Abstract: The association between level of cannabis consumption and development of schizophrenia during a 15-year follow-up was studied in a cohort of 45,570 Swedish conscripts. The relative risk for schizophrenia among high consumers of cannabis (use on more than fifty occasions) was 6.0 (95% confidence interval 4.0-8.9) compared with non-users. Persistence of the association after allowance for other psychiatric illness and social background indicated that cannabis is an independent risk factor for schizophrenia.
Untoward Mental Effects of Cannabis
1. Psychological responses such as panic, anxiety, depression or psychosis. These effects may be described as ‘toxic’ in that they generally relate to excess consumption of the drug.
2. Effects of cannabis on pre-existing mental illness and cannabis as a risk-factor for mental illness.
3. Dependency or withdrawal effects.
An appreciable proportion of cannabis users report short-lived adverse effects, including psychotic states following heavy consumption, and regular users are at risk of dependence. People with major mental illnesses such as schizophrenia are especially vulnerable in that cannabis generally provokes relapse and aggravates existing symptoms. Health workers need to recognise, and respond to, the adverse effects of cannabis on mental health.
Cannabis use may increase the risk of psychotic disorders and result in a poor prognosis for those with an established vulnerability to psychosis. A 3-year follow-up (1997-1999) is reported of a general population of 4,045 psychosis-free persons and of 59 subjects in the Netherlands with a baseline diagnosis of psychotic disorder.
Substance use was assessed at baseline, 1-year follow-up, and 3-year follow-up. Baseline cannabis use predicted the presence at follow-up of any level of psychotic symptoms (adjusted odds ratio (OR) = 2.76), as well as a severe level of psychotic symptoms (OR = 24.17), and clinician assessment of the need for care for psychotic symptoms (OR = 12.01).
The effect of baseline cannabis use was stronger than the effect at 1-year and 3-year follow-up, and more than 50% of the psychosis diagnoses could be attributed to cannabis use.
Discussion: Self reported use of cannabis in early adulthood was associated with an increased risk of developing schizophrenia. Risk increased in a dose dependent manner with increasing frequency of cannabis use, and this relation remained when analysis was restricted to subjects who had used only cannabis and no other drugs before conscription. The largest risk was seen in subjects reporting use of cannabis on more than 50 occasions. We found no association between cannabis and other psychotic illnesses, which implies that cannabis has a rather specific association with an increased risk of schizophrenia.
Conclusions: Frequent cannabis use in teenage girls
predicts later depression and anxiety, with daily users
carrying the highest risk. Given recent increasing
levels of cannabis use, measures to reduce frequent
and heavy recreational use seem warranted.
Comment: Using cannabis in adolescence increases the likelihood of experiencing symptoms of schizophrenia in adulthood. Our findings agree with those of the Swedish study and add three new pieces of evidence.
Firstly, cannabis use is associated with an increased risk of experiencing schizophrenia symptoms, even after psychotic symptoms preceding the onset of cannabis use are controlled for, indicating that cannabis use is not secondary to a pre-existing psychosis.
Secondly, early cannabis use (by age 15) confers greater risk for schizophrenia outcomes than later cannabis use (by age 18). The youngest cannabis users may be most at risk because their cannabis use becomes longstanding.
Thirdly, risk was specific to cannabis use, as opposed to use of other drugs, and early cannabis use did not predict later depression.
Although most young people use cannabis in adolescence without harm, a vulnerable minority experience harmful outcomes. A tenth of the cannabis users by age 15 in our sample (3/29) developed schizophreniform disorder by age 26 compared with 3% of the remaining cohort (22/730). Our findings suggest that cannabis use among psychologically vulnerable adolescents should be strongly discouraged by parents, teachers, and health practitioners.
Discussion:
Exposure to cannabis during adolescence and young adulthood increases the risk of psychotic symptoms later in life. The findings confirm earlier suggestions that this association is stronger for individuals with predisposition for psychosis and stronger for the more severe psychotic outcomes.
Frequent use of cannabis was associated with higher levels of risk in a dose-response fashion. Associations were independent of other variables known to increase the risk for psychosis. Also, the effect of cannabis remained significant after we corrected for baseline use of other drugs, tobacco, and alcohol.
Finally, the data did not support the self medication hypothesis as baseline predisposition for psychosis did not significantly predict cannabis use at follow up.
Cannabisusein adolescenceleads to a two- to threefoldincreaseinrelativerisk for
schizophrenia or schizophreniformdisorder in adulthood. The earlier the age of
onset of cannabis use, the greater the risk for psychotic outcomes.
Cannabis does not appear to represent a sufficient or a necessary cause for the
development of psychosis but forms part of a causal constellation.
Aminority of individuals experience harmful outcome consequent to their use of
cannabis.However, thisminority is significantboth froma clinical point of viewand at
a population level. It is estimated that about 8% of schizophrenia could be prevented
by elimination of cannabis use in the population.
Conclusions: Cases of psychotic disorder could be prevented by discouraging cannabis use among vulnerable youths.Research is needed to understand the mechanisms by which cannabis causes psychosis.
Measurements: Subjects filled in the 40-item Community Assessment of Psychic
Experiences, measuring subclinical positive (paranoia, hallucinations,
grandiosity, first-rank symptoms) and negative psychosis dimensions and
depression. Drug use was also reported on.
Use of cannabis was associated positively with both positive and negative
dimensions of psychosis, independent of each other, and of depression. An
association between cannabis and depression disappeared after adjustment for
the negative psychosis dimensions. First use of cannabis below age 16 years was
associated with a much stronger effect than first use after age 15 years, independent
of life-time frequency of use. The association between cannabis and
psychosis was not influenced by the distress associated with the experiences,
indicating that self-medication may be an unlikely explanation for the entire
association between cannabis and psychosis.
