07-02-2006
Dr Russell Newcome on the ACMD report on cannabis

Russell Newcombe, Lifeline Publications, Manchester; February 2006
In 2002, the Advisory Council on the Misuse of Drugs (ACMD) reviewed the evidence about the harmfulness of cannabis, and advised the government that it should be downgraded from Class B to C. So, in January 2004, the government amended the 1971 Misuse of Drugs Act to put all cannabis products in Class C. This meant a reduced maximum sentence of two years for cannabis possession, though the 14 year penalty for trafficking offences remained, because penalties for trafficking Class C drugs were simultaneously increased to those of Class B drugs. Around the same time, the police also adjusted their policies to allow possession of cannabis to be dealt with by Formal Warnings, rather than arrest followed by a caution or prosecution. But in March 2005, the Home Secretary asked the ACMD to review its advice on the reclassification of cannabis ‘ because of new research between 2002 and 2005 which suggested a link between cannabis use and mental disorder – or more likely because the tabloid press raised the political heat with their ‘Skunk is Turning Our Kids Schizo’-type headlines.
The ACMD published their report – Further Consideration of the Classification of Cannabis ‘ in January 2006. While focusing on mental health issues, the report also briefly addressed physical health and potency issues. On physical health, they noted that apart from possible respiratory damage among those who smoke cannabis, the main risks are to people with health problems and pregnant women. As regards potency, they emphasised that the purity figures produced from forensic analyses of seized cannabis are beset by methodological problems, and concluded that annual figures for the decade ending 2005 showed no evidence of trends. But when the figures are broken down by different products, they do show a clear rise in potency for sinsemilla (skunk) ‘ from 6% in 1995 to 14% in 2005.
But mental health was the main concern, and the report proposes that there are six main links between cannabis use and mental disorder: dependence, psychological and behavioural impairment, acute intoxication, depression and anxiety, relapse in schizophrenics, and psychosis (including schizophrenia). Dependence and intoxication-related mental and behavioural disorders (MBDs) are probably the two most common psychological problems found among cannabis users, and the ones really worthy of more research attention ‘ even though, as the ACMD note, compared with heroin dependence and the gross effects of alcohol on cognition and behaviour, they are far less likely and far less serious. Research reporting links with depression and anxiety is described as ‘not persuasive’, due to methodological limitations, and their small and inconsistent findings. But the ACMD conclude that ‘there is clear evidence that the use of cannabis may worsen the symptoms of schizophrenia and lead to relapse in some patients.’ (4.4) ‘ though this is widely accepted and uncontroversial. They also noted that cannabis use may be popular among schizophrenics because it reduces symptoms ‘ of both the illness and medication.
The fifth condition covered is acute intoxication ‘ the cannabis equivalent of being very drunk on alcohol, characterised by confusion, paranoia and panic. The report notes that in the most extreme cases, treatment for ‘a temporary psychotic state’ is required in hospital for a few days (about 100-140 cases a year in England). However, no mention whatsoever is made of two other cannabis-related MBDs listed in the latest International Classification of Diseases (ICD10), which have a similar annual level of cases – ‘cannabis psychosis’ (300-400) and ‘harmful use’ (100-125). Since both MBDs are of dubious validity, falling between the stools of acute intoxication and cannabis-triggered schizophrenia, I sympathise with the ACMD’s desire to ignore them, but they surely require addressing in a report such as this. In particular, cannabis psychosis (coded F10.5 in ICD10) sounds about as close as you can get to cannabis-induced schizophrenia without actually being it, so its difficult to see why it was passed over. Perhaps because, in reality, cannabis psychosis is nothing more than the extreme end of acute intoxication. For instance, hospitalised cases of cannabis psychosis have very similar demographic characteristics to acute intoxication cases (eg. mid-20s, compared with a mean age of 40 for schizophrenics), and are also typically released within a month ‘ compared with four or five months for schizophrenics. Similar points can be made about ‘harmful cannabis use’. Hopefully, ICD-11 will be based on a thorough review of categories of mental disorder ‘ including the deletion of ‘cannabis psychosis’ and ‘harmful cannabis use’.
