Résumé du résumé : on s'en doutait un peu mais c'est désormais confirmé : les psychoses et schizophrénies attribuées au cannabis ne sont pas dues aux composants naturels de la plante, mais bien plutôt aux produits chimiques toxiques contenus dans les savonnettes de hasch (voir l'étude du CRISP en fin de message).
D'où le cri d'alarme du Dr Newcombe :
« De toute évidence, il s'agit d'un problème de santé publique pouvant affecter des millions de personnes, la plupart d'entre eux n'étant pas conscients du fait qu'ils s'exposent eux-mêmes à un cocktail de substances chimiques toxiques à chaque fois qu'ils fument ou ingèrent du haschich en barrettes. Et c'est un problème qui ne sera pas aisément traité tant qu'une politique internationale de prohibition empêchera les gouvernements nationaux de développer la seule stratégie pragmatique capable de protéger ses citoyens consommateurs de cannabis : fournir un approvisionnement légal de cannabis de qualité contrôlée, et/ou autoriser la culture pour usage personnel.»
[Traduction perso : Raph <raph_cannabistrot.net>]
Introduction. Des publications récentes ont conclu que la notion de psychose induite par l'usage de cannabis manquait de validité conceptuelle et empirique. Cet article (résumé d'un long rapport non publié - Newcombe 2004) se focalise sur la 'vraie' psychose de cannabis (PC) - un trouble psychique unique résultant d'une intoxication aux cannabinoïdes, persistant au-delà de leur métabolisation et survenant en l'absence de prédisposition à la psychose.
Méthodes. Une étude de recherche documentaire a été conçue pour évaluer l'hypothèse que l'usage de cannabis (UC) est une cause de psychose, soit générale (schizophrénie) soit unique (vraie PC). Cette hypothèse a engendré deux pronostics testables : (1) les tendances à UC et PC doivent être positivement corrélées et (2) les caractéristiques démographiques et de traitement des cas de PC doivent différer des profils de chacun des cas de schizophrénie et autres désordres mentaux et comportementaux liés au cannabis (DMC) définis par le DCI-10 : l'intoxication de cannabis notablement aiguë (ICA) et l'usage nocif de cannabis (UNC).
Les statistiques officielles nationales ont été rassemblées à partir de (a) le nombre annuel et les caractéristiques des cas diagnostiqués de schizophrénie et de DMC liés au cannabis en Angleterre de 1998-99 (1995-96 pour la PC) à 2002-03 (Statistique Hospitalière); et (b) la fréquence des UC lors des années passées, parmi les 16-59 ans en Angleterre et au Pays de Galles, pendant la décennie s'achèvant en 2002-03 (Enquête sur la criminalité Britannique).
Résultats. Le taux annuel de PC parmi les UC anglais était en moyenne aussi bas qu'un pour 10.000. Mais bien que l'UC des années précédentes ait grimpé de 2,55 million (8,7 %) en 1994 à 3,36 millions (10,9 %) en 2002-03, il n'y a pas eu d'évolution significative (clear trend) soit des schizophrénies (36.000-38.500 cas annuels) soit des cas de PC (280-380). Chacun des deux pronostics ont été infirmés. Premièrement, la corrélation entre les UC et le nombre de PC, comparés sur une période de six années, s'est révélée petite et non significative. Deuxièmement, bien que les cas de PC différaient clairement des cas de schizophrénie - l'âge moyen des PC étant de 15 ans plus jeune que l'âge moyen des cas de schizophrénie, et la durée d'hospitalisation moyenne pour PC étant d'un mois seulement contre 4 à 5 mois pour les schizophrénies - leur profil était très semblable à chacun des cas d'ICA et d'UNC. Enfin, la recherche de preuves au sujet de la consommation de cannabis au cours de la période étudiée n'a trouvé aucun changement significatif des variables appropriées (par ex. le dosage, la puissance du taux de THC).
Conclusions. Il n'existe aucun élément tangible pour prétendre que l'usage de cannabis peut causer une psychose, ni une "vraie" PC. Au lieu de cela, les cas de PC étaient probablement des diagnostics erronés de cas extrêmes d'ICA et d'UNC, et/ou de DMC résultant d'un usage d'autres ou de plusieurs drogues. Une recherche urgente est nécessaire pour déterminer quels ingrédients du cannabis sont responsables des désordres mentaux attribués à son usage, en particulier depuis que la substance britannique la plus populaire - la savonnette de hasch marocain - est altérée par des produits chimiques toxiques.
Fin de la conclusion :
Selon l'étude Atha (2001), une majorité avérée d'usagers de cannabis, bien au-delà de 2 millions, sont actuellement, selon tout probabilité, des consommateurs de haschich en barrettes, avec un usage régulier moyen équivalent à une ounce par mois (environ 30 g). Par conséquent, les psychoses et autres problèmes de santé attribués à l'usage de cannabis en Angleterre peuvent vraisemblablement être attribués à une ou plusieurs substances diverses telles que la colle ou la ketamine - plutôt qu'aux cannabinoïdes. Des recherches complémentaires sont donc rapidement nécessaires pour identifier les substances chimiques que les usagers de cannabis consomment effectivement ; et pour évaluer les effets qu'un usage régulier de ces substances peut entraîner sur leur santé mentale et physique.
De toute évidence, il s'agit d'un problème de santé publique pouvant affecter des millions de personnes, la plupart d'entre eux n'étant pas conscients du fait qu'ils s'exposent eux-mêmes à un cocktail de substances chimiques toxiques à chaque fois qu'ils fument ou ingèrent du haschich en barrettes. Et c'est un problème qui ne sera pas aisément traité tant qu'une politique internationale de prohibition empêchera les gouvernements nationaux de développer la seule stratégie pragmatique capable de protéger ses citoyens consommateurs de cannabis : fournir un approvisionnement légal de cannabis de qualité contrôlée, et/ou autoriser la culture pour usage personnel.
Date: Thu, 14 Apr 2005 00:35:17 +0200
From: Peter Webster <firstname.lastname@example.org>
Subject: [DN] Does Cannabis Use Cause Psychosis? A Study Of Trends
DOES CANNABIS USE CAUSE PSYCHOSIS? A STUDY OF TRENDS IN CANNABIS USE AND PSYCHOSIS IN ENGLAND, 1995-2003
Dr. R.D. Newcombe, Liverpool John Moores University, Liverpool, England
Introduction. Recent literature reviews have concluded that the notion of cannabis-induced psychosis lacks conceptual and empirical validity. This paper focuses on 'true' cannabis psychosis (CP) - a unique mental disorder arising from intoxication by cannabinoids, persisting beyond their metabolisation, and occurring without predisposition to psychosis.