Findings
Regression models adjusting for observed and non-observed confounding
suggested that daily users of cannabis had rates of psychotic symptoms
that were between 1.6 and 1.8 times higher than non-users of
cannabis. Structural equation modelling suggested that these associations
reflected the effects of cannabis use on symptom levels rather than the effects of
symptom levels on cannabis use.
Conclusions:
The results of the present study add to a growing body of evidence
suggesting that regular cannabis use may increase risks of psychosis. The
present study suggests that: (a) the association between cannabis use and psychotic
symptoms is unlikely to be due to confounding factors; and (b) the direction
of causality is from cannabis use to psychotic symptoms.
Cannabis use, in individuals who did not have psychotic symptoms
before they began using cannabis, predicted future psychotic symptoms (hazard
ratio = 2.81; 95% confidence interval = 1.79窶4.43). However, psychotic symptoms
in those who had never used cannabis before the onset of psychotic symptoms
also predicted future cannabis use (hazard ratio = 1.70; 95% confidence
interval = 1.13窶2.57).
Conclusions: The results imply either a common vulnerability with varying order of onset or a bi-directional causal relationship between cannabis use and psychosis. More research on patterns and timings of these relationships is needed to narrow down the possibilities.
Conclusions: These findings provide evidence of a gene X environment interaction and suggest that a role of some susceptibility genes is to influence vulnerability to environmental pathogens.
Conclusion: The observed deleterious effect of cannabis use on the prognosis of patients with psychotic disorder may involve the same mechanism as the observed deleterious effect of cannabis use on the prognosis of individuals with high levels of liability to psychosis. Further study of gene-environment interactions is likely to help elucidate the exact role of cannabis in the onset and the persistence of psychotic disorders but there is an urgent need for human and animal studies
examining the biological mechanisms involved.
Results: Schizophrenia-spectrum disorders were diagnosed in 44.5% of the sample. New psychotic episodes of any type were diagnosed in 77.2%. Male gender and young age were associated with increased risk. Development of schizophrenia-spectrum disorders was often delayed, and 47.1% of patients received a diagnosis more than a year after seeking treatment for a cannabis-induced psychosis. The patients developed schizophrenia at an earlier age than people in the comparison group (males, 24.6 v. 30.7 years, females, 28.9 v. 33.1 years).
Cannabis use in Denmark: The incidence of cannabis-induced psychotic disorders in Denmark was estimated to be 2.7 per 100 000 person-years. This confirms that such conditions are rare. In the interpretation of this number, it is important to note that in Denmark cannabis is predominantly smoked as hashish, which is more potent than marijuana. A recent publication from the Danish National Board of Health (2003) shows that 40.9% of all Danish citizens aged 16窶24 years have used cannabis at some point in their lifetime, and that 19.7% had used the substance in the previous month.
We report two cases of healthy subjects who were occasional but regular
cannabis users without psychiatric history who developed transient psychotic symptoms
(depersonalization, paranoid feelings and derealisation) following oral administration of cannabis.
CONCLUSION: These data suggest that cannabis use is associated with an exacerbation of abnormal developmental trajectories of prefrontal cortex in schizophrenia. The relationship between lower FA values in the SMA and working memory provide further support for a hypothesis that adolescence-related neurodevelopmental events may contribute to the pathophysiology of cognitive dysfunction in schizophrenia.
CONCLUSIONS: These data provide evidence for neural synchronization and early-stage sensory processing deficits in cannabis use. This finding, along with the observed increased rates of schizotypy in cannabis users, adds support for a cannabinoid link to schizophrenia spectrum disorders.
AIMS: To estimate long-term trends in cannabis use and projections of schizophrenia assuming a causal relation between cannabis use and schizophrenia.
CONCLUSIONS: Our data provide no direct evidence on whether cannabis use causes schizophrenia. They appear to confirm assumptions of substantial increases in cannabis use in the UK population over the last 30 years, and suggest a shift to more prolonged use initiated at younger ages. This shift is relatively recent and its full impact on population levels of schizophrenia, if cannabis use does cause schizophrenia, may not yet be apparent. However, this impact should become apparent within the next 5 years. Consideration of these questions is constrained significantly by the lack of reliable data on trends in both cannabis use and schizophrenia, emphasizing the importance that these data be collected in future through robust surveillance systems.
Methods: We searched Medline, Embase, CINAHL, PsycINFO, ISI Web of Knowledge, ISI Proceedings, ZETOC,
BIOSIS, LILACS, and MEDCARIB from their inception to September, 2006, searched reference lists of studies selected for inclusion, and contacted experts. Studies were included if longitudinal and population based. 35 studies from 4804 references were included. Data extraction and quality assessment were done independently and in duplicate.
Findings: There was an increased risk of any psychotic outcome in individuals who had ever used cannabis (pooled adjusted odds ratio=1・41, 95% CI 1・20窶1・65). Findings were consistent with a dose-response effect, with greater risk in people who used cannabis most frequently (2・09, 1・54窶2・84). Results of analyses restricted to studies of more clinically relevant psychotic disorders were similar. Depression, suicidal thoughts, and anxiety outcomes were examined separately. Findings for these outcomes were less consistent, and fewer attempts were made to address non-causal explanations, than for psychosis. A substantial confounding effect was present for both psychotic and affective outcomes.