Turning to the sixth and main issue, they note that research on the links between cannabis use and psychosis has many methodological problems ‘ including the use of symptoms rather than full-blown mental illness as the ‘measure’ of psychosis; and the neglect of the effects of poly-drug use and other confounding variables. But the point that most studies focus on psychotic symptoms rather than illnesses should have been given more weight than it was, because there are several reasons why cannabis users may be more likely to report psychotic symptoms ‘ not least of which is that such ‘symptoms’ (strange thoughts, hallucinations, etc.) may be the direct effects of cannabis intoxication! Even if drug-induced symptoms are ruled out by some studies, as the ACMD note, there is still the possibility that there are subtle confounding variables caught up with cannabis use that are the real triggers of psychotic symptoms/illness, rather than THC. Few studies mention these factors let alone rule them out ‘ for instance, stress from being involved in illegal activity; personality factors which lead to cannabis use also predisposing to psychosis; deeper inhalation of tobacco/nicotine by joint smokers; exposure to adulterants in cannabis, etc. etc..
The ACMD claimed that just five studies had enough methodolological ‘clout’ to be worth considering, though ‘only one study has used the appropriate measures, and has had the statistical power, to assess whether cannabis use precedes the onset of an illness that meets the full diagnostic criteria for schizophrenia’ (4.9.4). Furthermore, their report does not give details of the main problems with these five studies. For instance, the New Zealand study reported a significantly greater level of later adult experience of psychotic symptoms among teen cannabis users compared with non-users: 10% compared with 3%. Yet the former figure was based on just three out of 30 cannabis users in the sample ‘ if just one had answered differently, the figure would have dropped to 7% and the effect would have been non-significant. Also, although some of these studies go beyond the vague label of psychosis to suggest a link with schizophrenia, this itself is a broad heading for a group of distinct mental illnesses. Paranoid schizophrenia is often the implied type of schizophrenia in these studies, but they are rarely explicit or precise enough to incicate which type they are talking about.
In short, the ACMD report does not bother with the details of the five studies, but simply points to an existing review paper (Arsenault et al, 2004) and moves straight to the conclusions: ‘collectively, the weight of these studies suggests an association between cannabis use and the development of psychotic symptoms which is consistent between studies and which remains after adjustment for confounding factors (4.10.1). However, they also point out that this association is very small: ‘at worst, using cannabis increases the lifetime risk of developing schizophrenia by 1% (4.10.2)’. In short, adopting the ‘official estimate’ that 1% of the population gets diagnosed as schizophrenic (at the rate of about 35-40,000 a year), this indicates a rate of about 2% among the minority who use cannabis. The report further notes that one in four individuals are at greater genetic risk than others for developing schizophrenia if they use cannabis, referring to a recent study which found an association between having two defective copies of the COMT gene and adult psychosis in people who used cannabis during their teens ‘ an example of how cannabis use can trigger psychosis in the genetically predisposed individual.
But the report pays no attention to the arguments and evidence concerning trends in levels of cannabis use and psychosis. That is, if cannabis use causes psychotic disorders like schizophrenia, then there should be a significant correlation between trends across time in the two variables. Yet studies in both Australia (Hall) and the UK (me) have reported that there is no such relationship. Similarly, recent research has also found anti-psychotic effect for CBD, a cannabinoid found mainly in resin rather than skunk, though this is also left unmentioned by the report.
The ACMD conclude that ‘the consumption of cannabis is neither a necessary nor a sufficient cause for the development of schizophrenia’ (6.4), reflecting the two facts that (a) 90% of schizophrenia episodes are not triggered by cannabis use, and (b) only a quarter of us have the genetic predisposition required for cannabis use to bring about schizophrenia – and other factors are also likely to be involved. They recommend that ‘cannabis products should remain Class C’ (6.6), giving the four main reasons for this advice as (1) that ‘at worst, the risk to an individual of developing schizophrenia as a result of using cannabis is very small’ (6.6.1); (2) cannabis is substantially less harmful than other Class B drugs (as well as alcohol and tobacco); (3) reclassification did not lead to an increased prevalence of use among young adults (but rather to a slight decline), and saved about 200,000 hours of police time; and (4) the potency of cannabis has not increased in the last decade (6.7). Lastly, there is no mention of the specific proposal voiced last year that, because of its relatively high THC content, skunk should be in Class B or A ‘ which is just as well, because it is both unjustifiable and unworkable. So, instead of returning cannabis to Class B, the ACMD recommend ‘a sustained public education and information strategy’, aimed at children and young adults (7.2); a review of health services for cannabis dependent people (7.3); measures to protect schizophrenics from exposure to cannabis (7.4); and, ‘a substantial research programme into the relationship between cannabis use and mental health’ (7.5).