Methods. A documentary research study was designed to evaluate the hypothesis that cannabis use (CU) is a cause of psychosis either general (schizophrenia) or unique (true CP). This hypothesis generated two testable predictions: (1) trends in CU and CP should be positively correlated, and (2) the demographic and treatment characteristics of CP cases should be different from the profiles of both cases of schizophrenia and other cannabis-related mental and behavioural disorders (MBDs) defined by ICD-10 notably acute cannabis intoxication (ACI) and harmful cannabis use (HCU). National official statistics were collected on (a) the annual number and characteristics of diagnosed cases of schizophrenia and cannabis-related MBDs in England from 1998/99 (1995/96 for CP) to 2002/03 (Hospital Episode Statistics); and (b) the prevalence of past-year CU among 16-59s in England & Wales in the decade ending 2002/03 (British Crime Survey).
Findings. The annual rate of CP among English CUs was typically as low as one in 10,000. But although past-year CU climbed from 2.55 million (8.7%) in 1994 to 3.36 million (10.9%) in 2002/03, there were no clear trends in either schizophrenia (36,000-38,500 cases annually) or CP cases (280-380). Both predictions were disconfirmed. First, the correlation between CU and CP numbers over six comparison years was found to be small and non-significant. Second, although CP cases were clearly different from schizophrenia cases - including being a mean 15-years younger, and averaging one (rather than 4-5) months in-patient treatment - their profile was very similar to that of both ACI and HCU cases. Lastly, assessment of research evidence about cannabis consumption over the study period found no significant changes in relevant variables (eg. dosage, THC potency).
Conclusions. There was no support for the claim that cannabis use can cause psychosis, nor for a 'true' CP. Instead, CP cases were arguably misdiagnoses of extreme cases of ACI and HCU, and/or MBDs arising from other/multiple drug use. Urgent research is also needed into which ingredients of cannabis are responsible for any mental disorders which are attributed to its use, particularly since Britain's most popular product - Moroccan soap-bar/formula - is routinely adulterated with toxic chemicals.
Main abbreviations: CU cannabis use CUs cannabis users
CP cannabis psychosis ACI acute cannabis
intoxication HCU harmful cannabis use
THC tetrahydrocannabinol the main active ingredient among about a dozen
MBDs mental & behavioural disorders ICD-10 International
Classification of Diseases, 10th revision
HES Hospital Episode Statistics BCS British Crime Survey
DOES CANNABIS USE CAUSE PSYCHOSIS? A STUDY OF TRENDS IN CANNABIS USE AND
PSYCHOSIS IN ENGLAND, 1995-2003
Dr. R.D. Newcombe, School of Psychology, Liverpool John Moores University,
Edited version published in Adiktologie, 4(4), 492-507 (2004).
Background. Does cannabis use cause psychosis? There are two main versions of this argument, which are not always identified explicitly by researchers: (1) cannabis use is a cause of general schizophrenia; and (2) cannabis use is the cause of a unique schizophrenia-like psychosis (cannabis psychosis). A comprehensive review of the literature is outside the scope of this paper, but two major reviews have been published which provide useful definitions and conclusions (see also Castle & Murray 2004). First, Poole & Brabbins (1996) reviewed the literature on drug psychoses in general, and their 4-point definition of 'true drug-induced psychosis' has been adapted for use in the present study: 1. There are psychotic symptoms arising from intoxication which persist beyond the metabolic elimination of the drug this distinguishes drug psychosis from short-term psychological reactions to drugs, notably acute intoxication (see below);
2. The psychosis generally remits if abstinence is continued, but recurs if the drug is used again;
3. The onset and development of the psychosis is related to the drug (consumption factors), set (biological and psychological factors), and setting (socio-cultural factors);
4. Drug psychosis has a different structure and process to standard functional psychosis, and, like other drug-related mental disorders, has specific diagnostic criteria - otherwise there would be no need to distinguish it from either general schizophrenia or drug dependence etc..
Poole & Brabbins concluded that the empirical evidence did not support the existence of such a 'drug-induced psychosis', and that we should "discontinue use of the term ... which is ambiguous and unsustainable" (1996: 137).
Second, Hall (1998) focused on the literature on cannabis psychosis (CP), concluding that there was much support for the hypothesis that cannabis use (CU) increases symptoms of manifest schizophrenia, and some support for the hypothesis that it triggers latent schizophrenia. However, there was little support for 'true' CP - the hypothesis that CU causes a psychosis which would not otherwise have occurred (i.e. no family or personal history of psychosis), and which endures beyond its metabolisation but usually remits with continued abstinence. Hall concluded that if true CP exists, it would have to be very rare, and "would require very high doses of THC, the prolonged use of highly potent forms of cannabis... [or] concurrent use of amphetamines" (Hall, 1998: 433). He argued that claims about the existence of 'true' CP are typically based on research with conceptual and methodological flaws. Clearly, more well-designed studies employing a variety of approaches are required to properly evaluate the theoretical and empirical validity of this 'alleged' mental disorder. The rationale for testing the hypothesis of a causal relationship between cannabis use and psychosis has been spelled out by Hall (1998): 1 Cannabis use should precede psychosis in individual cases; 2 There should be a positive association between cannabis use and psychosis (across groups, time, etc.);
3 The role of other potential causal factors should be excluded (or else quantified) - such as other drugs used by cannabis users, and/or psychological predispositions to both CU and psychosis.
The study reported here focused on assessing the second of these three types of evidence, though also examined some key evidence under the third type, namely trends in cannabis consumption. The rationale is based on the argument of Hall & Solowij (1997) that although CU can trigger pre-existing psychoses, "it is less likely that cannabis use can precipitate schizophrenic illness that would not otherwise have occurred, because the incidence of schizophrenia has not increased in countries such as Australia, which have had dramatic increases in the prevalence of adolescent cannabis use over the past two decades" (p.108). It also follows on from Hall and his colleagues' more recent conclusion from a study of the prevalence of cannabis use and schizophrenia in Australia between 1940 and 1979: "cannabis use does not appear to be causally related to the incidence of schizophrenia" (Degenhardt, Hall & Lynskey, 2003: 37).
Aims and rationale. The present study examined national official statistics for England between the mid-1990s and 2002/03 on (1) the number of cannabis users (CUs), and (2) the number and characteristics of diagnosed cases of both general schizophrenia and cannabis-related disorders, notably CP. The main aim was to assess the relationship between trends in the prevalence of CU and diagnoses of psychosis, though a secondary aim was to assess whether the characteristics of CP cases were different from those of other mental disorders related to either cannabis use or general psychosis (see below).
What is the official status of CP in England? British psychiatrists employ the 10th revision of the International Classification of Diseases (ICD-10) to classify drug-related mental and behavioural disorders (MBDs). Depending on which of ten psychoactive drug groups is involved - alcohol, opioids, cannabinoids, sedatives, cocaine, other stimulants (notably amphetamines), hallucinogens (notably LSD and magic mushrooms), tobacco, volatile substances (solvents), and other/unspecified drugs these disorders are coded as F10 to F19. Sartorious (1992), the WHO Director of Mental Health, has advised that MBDs should be attributed to a single drug - the one most frequently used - whenever possible (see Discussion); and, that identification of the causal drug(s) should be based on more than one source of evidence, including self-reports, reports by third parties, tests of body fluids, and clinical observations. ICD-10 makes ten more distinctions between types of disorder across all ten drug groups: acute intoxication (F1x.0), harmful use (F1x.1), dependence (F1x.2), withdrawals (F1x.3), withdrawals with delirium (F1x.4), psychosis (F1x.5), amnesia (F1x.6), and residual psychosis (F1x.7) along with other disorders (F1x.8), and unspecified disorders (F1x.9). As well as being associated with specific diagnostic criteria (signs/symptoms), most of the eight main groups of MBDs also have sub-types based on the predominant signs/symptoms. In short, the ten groups of mental disorders include three related to addiction (dependence, and withdrawals with or without delirium); two based on psychosis (regular and residual psychosis); three groups based on more transient disorders typically related to consumption factors (acute intoxication, harmful use, amnesia); and two miscellaneous groups (other and unspecified).