Conclusion: we have described a consistent association between cannabis use and psychotic
symptoms, including disabling psychotic disorders. The possibility that this association results from confounding factors or bias cannot be ruled out, and these uncertainties are unlikely to be resolved in the near future. Despite the inevitable uncertainty, policymakers need to provide the public with advice about this widely used drug. We believe that there is now enough evidence to inform
people that using cannabis could increase their risk of developing a psychotic illness later in life. The evidence that cannabis use leads to affective outcomes is less strong than for psychosis but is still of concern. Although individual lifetime risk of chronic psychotic disorders such as schizophrenia, even in people who use cannabis regularly, is likely to be low (less than 3%), cannabis use can be expected to have a substantial effect on psychotic disorders at a population level because exposure to this drug is so common.
いずれにしても、この論文の精度と作成理由についてこの研究を率いたザミット教授は、ランセットが配信しているポッドキャストのインタビューの中で、「カナビスの使用が本当に精神病のリスクを増加させるのでしょうか?」 という質問に対して、次のように答えている。(Soft Sercret Magazine Issue 6 - 2007 30p, Cannabis, Mental Health and the Media)
Abstract
There is controversy over whether the incidence rates of schizophrenia and psychotic disorders have changed in recent decades. To detect deviations from trends in incidence, we analysed admission data of patients with an ICD-8/9/10 diagnosis of psychotic disorders in the Canton Zurich / Switzerland, for the period 1977窶2005. The data was derived from the central psychiatric register of the Canton Zurich. Ex-post forecasting with ARIMA (Autoregressive Integrated Moving Average) models was used to assess departures from existing trends. In addition, age-period-cohort analysis was applied to determine hidden birth cohort effects. First admission rates of patients with psychotic disorders were constant in men and showed a downward trend in women. However, the rates in the youngest age groups showed a strong increase in the second half of the 1990's. The trend reversal among the youngest age groups coincides with the increased use of cannabis among young Swiss in the 1990's.
Abstract
Objective: Cannabis use increases the risk for psychosis, but psychotogenic effects of cannabis may be restricted to exposure during early adolescence.
Method: Four hundred and seventy-two participants (aged 12窶23 years), randomly selected from the general population in Trinidad, completed questionnaires on past and current cannabis use and psychotic symptoms (using the Community Assessment of Psychic Experiences).
Results: Cannabis use increased the risk of experiencing psychotic symptoms and this effect was conditional on early exposure, defined around the mean age of onset of cannabis use. Thus, exposure before but not after the age of 14 years predicted psychotic symptoms (respectively β: 0.71, 95% CI 0.22; 1.19, P = 0.004 and β: -0.11, 95% CI -0.57; 0.36, P = 0.66). The developmental effect of cannabis use was independent of use of other drugs or current use of cannabis.
Conclusion: Early adolescence may be a critical period with regard to the psychotogenic effect of cannabis across geographical settings and ethnic groups.
Summary
Recent interest has focused on the association between cannabis use and risk
of psychosis. In the largest unselected, population-based study on this
topic to date, we examined cannabis use and prodromal symptoms of psychosis
at age 15窶16 years among 6330 adolescents. Those who had tried cannabis
(n=352; 5.6% of the total sample) were more likely to present three or more
prodromal symptoms even after controlling for confounders including previous
behavioural symptoms (OR=2.23; 95% CI 1.70窶2.94). A dose窶途esponse effect was
seen. We conclude that cannabis use is associated with prodromal symptoms of
psychosis in adolescence.
Heavy cannabis use is strongly suspected to be associated with both
psychotic symptoms and schizophrenia. 1
Whether cannabis causes psychoses beyond intoxication, however, remains
controversial, as some studies describing associations between cannabis use
and psychosocial harm are subject to bias or confounding. 2
Our aim was to examine associations between cannabis use and prodromal
symptoms of psychosis in a prospective general population-based birth cohort
study.
The harms must not be overstated: cannabis is neither poisonous
nor highly addictive, and we do not believe that it can
cause schizophrenia in a previously well user with no predisposition to
develop the disease.
Objective: This paper evaluates evidence for two hypotheses about the relationship
between cannabis use and psychosis: (i) that heavy cannabis use causes a
‘cannabis psychosis’, i.e. a psychotic disorder that would not have occurred in the
absence of cannabis use and which can be recognised by its pattern of symptoms
and their relationship to cannabis use; and (ii) that cannabis use may precipitate
schizophrenia, or exacerbate its symptoms.
Results: There is limited clinical evidence for the first hypothesis. If ‘cannabis
psychoses’ exist, they seem to be rare, because they require very high doses of
tetrahydrocannabinol, the prolonged use of highly potent forms of cannabis, or a preexisting
(but as yet unspecified) vulnerability, or both. There is more support for the
second hypothesis in that a large prospective study has shown a linear relationship
between the frequency with which cannabis had been used by age 18 and the risk
over the subsequent 15 years of receiving a diagnosis of schizophrenia.
Cannabis-induced chronic psychosis
There is currently no clear evidence that cannabis use may lead to the persistence of a specific
psychotic illness after abstinence, but the topic is controversial.Existing studies of ‘cannabis psychosis’ are undermined by methodological problems (imprecise
characterisation of syndromes, lack of toxicological evidence and simplified models of causal
associations) .
The various studies generally mix up cases of shorter duration psychotic episodes (patients apparently suffering from toxic psychosis) with cases of chronic psychotic states. There is no clear evidence that the latter are not schizophrenic patients using cannabis . McGuire et al matched 23 psychotic patients who tested positive for cannabis in urinary screening with 46 drug-free controls, and found no difference in terms of their characteristic psychopathology and mode of onset.