Few people would question the recommendation for further research ‘ we need to understand more about the COMT gene and its triggers, and more about which consumption factors (dose, frequency etc) and other variables are involved in any triggering effect of cannabis. But the ACMD failed to suggest research into the adulterants in cannabis products. Yet, during research over the last decade, numerous cannabis users have complained to me about the increasing adulteration of cannabis ‘ particularly soap-bar resin, Britain’s most popular cannabis product, but also pesticides in skunk. Indeed, one small study of five soap-bar samples seized by Customs in 2001 found huge adulteration by many toxic substances, including soil, glue, engine oil and animal shit ‘ any of these adulterants could contribute to the triggering of psychotic symptoms in users. This problem is never mentioned in official reports, and whenever I have asked government officials about this (eg. at conferences), they simply shake their heads at me and reply with stuff like ‘there is no evidence whatsoever of the adulteration of cannabis’. Yes, but that’s because there has been no research, and cannabis is not routinely analysed for adulterants by the FSS like powdered drugs are. Indeed, the belief that cannabis resin is not adulterated is found only among people with no first-hand experience of the British cannabis market. I challenge anyone to show a piece of standard soap-bar to coffee-shop managers in Amsterdam, and try to find one who recognises it as cannabis resin. Most would find visual assessment enough, but smelling it usually confirms its fake status (smoking it is neither necessary nor advisable).
Finally, the ACMD also provide no rationale for why a drug described by them as relatively harmless should be made illegal to possess and use. Where is the evidence that levels of use or harm are reduced by prohibiting cannabis? Indeed, there is plenty of evidence to the contrary – that is, that banning cannabis has led to an increase in prevalence of use and harm. Although I am sure that the ACMD would reply that this broader question is outside their remit, it would have been so refreshing to see just one or two statements questioning the corrupt ideology of prohibition – that in order to protect people from hurting themselves with drugs, we need to criminalise them for their use, while maximising the harmfulness of the drugs (adulterants, high prices, etc.). Never was there a better target for the metaphor of the Emperor’s new clothes than the ‘war on drugs’.
In 2002, the Advisory Council on the Misuse of Drugs (ACMD) reviewed the evidence about the harmfulness of cannabis, and advised the government that it should be downgraded from Class B to C. So, in January 2004, the government amended the 1971 Misuse of Drugs Act to put all cannabis products in Class C. This meant a reduced maximum sentence of two years for cannabis possession, though the 14 year penalty for trafficking offences remained, because penalties for trafficking Class C drugs were simultaneously increased to those of Class B drugs. Around the same time, the police also adjusted their policies to allow possession of cannabis to be dealt with by Formal Warnings, rather than arrest followed by a caution or prosecution. But in March 2005, the Home Secretary asked the ACMD to review its advice on the reclassification of cannabis ‘ because of new research between 2002 and 2005 which suggested a link between cannabis use and mental disorder – or more likely because the tabloid press raised the political heat with their ‘Skunk is Turning Our Kids Schizo’-type headlines.
The ACMD published their report – Further Consideration of the Classification of Cannabis ‘ in January 2006. While focusing on mental health issues, the report also briefly addressed physical health and potency issues. On physical health, they noted that apart from possible respiratory damage among those who smoke cannabis, the main risks are to people with health problems and pregnant women. As regards potency, they emphasised that the purity figures produced from forensic analyses of seized cannabis are beset by methodological problems, and concluded that annual figures for the decade ending 2005 showed no evidence of trends. But when the figures are broken down by different products, they do show a clear rise in potency for sinsemilla (skunk) ‘ from 6% in 1995 to 14% in 2005.
But mental health was the main concern, and the report proposes that there are six main links between cannabis use and mental disorder: dependence, psychological and behavioural impairment, acute intoxication, depression and anxiety, relapse in schizophrenics, and psychosis (including schizophrenia). Dependence and intoxication-related mental and behavioural disorders (MBDs) are probably the two most common psychological problems found among cannabis users, and the ones really worthy of more research attention ‘ even though, as the ACMD note, compared with heroin dependence and the gross effects of alcohol on cognition and behaviour, they are far less likely and far less serious. Research reporting links with depression and anxiety is described as ‘not persuasive’, due to methodological limitations, and their small and inconsistent findings. But the ACMD conclude that ‘there is clear evidence that the use of cannabis may worsen the symptoms of schizophrenia and lead to relapse in some patients.’ (4.4) ‘ though this is widely accepted and uncontroversial. They also noted that cannabis use may be popular among schizophrenics because it reduces symptoms ‘ of both the illness and medication.