As these groupings suggest, there are similarities between the clinical definitions and a fair amount of 'overlap' between the diagnostic criteria for the five main MBDs and their sub-types. Acute intoxication is defined as a transient disorder arising directly from drug consumption, based on "disturbances in the level of consciousness, cognition, perception, affect or behaviour, or other psychophysiological functions and responses" (p.73) but without more persistent problems being present, as with harmful use or psychosis. It usually arises from use of high doses, so the symptoms gradually lessen over time, and complete recovery within a few days to a few weeks is the norm (if the patient abstains). Acute intoxication on alcohol is 'drunkenness', while acute intoxication on hallucinogens includes 'bad trips'. Harmful use is vaguer but fairly similar - diagnosis requires evidence that physical or psychological harm has been caused to the user (including impaired judgement or dysfunctional behaviour), and that drug use was substantially responsible for this damage. The main difference from acute intoxication is that harmful use may arise gradually over time from regular drug use, as well as from a single large dose. Drug-induced psychosis also arises from psychological or behavioural changes which begin during intoxication or within 48 hours of drug use, but which persist beyond both intoxication and metabolisation. The key symptoms are hallucinations and perceptual distortions (especially auditory), delusions (especially paranoid), ideas of reference, psychomotor disturbances (excitement or stupor), abnormal affect (eg. intense fear, ecstasy), and some clouding of consciousness (though severe confusion is rare). Sartorious states that when the drugs taken are hallucinogens (eg. LSD, cannabis), a diagnosis of drug psychosis requires more than just hallucinations or perceptual distortions - these symptoms alone would be more consistent with acute intoxication. It must also be distinguished from schizophrenia triggered or exacerbated by drug use. With continued abstinence, drug psychosis typically resolves at least partially within one month, and fully within six months. The same definition applies to residual psychosis, which seems to be distinguished from drug psychosis only by its identification of six conditions characterised by particular psychotic symptoms - namely flashbacks, personality or behaviour disorder, residual affective disorder, dementia, other persisting cognitive disorder, and late-onset psychotic disorder. Lastly, the drug-induced amnesia syndrome is based on chronic impairment of recent memory, usually along with disturbances of time sense in short, a highly specific memory disorder, in which other cognitive functions are generally unaffected (Note 1).
Furthermore, if the MBDs described above are unique conditions, then cases of each should be distinguishable not only by clear clinical definitions and diagnostic criteria (symptoms), but also by their demographic and treatment characteristics. This reasoning is based on the general observation that different types of mental disorder (a) disproportionately affect people in particular demographic groups (eg. sex, age, race) and (b) require different medical interventions (eg. admission, treatment duration and type). Consequently, in addition to assessing relationships between trends in the number of CUs and diagnoses of schizophrenia/CP, the present study also compared the limited official statistics available on the characteristics of diagnosed cases of CP, acute cannabis intoxication (ACI), harmful cannabis use (HCU), and general schizophrenia (see Methods).
In summary, the present study assessed the formal hypothesis that cannabis use can cause either a general psychosis (schizophrenia) or unique psychosis (true CP). Two testable predictions were derived from this hypothesis. First, between the mid-1990s and 2002/03, there should be a significant positive correlation between the annual number of past-year CUs and the annual number of cases of CP (while the population rate of CP cases should remain reasonably stable). Second, if CP is a unique mental disorder, cases should have a notably different demographic and treatment profile compared with cases of schizophrenia, and with cases of ACI and HCU. Lastly, the available evidence about trends in cannabis consumption over the same period was also examined, in order to check for the possible effects of potential confounding variables - such as frequency of cannabis use, THC potency, and other drug use on trends in relevant MBDs. 2. Methods of investigation
2.1 Data-collection research instruments and procedures
The documentary research method involves the identification, collection and processing of pre-existing information. In the present study, the main sources of documentary evidence were national official statistics deriving from monitoring systems and surveys, notably two key sources: Hospital Episode Statistics, and the British Crime Survey (a third source of independent evidence on cannabis consumption is discussed below). As with all official statistics, both sets of figures are based on various assumptions and procedures, which need to be clearly understood to make valid and reliable inferences.
First, the annual number and characteristics of primary diagnoses of general and drug-related MBDs by psychiatrists (based on ICD-10) are reported in the Department of Health's Hospital Episode Statistics (HES). Each year's figures are based on 'finished' hospital episodes in England, which means any admissions in or before that year whose 'stay' finished in that year (continuing cases are not included). Detailed figures on the number and characteristics of all types of mental disorder are available for the 5-year period 1998/99-2002/03. Additional statistics on annual numbers were also available from 1995/96 for CP, and from as far back as 1989/90 for drug-related psychoses (Hansard 1999). Information about the characteristics of cases of cannabis-related MBDs (particularly CP and ACI) and schizophrenia during the main 5-year study period was also collected and compared namely: sex, age, admission status (emergency or not), and length of stay (number of days in-patient treatment).
Second, the prevalence of CU among adults in England & Wales has been reported by the British Crime Survey (BCS), based on representative samples of 10,000+ respondents initially on a two-yearly calendar basis, from 1992 to 2000 (Ramsay, Baker, Goulden, Sharp & Sondhi, 2001; and previous reports); but upgrading to annual surveys by financial years in 2001/02 and 2002/03 (Aust, Sharp & Goulden, 2002; Condon.& Smith, 2003). The BCS reports present both sample percentages and estimated population numbers/ranges for three types of prevalence and 10 groups of drugs. The authors of the BCS reports usually stress that these figures are likely to under-estimate rather than over-estimate the true number of CUs. Figures on the prevalence of lifetime use and recent (past-month) use can be accurately related to the survey year. But the prevalence of past-year use (the relevant indicator for present purposes) is based on self-reported behaviour in the 12 months prior to the survey. Since BCS interviews are generally conducted in the first six months of the survey year, figures on past-year use may largely or partly concern the previous year. However, since HES figures on MBDs exclude ongoing cases and include only finished episodes, it seems likely that some cases of CP or other MBDs may also have begun in the year prior to that in which they were reported. For these reasons, no temporal adjustments were made to the comparisons of the figures from each source except for matching calendar years to financial years (see below). The age-range of the BCS sample is 16-59 years (12-59 years in 1991), which further strengthens the basis for comparison with the HES figures, since over 99% of all cases of CP in the 5-year study period were aged 15 to 59 years.