There have been some case reports of individuals displaying acute psychotic states after each
cannabis use. These cases are generally interpreted as the triggering of an underlying vulnerability
by cannabis use. It is difficult to establish whether such cases involve a repetition of toxic episodes, a specific chronic cannabis psychosis or an atypical sub-type of schizophrenia .
If cannabis use acts as a precipitant of psychosis, we would To model the impact of rising rates of cannabis use on the incidence and prevalence of psychosis under four hypotheses about the relationship between cannabis use and psychosis.
(1) that there is a causal relationship between cannabis use and schizophrenia; (2) that cannabis use precipitates schizophrenia in vulnerable persons; (3) that cannabis use exacerbates schizophrenia; and (4) that persons with schizophrenia are more liable to become regular cannabis users.
Results: There was a steep rise in the prevalence of cannabis use in Australia over the past 30 years and a corresponding decrease in the age of initiation of cannabis use. There was no evidence of a significant increase in the incidence of schizophrenia over the past 30 years. Data on trends the age of onset of schizophrenia did not show a clear pattern. Cannabis use among persons with schizophrenia has consistently been found to be more common than in the general population.
Conclusions: Cannabis use does not appear to be causally related to the incidence of schizophrenia, but its use may precipitate disorders in persons who are vulnerable to developing psychosis and worsen the course of the disorder among those who have already developed it.
In conclusion, our meta-analysis of studies that have attempted
to address the question of longer term neurocognitive
disturbance in moderate and heavy cannabis users has
failed to demonstrate a substantial, systematic, and detrimental
effect of cannabis use on neuropsychological performance.
It was surprising to find such few and small effects
given that most of the potential biases inherent in our analyses
actually increased the likelihood of finding a cannabis
effect.
Despite widespread concern, we have found no strong
evidence that use of cannabis in itself has important
consequences for psychological or social health. This
finding is not equivalent to the conclusion that use of
cannabis is harmless in psychosocial terms; problems with
the available evidence render it equally unable to support
this proposition. Better evidence is needed in relation to
cannabis, which is widely used, and in relation to other
drugs that, although less widely used, might have
important effects.
Abstract:
The current investigation uses a large non-clinical sample of undergraduate college students (N=189) to investigate schizotypal traits among cannabis and non-cannabis users, as well as the temporal order of the onset of these traits and cannabis use.
Findings suggest that regular cannabis users are significantly more prone to cognitive and perceptual distortions as well as disorganization, but not interpersonal deficits, than non-regular users and those who have never used. Additionally, the onset of schizotypal symptoms generally precedes the onset of cannabis use. The findings do not support a causal link between cannabis use and schizotypal traits.
The long-term use of cannabis, particularly at high intake levels, is associated with several adverse psychosocial features, including lower educational achievement and, in some instances, psychiatric illness. There is little evidence, however, that long-term cannabis use causes permanent cognitive impairment, nor is there is any clear cause and effect relationship to explain the psychosocial associations. There are some physical health risks, particularly the possibility of damage to the airways in cannabis smokers. Overall, by comparison with other drugs used mainly for ‘recreational’ purposes, cannabis could be rated to be a relatively safe drug...
A review of the literature suggests that the majority of cannabis users, who use the drug occasionally rather than on a daily basis, will not suffer any lasting physical or mental harm.
One obvious question is raised by their use of ten items from Symptom Checklist 90 as the only assessment tool for symptoms of psychosis. The items assessed focus heavily on paranoid ideation, e.g. ‘feeling other people cannot be trusted’, ‘feeling you are being watched or talked about by others’, and ‘having ideas or beliefs that other do not share.’ This is of concern because it is well known窶背idely reported in the literature [2] and commonly referenced in popular culture for decades [3,4]窶 that paranoid feelings are a relatively frequent effect of acute marijuana intoxication.
Cannabis use is among the least visibly problematic forms of illicit
drug use. Present evidence suggests that concerning the most
serious drug-related harm - death - the role of cannabis is negligible
compared to other legal, prescribed and illicit drugs (Blakemore
2003). Although it is increasingly clear that cannabis use incurs
risks, including mental health problems, millions of people use the
drug without obvious ill-effects. Regarding its potential to cause
serious mental health problems, it is also of note that alcohol has the
potential to cause a psychosis 窶 Korsakoff’s Syndrome; so in this
sense, the hazards of cannabis use are not unique.
Discussion:
Those who consume marijuana occasionally or even daily have lower levels of depressive symptoms
than those who have never tried marijuana. Specifically, weekly users had less depressed mood, more
positive affect, and fewer somatic complaints than non-users. Daily users reported less depressed mood and more positive affect than non-users. The groups did not differ on interpersonal symptoms. Our results add to the growing body of literature on depression and marijuana and are generally consistent with a number of studies that have failed to confirm a relationship between the two after controlling for relevant variables.
Conclusions After adjusting for differences in baseline risk factors of marijuana use and depression, past-year marijuana use does not significantly predict later development of depression. These findings are discussed in terms of their relevance for understanding possible causal effects of marijuana use on depression.
Conclusions: In a country with a liberal drug policy like The Netherlands, cannabis use is associated with aggression and delinquency, just as in other countries. Cannabis use was not associated with internalising problems. Alcohol use and regular smoking were strong confounding factors
Thus, these data lead to the likely conclusion that cannabis use, in at least moderate amounts, during adolescence does not appear to be neurotoxic, although we cannot exclude any adverse effects of heavier amounts than that used by the current subjects. These data are preliminary and need replication with larger numbers of subjects, although they do have implications for refuting the hypothesis that cannabis alone can cause a psychiatric disturbance such as schizophrenia by directly producing brain pathology.