The fifth condition covered is acute intoxication ‘ the cannabis equivalent of being very drunk on alcohol, characterised by confusion, paranoia and panic. The report notes that in the most extreme cases, treatment for ‘a temporary psychotic state’ is required in hospital for a few days (about 100-140 cases a year in England). However, no mention whatsoever is made of two other cannabis-related MBDs listed in the latest International Classification of Diseases (ICD10), which have a similar annual level of cases – ‘cannabis psychosis’ (300-400) and ‘harmful use’ (100-125). Since both MBDs are of dubious validity, falling between the stools of acute intoxication and cannabis-triggered schizophrenia, I sympathise with the ACMD’s desire to ignore them, but they surely require addressing in a report such as this. In particular, cannabis psychosis (coded F10.5 in ICD10) sounds about as close as you can get to cannabis-induced schizophrenia without actually being it, so its difficult to see why it was passed over. Perhaps because, in reality, cannabis psychosis is nothing more than the extreme end of acute intoxication. For instance, hospitalised cases of cannabis psychosis have very similar demographic characteristics to acute intoxication cases (eg. mid-20s, compared with a mean age of 40 for schizophrenics), and are also typically released within a month ‘ compared with four or five months for schizophrenics. Similar points can be made about ‘harmful cannabis use’. Hopefully, ICD-11 will be based on a thorough review of categories of mental disorder ‘ including the deletion of ‘cannabis psychosis’ and ‘harmful cannabis use’.
Turning to the sixth and main issue, they note that research on the links between cannabis use and psychosis has many methodological problems ‘ including the use of symptoms rather than full-blown mental illness as the ‘measure’ of psychosis; and the neglect of the effects of poly-drug use and other confounding variables. But the point that most studies focus on psychotic symptoms rather than illnesses should have been given more weight than it was, because there are several reasons why cannabis users may be more likely to report psychotic symptoms ‘ not least of which is that such ‘symptoms’ (strange thoughts, hallucinations, etc.) may be the direct effects of cannabis intoxication! Even if drug-induced symptoms are ruled out by some studies, as the ACMD note, there is still the possibility that there are subtle confounding variables caught up with cannabis use that are the real triggers of psychotic symptoms/illness, rather than THC. Few studies mention these factors let alone rule them out ‘ for instance, stress from being involved in illegal activity; personality factors which lead to cannabis use also predisposing to psychosis; deeper inhalation of tobacco/nicotine by joint smokers; exposure to adulterants in cannabis, etc. etc..
The ACMD claimed that just five studies had enough methodolological ‘clout’ to be worth considering, though ‘only one study has used the appropriate measures, and has had the statistical power, to assess whether cannabis use precedes the onset of an illness that meets the full diagnostic criteria for schizophrenia’ (4.9.4). Furthermore, their report does not give details of the main problems with these five studies. For instance, the New Zealand study reported a significantly greater level of later adult experience of psychotic symptoms among teen cannabis users compared with non-users: 10% compared with 3%. Yet the former figure was based on just three out of 30 cannabis users in the sample ‘ if just one had answered differently, the figure would have dropped to 7% and the effect would have been non-significant. Also, although some of these studies go beyond the vague label of psychosis to suggest a link with schizophrenia, this itself is a broad heading for a group of distinct mental illnesses. Paranoid schizophrenia is often the implied type of schizophrenia in these studies, but they are rarely explicit or precise enough to incicate which type they are talking about.
In short, the ACMD report does not bother with the details of the five studies, but simply points to an existing review paper (Arsenault et al, 2004) and moves straight to the conclusions: ‘collectively, the weight of these studies suggests an association between cannabis use and the development of psychotic symptoms which is consistent between studies and which remains after adjustment for confounding factors (4.10.1). However, they also point out that this association is very small: ‘at worst, using cannabis increases the lifetime risk of developing schizophrenia by 1% (4.10.2)’. In short, adopting the ‘official estimate’ that 1% of the population gets diagnosed as schizophrenic (at the rate of about 35-40,000 a year), this indicates a rate of about 2% among the minority who use cannabis. The report further notes that one in four individuals are at greater genetic risk than others for developing schizophrenia if they use cannabis, referring to a recent study which found an association between having two defective copies of the COMT gene and adult psychosis in people who used cannabis during their teens ‘ an example of how cannabis use can trigger psychosis in the genetically predisposed individual.