The annual rates of CP cases among CUs in 1995/96, 1996/97, 1998/99, 2000/01, 2001/02 and 2002/03 were calculated by dividing the number of CP cases for each financial year by the estimated number of past-year CUs either in the same year (2001/02 and 2002/03), or the year with the closest calendar-year correspondence (1994, 1996, 1998 and 2000). The pairing of figures from the 1994 BCS with those in the 1995/96 HES is the only comparison in which the years do not either match or at least share eight months overlap. Thus, BCS figures on CU are 'missing' for just two of the eight successive years for which HES figures on CP are available - namely 1997/98 and 1999/2000. Another limitation of the CP rate estimated here is that the numerator (number of CP cases) relates to England only while the denominator (number of past-year CUs) relates to England and Wales though the resulting under-estimation of the CP rate is negligible.
In addition to the two sources of official national statistics, a third source of evidence involved the findings of annual surveys of several thousand cannabis users in Britain, conducted between 1994 and 2000 by the Independent Drugs Monitoring Unit (Atha 2001). This evidence was examined to identify trends in drug consumption among cannabis users over the study period - including frequency of use, amounts purchased and used, and other drugs used. Since these were potential confounding variables in the predicted correlation between the prevalence of cannabis use and CP trends, the aim was to assess whether there were signs of any similar positive associations between consumption trends and CP trends.
2.2 Data processing and statistical analysis
As regards the first prediction, parametric correlation was ruled out because of violated assumptions, including the Pearson test requiring a sample size of over 30, as well as normally distributed data, homoscedasticity, etc.. The chi-square test was also rejected as a tool of analysis for testing either prediction because of failure to meet applicability criteria for instance, the summarised form of this documentary data meant that it was not possible to check whether respondents were in more than one comparison group (eg. years, diagnostic categories). Consequently, the non-parametric Spearman Rank Correlation test was employed to assess the first prediction concerning the size and significance of correlations between the annual number of CUs and the annual number of CP cases over the six points of the study period. The Spearman test is less powerful than the Pearson test because it works with ordinal (rank-ordered) rather than interval-level data, thereby losing information about the size of the differences between scores/values. But the test requires a minimum sample size of just five, though an almost perfect correlation is required to achieve significance when N = 5. Thus, in practice, a minimum sample size of six is required which means that a correlation greater than 0.83 would be significant at the 95% probability level (0.89 for a two-tail test). Hence the inclusion of the 1994 BCS to compare with 1995/96 figures for CP, because this brings the number of comparison years to a total of six. Unfortunately, reports on the 1996, 1998 and 2000 BCS did not present population numbers for past-year CUs and the reported sample rates for past-year CUs were also rounded to the nearest whole percentage (9% in each year). Consequently, the number of past-year CUs for these three years had to be estimated employing census statistics. Given the rounded-up 9% sample rate presented for each year, this produced an estimate of about 2.75 million for each of the three years - a 'plateau phase' in an otherwise steady upward trend.
Lastly, no attempts were made to correlate annual numbers of CUs with annual numbers of cases of general schizophrenia, ACI or HCU - because paired values were available for only four of the five years on which statistics were available for these three MBDs, and, as noted, a Spearman test requires six points to be feasible.
Before turning to the findings relevant to the two predictions (3.3 and 3.4), it will first be useful to summarise two sets of relevant figures from the main sources for the present analysis, namely: the prevalence of CU (3.1); and, the annual numbers of cannabis-related MBDs and general schizophrenia cases (3.2). The final section (3.5) assesses the available evidence about a set of potential confounding variables: trends in cannabis consumption.
3.1 Prevalence of cannabis use
According to the BCS, the estimated number of lifetime CUs in England & Wales more than doubled during the 1990s - climbing from 4.2 million in 1992 to 6.6 million in 1996, 8.2 million in 1998, and 10.1 million in 2000 (not reported after 2000). Following earlier estimates for 1981 (2%) and 1983 (4%), the past-year prevalence of CU continued to climb from the start of the 1990s - 5% in 1992, 8.7% in 1994, hovering around 9% from 1996 to 2000, then climbing again to 10.6% in 2001/02, and 11.3% in 2002/03. In population numbers, this represents a rise in past-year CUs from 1.3 million in 1992 and 2.55 million in 1994, through around 2.75 million in 1996, 1998 and 2000, to 3.29 million in 2001/02 and 3.36 million in 2002/03 (Table 2). The reliability of the BCS figures was confirmed by the findings of the British Psychiatric Morbidity Survey of 8,900 16-75 year olds in 2000 - 10% reported past-year CU, the same rate as in the 2000 BCS (Office for National Statistics 2001).
3.2 Annual numbers of cases of cannabis-related and schizophrenic mental disorders
The total number of drug-related psychoses gradually trebled from 860 in 1989/90 to 2,530 in 1994/95, before falling again through second half of the 1990s, but then rising again in the 2000s, reaching 2,327 in 2002/03 - the highest number reported except for 1994/95 (Hansard 1999; DOH 2004). In the 8-year period from 1995/96 to 2002/03, the annual proportion of drug-related psychoses involving CP varied erratically between 14% and 21%. The total number of cannabis-related MBDs fell from 669 in 1998/99 to 626 in 2000/01, before rising up to 788 in 2002/03 (Table 1). The proportion of cannabis-related MBDs classified as CP cases approached half in each year (43%-48%), making CP the most common cannabis-related MBD (280-380 cases per year). The only other two common cannabis-related MBDs were ACI (about 110-140 cases per year) and HCU (about 90-120 cases per year). Together, these three disorders consistently accounted for 86-87% of the annual number of cannabis-related MBDs (excluding unspecified disorders which doubled from 46 in 1998/99 to 92 in 2002/03). That is, the other four specified cannabis-related MBDs were fairly rare, including dependence (45-60 cases per year), related withdrawals (10-25 cases per year), residual psychoses (3-11 cases per year) and amnesia (0-6 cases per year).
Both the annual number of cases of 'general' schizophrenia (all sub-types) and 'regular' schizophrenia (main sub-type) followed a similar course to cannabis-related MBDs, dropping steadily from 1998/99 to 2000/01, before slowly rising again up to 2002/03. In short, there were no clear, consistent trends - about 36,000 to 38,500 cases of general schizophrenia each year, of which about two-thirds were 'regular' (unprefixed) schizophrenia (Table 1). The other three most common types of general schizophrenia, each numbering about 2,000-4,500 cases per year, were schizo-affective disorder, acute and transient psychotic disorders, and persistent delusional disorder. The first two types exhibited fairly stable (unchanging) trends over the five-year period, though there was a minor but consistent trend for persistent delusional disorder, which declined steadily from 3,019 to 2,442. These statistics are consistent with independent evidence that the rate of schizophrenia has remained below 0.5% over the last decade - the population rate of psychosis reported by the survey of mental disorder in Britain in 1993/94 (OPCS 1995).