Aims: To examine whether variants within the cannabinoid receptor (CNR1) and {alpha}7 nicotinic receptor (CHRNA7) genes are associated with schizophrenia, and whether these effects vary according to cannabis or tobacco use. We also examined a putative interaction between cannabis and Val158Met within the catechol-O-methyltransferase gene (COMT).
Conclusions: Neither CNR1 nor CHRNA7 variation appears to alter the risk of schizophrenia. Furthermore, our results do not support the presence of different effects of cannabis use on schizophrenia according to variation within COMT.
Methods
Schizotypal Personality Questionnaire (SPQ) scores were compared in groups of people with different exposure to cannabis, with the use of other drugs serving as a covariate. Supplemental analyses compared users of legal and illicit drugs with cannabis use as a covariate.
Results
Weekly (n = 111) and monthly (n = 136) cannabis users had higher scores on the SPQ than former (n = 143) and non-users (n = 81). The use of other drugs accounted for the links between cannabis and schizotypy. Lifetime use of psychomotor stimulant drugs plus ecstasy accounted for associations between cannabis and scores on the SPQ and its different subscales. Dividing groups by type of drug use revealed that those who used only cannabis and legal drugs (CLDs) (n = 126) were no different from those who used only legal drugs (LDs) (n = 74) but both groups scored significantly lower on the SPQ than polydrug users (n = 247). When controlling for marijuana use in the last month, the significant difference across drug use groups remained.
Conclusions
The results suggest that research on marijuana and schizotypy requires careful assessment of the use of other drugs, especially psychomotor stimulants and ecstasy.
Some people who abuse drugs show symptoms similar to those of schizophrenia, and people with schizophrenia may be mistaken for people who are high on drugs. While most researchers do not believe that substance abuse causes schizophrenia, people who have schizophrenia abuse alcohol and/or drugs more often than the general population.
Substance abuse can reduce the effectiveness of treatment for schizophrenia. Stimulants (such as amphetamines or cocaine), PCP, and marijuana may make the symptoms of schizophrenia worse, and substance abuse also makes it more likely that patients will not follow their treatment plan.
Schizophrenia and Nicotine
The most common form of substance abuse in people with schizophrenia is an addiction to nicotine. People with schizophrenia are addicted to nicotine at three times the rate of the general population (75窶90 percent vs. 25窶30 percent).
Conclusions
Although the schizophrenia prodrome is associated with substantial diagnostic and management challenges, it is an area of intense study with considerable progress. The presentation of the young adolescent in the clinical vignette is characteristic of these challenges. The clinician’s most useful diagnostic tool窶杯he patient’s history of symptoms over time窶琶s limited in the early stages of the prodrome. In addition, developmental factors that can modulate the symptoms must be taken into account. For the patient in the clinical vignette, a diagnosis of a schizophrenia spectrum disorder would be premature, given the available history. However, she has a number of clinical features that place her at an increased risk. The timing and intensity of treatment in this case would be determined by weighing the effects of the prodromal symptoms on the patient’s developmental trajectory. After a thorough evaluation, this young patient would benefit from CBT with psychoeducation and possibly pharmacological intervention within an overall framework of a well-supported family network.
This study explored explanatory models used by individuals with schizophrenia in relation to continuing cannabis abuse. Cannabis is known to exacerbate positive symptoms, compound the effects of negative symptoms, and lead to relapse, having a negative effect upon quality of life. If this is so, why would people choose to continue the drug use? Most previous studies exploring this phenomenon have used quantitative methodology where the questions asked have been preset by the researchers and the subjective experience of the patient has been minimized. Qualitative methodology was utilized in this study in order to give voice to the patients' perspectives, and contribute to the knowledge of the frameworks of meanings employed by patients. The majority of participants in this study did not perceive that they had a mental illness and they held strong beliefs regarding the usefulness of cannabis. They gave explanations for their continuing cannabis use that expanded the understanding from previous studies. These included that they sought the drug effects of cannabis use for clarity of voices, control of symptoms, to feel normal, perceived improvement in cognitive function, reduced psychological pain and increased energy. These beliefs may influence a person's adherence with treatment and their future cannabis use. This research has implications for clinical practice as clinicians may lack insight into the importance of the phenomenological beliefs of a person with schizophrenia. This lack of insight by the clinician into the phenomenological beliefs may impact on the development of a therapeutic relationship.
Patients:
During the 21.9 million person-years of follow-up between 1994 and 2005, 609 individuals received treatment of a cannabis-induced psychosis and 6476 received treatment of a schizophrenia spectrum disorder.
Results:
In general, the rate ratios of developing cannabis-induced psychosis and schizophrenia spectrum disorder associated with predisposition to schizophrenia spectrum disorder, other psychoses, and other psychiatric disorders in first-degree relatives were of similar magnitude. However, children with a mother with schizophrenia were at a 5-fold increased risk of developing schizophrenia and a 2.5-fold increased risk of developing cannabis-induced psychosis. The risk of a schizophrenia spectrum disorder following a cannabis-induced psychosis and the timing of onset were unrelated to familial predisposition.
Conclusions:
Predisposition to both psychiatric disorders in general and psychotic disorders specifically contributes equally to the risk of later treatment because of schizophrenia and cannabis-induced psychoses. Cannabis-induced psychosis could be an early sign of schizophrenia rather than a distinct clinical entity.
