Panorama's "Cannabis: what teenagers need to know" explored the latest scientific research on the effects of cannabis on the human mind. In particular, the growing evidence of links between cannabis and psychotic illness in young people. What follows is a guide to the main theories and research in this field.
A cannabis leaf
Four hypotheses have been proposed about the relationship between cannabis use and mental health:
The first, the causal hypothesis, suggests that heavy cannabis use can cause mental disorders such as psychosis.
Second, the dormant hypothesis argues that cannabis use may precipitate a mental disorder that was previously dormant in individuals prone to mental health disorders.
Third, the common cause hypothesis states that mental illness and cannabis use may simply occur together as a result of common variables, such as unemployment, family difficulties and other drug use.
The fourth is the self-medication hypothesis, that people use cannabis after experiencing signs of a mental health disorder in order to alleviate symptoms.
Until recently the consensus amongst the scientific community was that the fourth hypothesis which stated that people suffering from psychosis or schizophrenia used cannabis to alleviate some of the symptoms they were experiencing was the most likely explanation.
However the new research is generating more interest in the first hypothesis; namely that cannabis use itself can cause psychosis. This research is based on studies where large numbers of people are followed through a process of questionnaires over ten to twenty years. The conclusions drawn from these statistical analyses have shown that there is an association between cannabis use by adolescents who are predisposed to mental health problems and later mental health problems.
The publication of a Swedish study in 1987 was the first to suggest a link between cannabis and long-term mental health problems. The records of all the young men who had done national service in the Swedish army in 1969 and 1970 - 50,087 in total, representing about 97 per cent of the male population aged 18 to 20, were analysed. The research team then examined each man's medical history up to the mid-1980s. They found that those who had smoked cannabis before being called up were six times as likely to end up in hospital with schizophrenia as non-users. This, the team concluded, provided clear evidence that smoking cannabis was a risk factor for psychosis.
However critics pointed out methodological flaws which severely undermined the conclusions drawn. However the findings led others to examine the link with new studies that were better designed to avoid the mistakes of the Swedish study.
One of the new studies from New Zealand found that those who had smoked cannabis three times or more before the age of 15 were much more likely to suffer symptoms of schizophrenia by the time they were 26. The team, which included Professor Murray, concluded that there is a vulnerable minority of teenagers for whom cannabis is harmful. "We're not saying that cannabis is the major cause of schizophrenia but it's a risk factor."
A re-analysis of an original Swedish study from the 1980s also found similar results. Last year Dutch researcher Prof Jim van Os and his team published the results of following a group of nearly 2500 14 to 24-year-olds living in and around Munich, Germany, over four years. After correcting for all the additional factors they could think of, they found that smoking cannabis as an adolescent moderately raised the risk of developing signs of psychosis later on, from 16 per cent to 25 per cent. However when they focused on individuals who were known to be susceptible to psychosis - those who were showing signs of disturbed thought processes by age 11 - they found a much stronger link. Susceptible individuals who avoided cannabis had a 25 per cent chance of developing psychosis. Susceptible individuals who smoked it had a 50 per cent risk. And the more cannabis they smoked, and the earlier they smoked it, the worse the outcome.
Criticisms of the link theory
The big criticism of research on any link between cannabis and psychosis has been that its not clear whether the symptoms are caused by cannabis use or whether people who are likely to develop psychotic symptoms happen also to be more likely to be attracted to cannabis. David Fergusson (New Zealand - Christchurch 25-year study group) took all confounding factors into account and found: a clear increase in rates of psychotic symptoms after the start of regular use, with daily users of cannabis having rates that were over 150% those of non users. His findings clearly show cause and effect from cannabis to psychosis not other way round.
However, critics of the new research point out that other factors which can also cause mental health issues cannot always be adequately accounted for and that they may serve to lessen the power of the association between cannabis and mental health that these studies revealed.