Table 1: The annual number of cases of (a) cannabis-related mental
disorders, and (b) general and regular schizophrenia - England 1998/99-2002/03
98-99 99-00 00-01 01-02 02-03
Cannabis-related MBD 669 632 626 741 788
Psychosis 296 279 287 322 380
Acute intoxication 134 107 122 140 127
Harmful use 115 109 88 117 97
Dependence 45 45 48 59 51
delirium 4 3 6 12 13
Withdrawals 11 8 7 11 8
Residual psychosis 11 11 6 6 3
Amnesia 5 6 6 0 2
Other 2 8 9 9 15
Unspecified 46 56 47 65 92
General schizophrenia 38517 36806 36109 37086 37736
Regular schizophrenia 25967 24696 24454 25224 25269
Source: Dept. Health (2000-04). Hospital Episode Statistics (primary
diagnoses & finished episodes)
In summary, there were no signs of any consistent rising or falling trends in either the number of cases of cannabis-related MBDs or general schizophrenia, nor in their main sub-types CP and regular schizophrenia respectively.
3.3 Relationship between cannabis use and cannabis psychosis
Turning to the first of the two predictions, Table 2 shows the annual number of past-year CUs and the annual number of diagnosed cases of CP for the six years between 1995/96 and 2002/03 for which both sets of figures were available. It can be seen that there was a gradual rise in the number of past-year CUs (with a plateau phase in the middle years), though the number of CP cases exhibited no clear trend. The Spearman Rank Correlation Test was used to assess the size and significance of the relationship between the two sets of rank-ordered figures. In order to achieve significance at the minimum 95% level of probability, the correlation would need to be greater than 0.89 (2-tailed) or 0.83 (one-tailed). But the test produced a small positive correlation of 0.37, which was clearly non-significant.
Additional analyses were conducted to assess whether the correlation was significant when the figures were adjusted to reflect plausible assumptions namely when (a) the annual number of past-year CUs exhibited a consistent, rising trend (rather than an intermediate plateau); and (b) the number of past-year CUs was estimated for the two missing years (1997/98 and 1999/2000), providing 8 points for correlation. However, the correlation remained small and non-significant in both cases.
Table 2: The number (%) of past-year cannabis users (CU), the number of
psychosis (CP) cases, and the rate of CP in England,
Hospital Episode Stats British Crime Survey (BCS) Rate of CP cases per
Year CP Year CU: number
(%) past-year cannabis users
1992 1,297,000 (5)
1995/96 360 1994 2,550,000 (8.7)
1996/97 280 1996 2,750,000* (9)
1998/99 296 1998 2,750,000* (9)
2000/01 287 2000 2,750,000* (9)
2001/02 322 2001/02 3,290,000 (10.6)
2002/03 380 2002/03 3,360,000 (10.9)
The annual rate of cannabis psychosis. Table 2 shows that the rate of CP in England - the number of cases divided by the number of past-year CUs though starting from a peak of 14 per 100,000 in 1995/96, remained fairly stable at around 10 per 100,000 in subsequent years, only changing again in 2002/03, when it rose slightly to 11 per 100,000. In short, the annual rate of CP was typically stable, hovering around one in 10,000 CUs or about one in 100,000 of the general adult population. Since only about 0.01% of CUs are diagnosed with CP over a typical year, this suggests that even the lifetime rate of CP is likely to be lower than 1%.This is supported by Atha's (2001) research on several thousand British CUs, which found in 1999 that less than 5% reported having experienced psychotic symptoms, with less than 1% reporting either regular or severe symptoms of psychosis.
There are also notable gender differences. The sex ratio of adult past-year CUs is generally around 65%-35% (eg. 12% for males and 7% for females in both the 2000 BCS and BPMS). But around eight in ten CP cases were male. Based on the 2001/02 BCS, the CP rate (about 10 per 100,000 overall), when adjusted for each sex, was about 14 per 100,000 for males (287 in 2,107,000), and about 3 per 100,000 for females (35 in 1,185,000). In short, the annual rate of CP is typically almost five times higher amongst male CUs compared with female users. Lastly, the BCS also indicates that there are notable racial differences in cannabis use . for instance, in 2001/02, past-year CU was around 5% for Asians, 11% for both Blacks and Whites, and 25% among Mixed Race respondents (Aust & Smith 2003). However, HES reports do not provide racial breakdowns, so no comparisons can be made with the BCS.
3.4 Characteristics of cases of three cannabis-related mental disorders and schizophrenia
Table 3 shows that the typical case of cannabis-related MBD was male (around eight in ten) and aged 26-27 years. About eight in ten were admitted as emergencies, and the mean duration of hospitalisation was about three to four weeks. CP cases were very similar in age and sex characteristics to the overall group, and to each of the two other main sub-groups of cannabis-related disorders (ACI and HCU). Over the 5-year period, CP cases were typically around a year older than ACI and HCU cases, though the only salient difference was that CP cases had longer stays in hospital - annual means ranged from 31 to 43 days, compared with 13-20 days for ACI, and 14-27 days for HCU. Glossing over these findings, it can be stated that the typical CP case is hospitalised for around four to five weeks, compared with about two weeks for ACI, and two to four weeks for HCU. Median figures, though smaller, reflected the same differences.
Table 3: The characteristics of hospital patients diagnosed with
disorders in England, 1998/99-2002/03 - with breakdowns for three
All cannabis-linked mental disorders Cannabis
Number Male Age Emerg Stay Number Male Age Emerg Stay
98-99 669 80% 26 79% 29 296 80% 26 83% 43
99-00 632 77% 27 83% 23 279 74% 27 86% 33
00-01 626 77% 27 86% 24 287 77% 26 80% 33
01-02 741 82% 26 83% 26 322 84% 26 73% 31
02-03 788 79% 27 80% 26 380 82% 27 81% 33
Acute cannabis intoxication Harmful cannabis use .
Number Male Age Emerg Stay Number Male Age Emerg Stay
98-99 134 78% 25 87% 20 115 82% 25 85% 14
99-00 107 80% 25 87% 15 109 78% 28 85% 15
00-01 122 73% 26 92% 15 88 86% 26 95% 18
01-02 140 78% 25 79% 13 117 81% 26 82% 27
02-03 127 72% 25 82% 13 97 80% 25 87% 21
Key: Age = mean age at admission Emerg = percentage of cases
where admission was an emergency
Stay = mean number of days between admission and discharge from
hospital (finished episode)
Source: Dept. Health (2000-04). Hospital Episode Statistics (primary
diagnoses & finished episodes)
In short, although the demographic characteristics of cases of CP, ACI and HCU were generally similar, there was a notable difference in duration of hospitalisation - typically up to twice as long for CP cases. However, it could be the 'labelling' of patients as CP cases rather than as just acutely intoxicated or harmed by their use of cannabis - which leads medical staff to retain them for treatment as in-patients for a longer period. Or, CP cases may simply be the more severe (extreme) forms of ACI and/or HCU.