Background
It is unclear if research findings support clinical opinion that cannabis use leads to worse outcomes in people with psychosis, or whether this impression is confounded by other factors.
Aims
To systematically review the evidence pertaining to whether cannabis affects outcome of psychotic disorders.
Method
We searched 10 relevant databases (to November 2006), reference lists of included studies and contacted experts. We included 13 longitudinal studies from 15 303 references. Data extraction and quality assessment were conducted independently and in duplicate.
Results
Cannabis use was consistently associated with increased relapse and non-adherence. Associations with other outcome measures were more disparate. Few studies adjusted for baseline illness severity, and most made no adjustment for alcohol, or other potentially important confounders. Adjusting for even a few confounders often resulted in substantial attenuation of results.
Conclusions
Confidence that most associations reported were specifically due to cannabis is low. Despite clinical opinion, it remains important to establish whether cannabis is harmful, what outcomes are particularly susceptible, and how such effects are mediated. Studies to examine this further are eminently feasible.
The aim of the presented study was to compare schizophrenia and schizoaffective patients early in the course of the disease with and without comorbid substance abuse disorder (SUD vs. NSUD) with regard to brain morphology.
In a prospective design 41 patients (20 SUD vs. 21 NSUD) diagnosed as recent-onset schizophrenia or schizoaffective disorder consecutively admitted to hospital received standardized psychopathological evaluation (BPRS, SANS, MADRS, CGI, GAF) and MRI scanning with volumetric measurement of superior temporal gyrus (STG), amygdala-hippocampal complex, and cingulum.
Patients with SUD (primarily cannabis) were significantly younger, predominantly male and had a lower socioeconomic status. Despite less attentional impairment (SANS subscore) and elevated anxiety/depression (BPRS subscore) in patients with SUD compared to NSUD, no other psychopathological differences could be detected. There were no differences in the assessed temporolimbic brain morphology between the two subgroups.
In conclusion, in this study substance abuse in recent-onset psychosis had no effect on brain morphology and the earlier onset of psychosis in patients with comorbid SUD could not be explained by supposed accentuated brain abnormalities in temporolimbic regions.
Schizophrenia is a severe psychiatric disorder with a world-wide prevalence of 1%. The pathophysiology of the illness is not understood, but is thought to have a strong genetic component with some environmental influences on aetiology.
To gain further insight into disease mechanism, we used microarray technology to determine the expression of over 30 000 mRNA transcripts in post-mortem tissue from a brain region associated with the pathophysiology of the disease (Brodmann area 10: anterior prefrontal cortex) in 28 schizophrenic and 23 control patients.
We then compared our study (Charing Cross Hospital prospective collection) with that of an independent prefrontal cortex dataset from the Harvard Brain Bank. We report the first direct comparison between two independent studies.
A total of 51 gene expression changes have been identified that are common between the schizophrenia cohorts, and 49 show the same direction of disease-associated regulation.
In particular, changes were observed in gene sets associated with synaptic vesicle recycling, transmitter release and cytoskeletal dynamics. This strongly suggests multiple, small but synergistic changes in gene expression that affect nerve terminal function.
We are reporting improvement of symptoms of schizophrenia in a small group of patients who received the cannabinoid agonist dronabinol (synthetic Δ-9-tetrahydrocannabinol).
Before this report, cannabinoids had usually been associated with worsening of psychotic symptoms. In a heuristic, compassionate use study, we found that 4 of 6 treatment-refractory patients with severe chronic schizophrenia but who had a self-reported history of improving with marijuana abuse improved with dronabinol.
This improvement seems to have been a reduction of core psychotic symptoms in 3 of the 4 responders and not just nonspecific calming. There were no clinically significant adverse effects.
These results complement the recent finding that the cannabinoid blocker rimonabant does not improve schizophrenic symptoms and suggest that the role of cannabinoids in psychosis may be more complex than previously thought. They open a possible new role for cannabinoids in the treatment of schizophrenia
Background: Cannabis use in early adolescence may be a risk factor for development of schizophrenia. In animals, Delta9-tetrahydrocannabinol (THC) increases the rate of dopamine neuronal firing and release in the striatum. Thus cannabis use may increase dopamine release in the human striatum leading to vulnerability to psychosis
Aims: To investigate whether THC, the main psychoactive component of cannabis, can produce dopamine release in the human striatum.
Methods: 13 healthy volunteers, with previous cannabis experience, underwent two [11C]-raclopride positron emission tomography (PET) scans to indirectly measure striatal dopamine levels following either 10mg THC or placebo.
Results: Although THC markedly increased psychosis-like symptoms on the Psychotomimetic States Inventory (PSI), there was no significant effect of THC on [11C]-raclopride binding
Conclusion: In the largest study of its kind so far, we have shown that recreational cannabis users do not release significant amounts of dopamine from an oral THC dose equivalent to a standard cannabis cigarette. This result challenges current models of striatal dopamine release as the mechanism mediating cannabis as risk factor for schizophrenia.
A recent systematic review concluded that cannabis use increases risk of psychotic outcomes independently of confounding and transient intoxication effects. Furthermore, a model of the association between cannabis use and schizophrenia indicated that the incidence and prevalence of schizophrenia would increase from 1990 onwards. The model is based on three factors: a) increased relative risk of psychotic outcomes for frequent cannabis users compared to those who have never used cannabis between 1.8 and 3.1, b) a substantial rise in UK cannabis use from the mid-1970s and c) elevated risk of 20 years from first use of cannabis.