But the report pays no attention to the arguments and evidence concerning trends in levels of cannabis use and psychosis. That is, if cannabis use causes psychotic disorders like schizophrenia, then there should be a significant correlation between trends across time in the two variables. Yet studies in both Australia (Hall) and the UK (me) have reported that there is no such relationship. Similarly, recent research has also found anti-psychotic effect for CBD, a cannabinoid found mainly in resin rather than skunk, though this is also left unmentioned by the report.
The ACMD conclude that ‘the consumption of cannabis is neither a necessary nor a sufficient cause for the development of schizophrenia’ (6.4), reflecting the two facts that (a) 90% of schizophrenia episodes are not triggered by cannabis use, and (b) only a quarter of us have the genetic predisposition required for cannabis use to bring about schizophrenia – and other factors are also likely to be involved. They recommend that ‘cannabis products should remain Class C’ (6.6), giving the four main reasons for this advice as (1) that ‘at worst, the risk to an individual of developing schizophrenia as a result of using cannabis is very small’ (6.6.1); (2) cannabis is substantially less harmful than other Class B drugs (as well as alcohol and tobacco); (3) reclassification did not lead to an increased prevalence of use among young adults (but rather to a slight decline), and saved about 200,000 hours of police time; and (4) the potency of cannabis has not increased in the last decade (6.7). Lastly, there is no mention of the specific proposal voiced last year that, because of its relatively high THC content, skunk should be in Class B or A ‘ which is just as well, because it is both unjustifiable and unworkable. So, instead of returning cannabis to Class B, the ACMD recommend ‘a sustained public education and information strategy’, aimed at children and young adults (7.2); a review of health services for cannabis dependent people (7.3); measures to protect schizophrenics from exposure to cannabis (7.4); and, ‘a substantial research programme into the relationship between cannabis use and mental health’ (7.5).
Few people would question the recommendation for further research ‘ we need to understand more about the COMT gene and its triggers, and more about which consumption factors (dose, frequency etc) and other variables are involved in any triggering effect of cannabis. But the ACMD failed to suggest research into the adulterants in cannabis products. Yet, during research over the last decade, numerous cannabis users have complained to me about the increasing adulteration of cannabis ‘ particularly soap-bar resin, Britain’s most popular cannabis product, but also pesticides in skunk. Indeed, one small study of five soap-bar samples seized by Customs in 2001 found huge adulteration by many toxic substances, including soil, glue, engine oil and animal shit ‘ any of these adulterants could contribute to the triggering of psychotic symptoms in users. This problem is never mentioned in official reports, and whenever I have asked government officials about this (eg. at conferences), they simply shake their heads at me and reply with stuff like ‘there is no evidence whatsoever of the adulteration of cannabis’. Yes, but that’s because there has been no research, and cannabis is not routinely analysed for adulterants by the FSS like powdered drugs are. Indeed, the belief that cannabis resin is not adulterated is found only among people with no first-hand experience of the British cannabis market. I challenge anyone to show a piece of standard soap-bar to coffee-shop managers in Amsterdam, and try to find one who recognises it as cannabis resin. Most would find visual assessment enough, but smelling it usually confirms its fake status (smoking it is neither necessary nor advisable).
Finally, the ACMD also provide no rationale for why a drug described by them as relatively harmless should be made illegal to possess and use. Where is the evidence that levels of use or harm are reduced by prohibiting cannabis? Indeed, there is plenty of evidence to the contrary – that is, that banning cannabis has led to an increase in prevalence of use and harm. Although I am sure that the ACMD would reply that this broader question is outside their remit, it would have been so refreshing to see just one or two statements questioning the corrupt ideology of prohibition – that in order to protect people from hurting themselves with drugs, we need to criminalise them for their use, while maximising the harmfulness of the drugs (adulterants, high prices, etc.). Never was there a better target for the metaphor of the Emperor’s new clothes than the ‘war on drugs’.
Link to the Home Office Report (PDF)