One explanation for the lack of correlation between levels of CU and CP over the past decade in England is that psychiatrists may be wrongfully diagnosing some cases of CP as schizophrenia. However, this seems unlikely given the notably different characteristics of cases of general and regular schizophrenia compared with CP cases Table 4 shows that up to two-thirds of schizophrenics were male, and their mean age was around 40-41 years. Similarly, about two-thirds to three-quarters of cases each year were admitted as emergencies, and the mean 'stay' was 15 to 20 weeks. The only notable difference between schizophrenic patients overall and the main sub-category of 'regular' schizophrenia was that the former were generally hospitalised for a much shorter period - from about one to about three months, compared with about five months for 'regular' schizophrenia.
Table 4: The number and characteristics of hospital patients diagnosed with
general schizophrenia in England, 1998/99 to 2002/03
All schizophrenia-type disorders (F20-9) 'Regular'
schizophrenia (F20) .
Number Male Age Emerg Stay Number Male Age Emerg Stay
98-99 38,517 59% 41 68% 121 25,967 65% 40 66% 150
99-00 36,806 59% 41 77% 105 24,696 65% 40 75% 129
00-01 36,109 59% 41 77% 118 24,454 64% 40 76% 145
01-02 37,086 61% 41 73% 112 25,224 66% 41 72% 138
02-03 37,736 62% 41 71% 102 25,269 68% 40 69% 122
Key: Age = mean age at admission Emerg = percentage of cases
where admission was an emergency
Stay = mean number of days between admission and discharge from
hospital (finished episode)
Source: Dept. Health (2000-04). Hospital Episode Statistics (primary
diagnoses & finished episodes)
To summarise, in addition to exhibiting different signs and symptoms, the typical schizophrenic is notably different from the typical CP patient - for instance, they are about 15 years older on average, about 20% more likely to be female, up to 10% less likely to be admitted as an emergency, and spending a significantly longer time in hospital - about 4-5 months, compared with nearer 4-5 weeks for CP. These very different profiles suggest that the misdiagnosis of schizophrenia as CP is probably quite rare.
3.5 Trends in cannabis consumption
As noted earlier, the third rule of causality requires that other causal factors (confounding variables) be excluded (or at least quantified), if the empirical cause of an effect - i.e. the factor which both precedes and is associated with the effect - is to be confirmed as the only (or main) cause. Though assessment of all potential confounding variables is outside the scope of a single study, one variable closely related to prevalence of CU will be briefly assessed. That is, CP levels may also have been affected by changes in consumption factors beyond simple prevalence of use notably the amounts of cannabis used, the potency of THC, and the extent of use of other drugs. Annual surveys of several thousand CUs in the UK have been conducted by the Independent Drugs Monitoring Unit from 1994 to 2000, and remain the only source of evidence about changes in the behaviour and experiences of cannabis consumers in Britain over the last decade (Atha 2001). This study concluded that there have been few significant trends over the second half of the 1990s in either (a) cannabis consumption - including frequency of use, monthly amounts used, number of reefers smoked, and monthly spending - or (b) prevalence and frequency of use of other drugs by CUs. Similarly, though there have been many claims that the potency (THC content) of cannabis has increased since the 1960s, there is no evidence of this trend in Europe (European Union 2004). In Britain, the average THC content of cannabis has remained fairly constant at around 6%, though since 1990 there has been a polarisation effect. That is, the British market is now dominated by two products (Atha 2001): Moroccan resin, known as soap-bar (typically 1-3% purity) and hydroponic herbal cannabis, known as skunk (8-16% purity) though there is no evidence that the growing popularity of skunk since the mid-1990s was associated with any parallel trend in CP cases.
To summarise: an assessment of relevant official statistics and surveys in Britain over the last decade does not provide support for the hypothesis that use of cannabis causes psychosis, either general or unique. More specifically, it disconfirms two predictions derived from this hypothesis. First, while the prevalence of cannabis use exhibits a general upward trend, the number of diagnosed cases of CP have remained fairly erratic, with no clear trend resulting in a non-significant correlation between the two variables. Similarly, the number of cases of schizophrenic disorders in general have remained fairly constant, with no apparent rising/falling trends. Second, the characteristics of CP cases, though differing notably from those for schizophrenia cases, are fairly similar to those for ACI and HCU cases. Lastly, though it was not possible to assess the full range of potential confounding variables (i.e. to exclude all other possible causes of CP), a review of available evidence over the study period indicated no clear or relevant trends in the consumption of cannabis or other drugs among British cannabis users (amounts used, potency, etc.).
If CP is really a standard schizophrenia triggered by CU in some people, then it is not a unique mental disorder requiring a separate name - no more than a psychotic episode triggered by the death of a loved one needs to be identified as a unique 'bereavement psychosis'. Conversely, if CP is a unique syndrome arising from CU, then we would expect the number of CP cases to reflect an underlying positive correlation with the prevalence of CU - which they do not. But the present non-significant correlation between annual numbers of CUs and CP cases could be a statistical artifact, produced by problems in the recording, processing and reporting of information about hospital patients, as well as insufficient data at the present time (Note 2).
Regarding the second prediction, few characteristics of the patient or hospital episode distinguish CP from ACI or HCU, though they are notably different for cases of schizophrenia. Thus, though CP cases are very unlikely to be misdiagnosed cases of general schizophrenia, there is a strong possibility that most or all cases could actually represent misdiagnoses of (the more serious) cases of ACI and/or HCU particularly given the overlap in diagnostic criteria for these three MBDs. This is consistent with the fact that CP is only distinguishable from official characteristics of the latter two disorders by its tendency to require a few weeks more treatment on average (i.e. typically just over a month in hospital while schizophrenics usually require around 4-5 months in-patient treatment per episode, among other salient differences). Indeed, because THC is fat-soluble rather than water-soluble, heavy users find that it can take 30 days, or even longer, before their body fluids are clear of THC on drug tests. Thus, since the definition of a true drug-induced psychosis requires that the condition persists beyond the metabolic elimination of the drug, CP cases who are released from hospital within a month do not meet the definition of a true drug-induced psychosis - and so are arguably more likely to be cases of ACI or HCU.
An even more serious flaw in the ICD-10 guidelines is the advice that, in cases of poly-drug use, "the diagnosis of the disorder should be classified, whenever possible, according to the most important single substance (or class of substances) used" - where 'important' means the 'prime suspect', based on the criterion of "the drug or type of drug most frequently used" (Sartorious, 1992, p.72). The guidelines further state that 'multiple drug' attributions should be avoided unless their contribution is 'inextricably mixed' or the drug use is 'chaotic' (op. cit.). Since cannabis is one of the most frequently used illicit drugs among poly-drug users (perhaps only heroin has a higher proportion of daily users), it seems likely that it has often been routinely identified as the 'single drug' causing various MBDs, when other drugs were just as or even more likely to have been the cause (Note 3). For example, consider a scenario in which a poly-drug using man with no history of mental disorder has been admitted to hospital from a nightclub, exhibiting symptoms of drug-induced psychosis. He reported taking six tablets of ecstasy that night (MDMA confirmed by drug tests), and admitted using ecstasy (in similar doses) about twice a month, and smoking one or two 'joints' of cannabis on most days of the week. Under ICD-10 guidelines, his psychosis would be attributed to cannabis rather than ecstasy, based on the 'prime suspect' criterion of frequency of use - though the equally justifiable criteria of amounts used and recency of use each indicate ecstasy as the 'prime suspect'. Indeed, only alcohol is associated with a higher number of psychosis cases than cannabis (eg. 558 in 2002/03, compared with 380 for cannabis - and 190 for amphetamines, 53 for cocaine, and 41 for hallucinogens). But it should be noted that, despite the ICD-10 ruling that MBDs among poly-drug users should be routinely attributed to a single drug, multiple/other drug use is the most common attribution for drug-induced psychoses every year, typically accounting for just over half (though dropping to under half in 2002/03).