This paper investigates whether this has occurred in the UK by examining trends in the annual prevalence and incidence of schizophrenia and psychoses, as measured by diagnosed cases from 1996 to 2005. Retrospective analysis of the General Practice Research Database (GPRD) was conducted for 183 practices in England, Wales, Scotland and Northern Ireland. The study cohort comprised almost 600,000 patients each year, representing approximately 2.3% of the UK population aged 16 to 44.
Between 1996 and 2005 the incidence and prevalence of schizophrenia and psychoses were either stable or declining. Explanations other than a genuine stability or decline were considered, but appeared less plausible.
In conclusion, this study did not find any evidence of increasing schizophrenia or psychoses in the general population from 1996 to 2005.
Conclusions:
6.1 Cannabis is not a harmless substance and its use unquestionably poses
risks both to individual health and to society.
6.2 Cannabis, however, is less harmful than other substances (amphetamines,
barbiturates, codeine-like compounds) within Class B of Schedule 2 to the
Misuse of Drugs Act 1971. The continuing juxtaposition of cannabis with
these more harmful Class B drugs erroneously (and dangerously) suggests
that their harmful effects are equivalent. This may lead to the belief,
amongst cannabis users, that if they have had no harmful effects from
cannabis then other Class B substances will be equally safe.
6.3 The Council therefore recommends the reclassification of all cannabis
preparations to Class C under the Misuse of Drugs Act 1971.
6.4 If this recommendation is accepted, the Council has identified a number
of issues that it believes, while not directly related to the scientific
consideration, to be relevant and/or merit consideration. These are outlined
in Annex A of this Report.
7. Conclusions and recommendations:
7.1 Cannabis is harmful and its consumption can lead to a wide range of
physical and psychological hazards. Nevertheless, the Council does not
advise that the classification of cannabis-containing products should be
changed on the basis of the results of recent research into the effects on
the development of mental illness. Although it is unquestionably harmful,
its harmfulness does not equate to that of other Class B substances
either at the level of the individual or of society.
We live in a time in which the unrealistic and
unproductive paradigm of complete abstinence from
drugs is slowly dissipating. Proponents of a drug-free
society find this fact hard to accept, and responsible
politicians and doctors can find achieving an appropriate
position in the debate difficult. However, we must learn
to deal with drugs and their possible dangers without
fear.
13. Conclusions and Recommendations
Recommendation : Cannabis should remain a Class C drug.
13.4.1 The most worrying individual harms are the effects on mental health
but, since the Council’s previous review the evidence has become more,
rather than less, confused. Although there is a consistent (though weak)
association, from longitudinal studies, between cannabis use and the
development of psychotic illness, this is not reflected in the available
evidence on the incidence of psychotic conditions. The most likely (but
not the only) explanation is that cannabis 窶 in the population as a whole
窶 plays only a modest role in the development of these conditions. The
possibility that the greater use of cannabis preparations with a higher
THC content might increase the harmfulness of cannabis to mental
health cannot be denied; but the behaviour of cannabis users, in the
face of stronger products 窶 as well as the magnitude of a causal
association with psychotic illnesses 窶 is uncertain.
To enhance the attention of the peple and government of the world to effects of mental health problems and substance abuse on the social well-being and physical health of the world's underserved populations.A first step is to increase awarness and concern of the omportance of mental health throuth a series of key high profile regional and internatinal events. Secondly, efforts will be devoted to building up the will of the key political authorities to participate. Thirdly, and finally, efforts are to be directed as securring political commitments by decision makers.
Despite reports of falling first-admission rates for schizophrenia in the UK and other Western countries, it would be rash to conclude that the incidence of schizophrenia is falling. An attempt was made to tackle the many methodological problems and sources of bias influencing the relationship between admission rates and incidence in an analysis of inception rates for schizophrenia and other psychoses in Edinburgh between 1971 and 1989.
However it was calculated, the inception rate for schizophrenia fell significantly, but because there was evidence that diagnostic criteria for schizophrenia had narrowed between 1971 and 1989, and because a substantial and changing proportion of recorded first admissions were not true first admissions, it was impossible to conclude that the incidence of schizophrenia had fallen.
Changes in the incidence of psychiatric syndromes are difficult to establish, particularly in retrospect, and future studies must pay more attention to the many possible confounding influences.
Results There was a continuous and statistically significant increase in the incidence of schizophrenia, which was greatest in people under 35 years of age and was not gender-specific.
Conclusions The incidence of schizophrenia has doubled in south-east London over the past three decades.
Conclusions: Weekly cannabis use marks a threshold for increased risk of later dependence, with selection of cannabis in preference to alcohol possibly indicating an early addiction process.
The conclusion of this report is that there have been modest changes in THC
levels that are largely confined to the relatively recent appearance on the
market of intensively cultivated domestically produced cannabis. Cannabis
of this type is typically more potent, although it is also clear that the THC
content of cannabis products in general is extremely variable and that there
have always been some samples that have had a high potency.
A clear need exists to develop monitoring systems that can assess the market share of
different cannabis products and track changes over time. Currently this
information is to a great extent lacking. This is important, as a concern exists
that hydroponically produced cannabis grown in the EU may be increasing
its market share.
It is not known exactly how many people develop problems related to cannabis use.
There is no universally accepted definition of problem cannabis use. In international research,
a diagnosis of cannabis dependence is often based on the DSM psychiatric classification
system. By comparison with nicotine, heroin and alcohol, cannabis is not very
addictive. However, the risk of dependence increases with long-term frequent use and is
often accompanied by dependence on other substances. Younger people are more susceptible
to this than older people.