Indeed, as far as the development of an effective health policy is concerned, CP may be somewhat of a 'red herring', distracting the attention of researchers and policy-makers from more prevalent or problematic MBDs arising from drug use in general (eg. multi-drug psychoses) or cannabis use in particular (cf. Newcombe 1992). For instance, the British Psychiatric Morbidity Survey 2000 found that 3.1% of British adults self-reported cannabis dependence (Office for National Statistics 2001). This equates to about one in four past-year CUs experiencing dependence compared with a fraction of one per cent who experience psychosis. Similarly, with CP grabbing most of the research attention, the effects of cannabis on neuroses (eg. anxiety) and mood disorders (eg. depression) remains poorly understood, and research into these areas has just begun (eg. Patton et al. 2002).
In conclusion, the current 'fashionable' concern among researchers and policy-makers with cannabis-induced psychosis has contributed to an unjustifiable neglect of other cannabis-related mental disorders, such as dependence. In addition, ICD-10 guidelines and definitions contain serious flaws, which are likely to have resulted in (a) misdiagnoses of ACI and HCU as CP, and (b) attributions of mental disorders to cannabis instead of to more likely but less frequently used drugs (eg. ecstasy, cocaine). But perhaps more serious than any of these problems is the almost complete neglect of a major health risk now facing the majority of cannabis consumers in Britain - the ingestion of toxic adulterants. Though all illicit drugs are adulterated, there is scattered but consistent evidence that cannabis resin, particularly 'Moroccan', has become particularly affected by toxic additives as any regular cannabis user in Britain would undoubtedly confirm (especially after visiting Holland or Morocco). For instance, the Cannabis Resin Impurities Survey Project conducted preliminary research in 2001 on five samples of Moroccan 'soap-bar' resin provided by Customs & Excise (CRISP 2002). It was found that the psychoactive adulterants included glue (benzene and toluene), ketamine, caffeine, and aspirin while other additives, varying in toxicity, included liquorice, milk powder, boot polish, beeswax, turpentine, henna, vinyl, motor oil, dyes, pine resin, animal shit, soil, and phenols. Why does cannabis resin contain so many toxic adulterants and additives when other drugs do not? Traditionally, since profit is the main motive, household substances like sugars and bicarbonate of soda are added by dealers to drug powders like cocaine and heroin, because they look quite similar, and are cheap and easily obtained, but also because they are fairly harmless. By contrast, cannabis resin is a complex and unusual substance to reproduce, so a more extensive range of substances has to be mixed together and 'cooked' to produce a reasonable facsimile with a close enough appearance, taste and smell to trick consumers into purchasing it leading safety to be sacrificed for a cheap and passable simulation of the product. This has earned soap-bar the slang name of formula among some users (or Chernobyl in European countries with similarly adulterated cannabis products).
Based on Atha's (2001) research, a clear majority of cannabis users well over two million - are now likely to be using soap-bar/formula, with the average regular user smoking about an ounce per month. Consequently, psychoses and other health problems attributed to cannabis use in England could be realistically attributable to one or more of a variety of substances such as glue or ketamine - rather than to cannabinoids. More research is urgently needed to establish what chemicals cannabis users are actually consuming; and, what effects regular use of these can have on their mental and physical health. Clearly, this is a public health problem with the potential to affect millions of people, many of whom are unaware that they are exposing themselves to a cocktail of toxic chemicals each time that they smoke or eat soap-bar cannabis. And it is a problem which is not easily tackled while the international Prohibition policy prevents national governments from deploying the only pragmatic strategy which could protect their cannabis consuming citizens: providing a legal supply of quality-controlled cannabis, and/or permitting cultivation for personal use.
This paper is a summary of a longer unpublished report (Newcombe 2004)
Atha M. (2001). Cannabis use in Britain. Wigan: Independent Drugs Monitoring Unit.
Aust R. & Smith N. (2003). Ethnicity and drug use: key findings from the 2001/2002 British Crime Survey. London: Home Office (Findings 209).
Aust R., Sharp C. & Goulden C. (2002). Prevalence of drug use: key findings from the 2002/2003 British Crime Survey. London: Home Office (Findings 182).
Castle D. & Murray R. (eds) (2004). Marijuana and Madness: psychiatry and neurobiology. Cambridge: University Press. Condon J. & Smith N. (2003). Prevalence of drug use: key findings from the 2002/2003 British Crime Survey. London: Home Office (Findings 229).
CRISP (2002). Personal communication. Edinburgh University: Cannabis Resin Impurities Survey Project.
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Department of Health (2000-2004). Hospital Episode Statistics, England, 1998/99-2002/03. London: DOH.
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Newcombe R. (1992). The reduction of drug-related harm: a conceptual framework for theory, practice and research. In P. O'Hare et al. (eds), The Reduction of Drug-Related Harm. Londond: Routledge.
Newcombe R. (2004). Cannabis psychosis: mental disorder or myth? Unpublished report, Liverpool John Moores University. Office for National Statistics (2001). Psychiatric morbidity among adults, 2000. London: ONS.
Patton G., Coffey C., Carlin J., Degenhardt L., Lynskey M. & Hall W. (2002). Cannabis use and mental health in young people: cohort study. British Medical Journal, 325, 1195-1198.
Poole R. & & Brabbins C. (1996). Drug induced psychosis. British Journal of Psychiatry, 168, 135-38
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Sartorious N. (1992). The ICD-10 Classification of Mental and Behavioural Disorders: clinical descriptions and diagnostic guidelines. Geneva: World Health Organisation.
The ICD-10 guidelines also state that acute intoxication and harmful use should not be diagnosed when other MBDs are present - notably psychosis, residual psychosis or dependence - and that diagnostic precedence should be given to harmful use over acute intoxication (the criteria for drug-induced psychosis and residual psychosis are hardly distinguishable, the only clear difference being that diagnoses of the latter are based on six specific psychotic conditions). This implies a general hierarchy of severity for the three MBDs of present interest - with acute intoxication being the least severe, drug-psychosis the most severe, and harmful use occupying the intermediate position. Indeed, this is consistent with the argument that acute intoxication and harmful use are not 'genuine' psychiatric disorders or 'true' mental illnesses, but simply cases of excessive intoxication and/or consequent harm transient conditions superficially resembling mental illness, but lacking their structure and process. For instance, focusing on cannabis-related MBDs, and employing 'stoned' as shorthand for the effects of cannabis, many cases of acute cannabis intoxication (ACI) could be more accurately described as 'being so excessively stoned that they appeared psychotic' (cf. drunkenness), while many cases of harmful use (HCU) could be reinterpreted as 'being so excessively stoned that they were hurting themselves or others'. The argument in the main text is that cases of CP probably represent the extreme end of ACI/HCU cases ('...exceptionally stoned...' perhaps).
Moreover, there seems to be a large degree of overlap between the ICD-10 diagnostic criteria for acute CP and ACI. The seven sub-types of CP, based on predominant symptoms, include schizophrenia-like, delusional, hallucinatory, polymorphic, depressive, manic, and mixed (F12.56). The eight sub-types of ACI are uncomplicated, with trauma/bodily injury, with other medical complications, with delirium, with perceptual distortions, with coma, with convulsions, and with pathological intoxication. But the greatest potential for misdiagnosis is provided by the diagnostic criteria for these two conditions, which exhibit a fairly extensive amount of overlap. That is, signs and symptoms of acute CP include: (1) dysfunctional behaviour evidenced by either (a) apathy and sedation, (b) disinhibition, (c) psychomotor retardation, (d) impaired attention, (e) impaired judgement, and/or (f) interference with personal functioning; and (2) exhibition of such signs as (a) drowsiness, (b) slurred speech, (c) pupilary constriction, and /or (d) decreased level of consciousness. These bear strong resemblance to the diagnostic criteria for ACI, namely: (1) euphoria and disinhibition; (2) anxiety or agitation; (3) suspiciousness or paranoid ideation; (4) temporal slowing; (5) impaired judgement; (6) impaired attention; (7) impaired reaction time; (8) auditory, visual or tactile illusions; (9) hallucinations, with preserved orientation; (l0) depersonalisation; (11) derealization; and/or (12) interference with personal functioning. Lastly, the signs and symptoms of both of these cannabis-related mental disorders also exhibit a fair degree of overlap with the diagnostic criteria for general schizophrenia disorders (notably regular schizophrenia) though space constraints preclude a more detailed account here (see Newcombe 2004, for a more rambling exposition).
There are two major limitations of HES data which may have prevented proper assessment of the correlation between CUs and CP cases over time. First, it could at least partly derive from the small number of values used in running the statistical test, namely six comparison years between 1995/96 and 2002/03. It is possible that as more annual statistics emerge over the next decade, and the test is conducted again with ten or more values/years for each variable, a significant correlation will emerge for instance, a Spearman correlation of just 0.36 becomes significant when it is based on comparing 30 pairs of values and sample sizes over 30 permit assessments of correlation with the more powerful (parametric) Pearson test. Second, the lack of correlation overall may mask significant relationships between CU and CP in particular gender and race sub-groups - for instance, the rate of CP was about five times higher among male compared with female cannabis users. However, the lack of race breakdowns for CP cases in HES precluded any further investigation of this issue. Given that all countries vary in the type and amount of information they record about citizens diagnosed with mental disorders, further studies conducted in different countries would help gradually fill in the 'gaps' in our knowledge.
Given that ICD-10 guidelines advise that drug-induced psychoses be attributed to the single drug used most frequently by the patient, we might also have expected high numbers of tobacco-related psychoses to be reported in HES because tobacco probably has a higher proportion of daily users than any other drug. The fact that the tobacco psychosis figures are typically zero suggests that psychiatrists do not follow the 'most frequently used drug = primary cause of disorder' rule. If they have rejected this rule in favour of more acceptable criteria for a primary single cause, then wrongful attributions of multi-drug psychoses to cannabis may not be as widespread as was suggested in the main text.
De :Russell Newcombe (email@example.com)
Objet :Re: UK Cannabis Resin (Soapbar??) (Rocky??)
Groupes de discussion :uk.rec.drugs.cannabis
Date :2003-04-06 10:53:25 PST
SOAP-BAR/FORMULA - what the hell is it?
The adulterants in powdered drugs like speed, cocaine and heroin (notably caffeine and sugars) are regularly reported in Forensic Science Service publications (the Home Office agency who analyse drugs seized by police and customs). But, until recently, there was little hard evidence about adulterants in cannabis resin. However, CRISP (the Cannabis Resin Impurities Survey Project) at Edinburgh University, have been analysing the contents of cannabis products seized by British law enforcement authorities since 2001. Preliminary analysis of Moroccan soap-bar cannabis resin - the most popular cannabis product, accounting for about half the UK market - which were seized by HM Customs in 2001, found that some contained as little as 10-20% cannabis resin - for instance, one sample was 80% soil. The main adulterants identified so far include liquorice, boot polish, beeswax, turpentine, henna, coffee, vinyl, motor oil, dyes, animal shit, milk powder, and pine resin; and other drugs such as aspirin, ketamine, glue, toluene and benzene. The last two chemicals alone can have unpleasant and dangerous poisoning effects, including liver and kidney damage. More recent analyses of 'formula' cannabis products in 2002 found evidence of 'phenols' - aromatic hydrocarbons used in disinfectants. THC purities of 'formula' are often closer to zero than 1%, and are rarely above 2%. The UK Legalise Cannabis Alliance has distributed a leaflet warning cannabis users of the foul chemical make-up of Moroccan soapbar, and advising them not to buy it - though few other warnings have appeared from official bodies or in the press."
Le CRISP, un projet d'étude sur les impuretés de la résine de cannabis, mené par l'Université d'Edimbourg, a analysé la composition du cannabis saisi par les autorités britanniques depuis 2001. Les analyses préliminaires de la résine de cannabis en barrettes en provenance du Maroc - forme la plus répandue du cannabis, près de la moitié du marché britannique - qui a été saisie par les douanes en 2001 a découvert que certains échantillons contenaient à peine 10 à 20 % de résine de cannabis - l'un d'eux était composé de 80 % de terre par exemple. Parmi les impuretés principales identifiées jusqu'à présent : réglisse, cirage, cire d'abeille, résine de pin, henné, café, huile de moteur, déjections animales, lait en poudre ; et aussi aspirine, ketamine, colle, toluène et benzène. Ces deux derniers produits chimiques seuls peuvent avoir des effets déplaisants et dangereux d'empoisonnement, y compris des dommages sur le foie et les reins. Les analyses les plus récentes de ces dérivés du cannabis, en 2002, ont mis en évidence la présence de phénols - hydrocarbones aromatiques utilisés dans les désinfectants. La pureté du THC des barrettes de hasch marocain est souvent plus proche de zéro que de 1 %, et rarement au-dessus de 2 %. L'Alliance pour la Légalisation du Cannabis britannique a distribué un prospectus alertant les usagers de cannabis sur les immondes composants chimiques des savonnettes de résine de cannabis marocain, en leur conseillant de ne pas en acheter - bien que quelques autres avertissements aient été émis par les autorités ou sont apparus dans la presse.
CRISP (Cannabis Resin Impurities Survey Project) - Department of Social Anthropology, The University of Edinburgh, Adam Ferguson Blding, George Squ, Edinburgh. EH8 9LL. Tel: 0131 651 1529. E-mail: Neil.Montgomery@ed.ac.uk