The present study confirmed findings that alcohol moderates the link between cannabis use and dependence. The study examined a large, diverse national sample of 856 people who consumed cannabis and alcohol at least twice per week. The study possesses several methodological improvements over past research, including less subjective measures of cannabis use and interview-based data collection. Cannabis use and alcohol consumption interacted to predict cannabis dependence symptoms. Cannabis use covaried with cannabis dependence particularly in people who consumed greater amounts of alcohol. These data further support the hypothesis that alcohol increases problems associated with cannabis use.
Benefits of a more scientifically based scale of harm
48. A more scientifically based scale of harm than the current system would
undoubtedly be a valuable tool to inform policy making and education. (Paragraph
104)
49. It is vital that the Government’s approach to drugs education is evidence based. A
more scientifically based scale of harm would have greater credibility than the
current system where the placing of drugs in particular categories is ultimately a
political decision. (Paragraph 105)
50. In our view, it would be unfeasible to expect a penalty-linked classification system to
include tobacco and alcohol but there would be merit in including them in a more
scientific scale, decoupled from penalties, to give the public a better sense of the
relative harms involved. (Paragraph 106)
This report, prepared for the House of Commons Select Committee on Science and
Technology, presents the results of four case studies examining the evidence base for the
classification of illegal drugs in the context of the 1971 Misuse of Drugs Act. The objective
is to identify the main evidence base on the selected drugs and to examine the use of that
evidence in classifying each drug. The report also briefly examines the classification systems
in three other countries, to provide a context through other drug classification systems.
an introduction describing the history of drug classification in the UK and general
issues surrounding the types of evidence used in classifying drugs;
four individual drug case studies (amphetamines and ecstasy, cocaine, magic
mushrooms and cannabis) examining the evidence of physical, social, psychological
and economic harm associated with each drug and the use of evidence in
government policy;
an international learning section examining the classification systems in three other
countries (the USA, the Netherlands and Sweden) and the penalties and treatment
regimes associated with them.
In the UK at present, 20窶25% of 15-year-olds are regular smokers, with females now outnumbering
males; around 40窶50% are drinking alcohol at least weekly; and 20窶25% are using other drugs 窶
mainly cannabis 窶 at least monthly.
Among the 6.8 million 16窶24-year-olds in the UK, there are an estimated 2.1 million daily smokers, 1.9 million who drink more than twice the recommended daily alcohol limit at least once a week and 1 million who have used another drug in the past month. Because many young people use more than one drug, there is much overlap between these groups.
Findings
There are many factors which influence whether or not young people will use tobacco, alcohol or
other drugs hazardously. The most important of these include early life experiences, family
relationships and circumstances, and parental attitudes and behaviour. It is difficult to predict who
will develop serious problems.
While many young people first use tobacco, alcohol or other drugs in their early and mid-teens,
hazardous use often starts in the late teens or twenties.
Of all drugs, the use of alcohol has shown the greatest recent growth and causes the most
widespread problems among young people in the UK today. It is also the least regulated and the
most heavily marketed.
Most schools in the UK provide drug prevention programmes. Research indicates that these
probably have little impact on future drug use.
この論文は、カナビスと精神病問題では最もよく引き合いに出される「カナビスで精神病になる率が6倍に増える」という数字の出処になっている最も有名な論文。発表は1987年。
スエーデン新兵4万5570人を対象に、入隊時(平均年齢18才)でのカナビス使用状況を自己申告させ、15年後に統合失調症の発症具合を調べた。入隊時にカナビス経験を持つ人は9.4%、50回以上のヘビーな経験者は1.7%になっている。
15年後には、カナビスを使ったことのない人に比較して、少なくとも1回以上体験のあった人では統合失調症になった率が2.4倍に増え、50回以上のヘビー・ユーザーの場合は6倍になった。だが、ヘビー・ユーザーのおよそ半数(430/730)が入隊時以前に精神科の診断を受けていることを補正するとリスクは2.3倍になっている。しかし、ヘビー・ユーザーで統合失調症になった人の割合は3%に過ぎず、著者たちは、カナビスのよるリスクが精神病を発症しやすい精神脆弱性を持った人にだけ現れるのではないかとしている。(ジョーンズ、アーセンバウルト)
しかしながら、この研究には批判が多い。最も重大な欠陥は、調査時点が15年も離れているのに、その間のアルコール、アンフェタミンやLSDなどを始めとする統合失調症を起こすとされる他のドラッグ使用やカナビスの使用状況の変化などの調査が行われていないことが上げられる。また、統合失調症を、診断ではなく精神病院の入院歴でカウントしているという問題もある。
こうした批判に対して、2002年に、同じチームがデータから問題のあるケースを取り除き、新たなデータも加えて再分析を行った別の論文を発表している。結論では、「カナビスの使用は精神病を発症するリスクを高めるという一貫した因果関係が存在する」と前回の同じようになっているが、内容的にはかなり異なり、新たな問題点も指摘されている。
とは言え、カナビスに反対する人たちは、現在でも繰り返しこの研究を引用し続けている。さすがに、イギリスのリシンクのような分別のある団体では6倍という数字までは使っていないが、例えば、Schizophrenia.com という統合失調症全般の情報を扱ったサイトでは、カナビスのこととなると途端に科学的批判精神を忘れて、6倍を600%と大きく見えるように表記し、グラフまで使ってこの研究をページのトップに掲げている。
逆にいえば、その後にカナビスと統合失調症の因果関係を主張する論文が多数出てきたにもかかわらず、今だこの論文に頼らなければならないほど、実際の論拠が弱いことを表しているとも言えるかもしれない。