They also point out that such epidemiological studies are notoriously bad at proving cause and effect. Apart from the problem of identifying all the potential other factors the critics say that many of the conclusions are based on very small statistical differences. They point to one of the studies, which followed over 700 people, where the number of people who had smoked cannabis three times by the age of 15 was only 29. Of those 29 only three went on to develop psychosis.
The critics also point out that if cannabis really was causing schizophrenia then there should bean increased incidence to match the rise in teenage consumption of cannabis. However in 2003 researchers at the University of New South Wales in Sydney found that, despite a steep rise in cannabis use among Australian teenagers over the past 30 years, there had been no rise in the prevalence of schizophrenia.
However most recently researchers involved in the New Zealand study have found that there might genetic factors at work as well. The team led by Dr Avshalom Caspi, re-analysed the data, this time looking at the genetic makeup of their subjects. They investigated a gene called COMT, is involved with the breaking down of key brain chemical called dopamine. Dopamine is thought to be involved in psychosis- people with psychosis have increased dopamine in one area of the brain COMT comes in two forms.,
The team found that in people with two copies of the "normal" version of COMT, smoking cannabis had little effect on their mental health. In people with one normal and one "bad" form of the gene, smoking cannabis slightly increased their risk of psychosis. But for people with two copies of the bad gene, smoking cannabis as a teenager increased their likelihood of developing psychosis by a factor of 10. According to Professor Murray, 25% of the UK population carry two 'bad' copies of the COMT gene
Professor Robin Murray
Research published in the British Journal of Psychiatry (2004) 181, p110 - 117
Professor Murray is Head of Psychiatry at the Institute of Psychiatry. His research examines the evidence that cannabis causes psychosis using established criteria of causality. His team identified five studies that included a well-defined sample drawn from population-based registers or cohorts and used prospective measures of cannabis use and adult psychosis
His team's findings were:
On an individual level, cannabis use confers an overall twofold increase in the relative risk factor for later schizophrenia.
At the population level, elimination of cannabis use would reduce the incidence of schizophrenia by approximately 8%, assuming a causal relationship.
Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It is a component cause, part of a complex constellation of factors leading to psychosis.
His team concluded that cases of psychotic disorder could be prevented by discouraging cannabis use among vulnerable youths but also felt that further research is needed to understand the mechanisms by which cannabis causes psychosis
Professor Yasmin Hurd
Her research investigates the close relationship between psychiatric disorders and drug abuse. As drug abuse is 4-7 times more common in persons with depression or schizophrenic syndromes and 35-80% of drug abusers will suffer from psychiatric disorders during their lifetime. The strong association between drug abuse and psychiatric disorders suggests similar underlying neurobiological impairments.
Her research team is focused on the systematic study of human brains from subjects with drug abuse (stimulants and opiates) and psychiatric disorders. Their goal is to identify and map specific genes in which regulate emotional functions, and are thereby relevant to the disorders of interest.
Additional studies carried out by this group are designed to assess how drugs affect the development of the human brain during the foetal stage, which may later lead to psychiatric problems. As complement to studies of the human brain, animal models are used in this research group to simultaneously study changes in neurotransmitter levels (e.g., dopamine) during drug self-administration behaviour. Possible neural targets for the development of future treatments against depression and drug dependence have been identified and published by the research group.
(Professor Hurd's results are unpublished and have not been replicated at this time).
Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyl transferase gene: longitudinal evidence of a gene X environment interaction. Caspi et al., Biological Psychiatry. 2005 May 15; 57(10) p1117-27
Arseneault L, Cannon M, Poulton R, et al, 2002, Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study, BMJ 2002; 325:1212 -1213
Arseneault L, Cannon M, Witton J, Murray R M, 2004, Causal association between cannabis and psychosis: examination of the evidence, Br. J. Psychiatry, 2004; 184: 110 - 117
Hall W, Solowij N, 1998, Adverse effects of cannabis, Lancet 1998; 352:1611-16
van Os J, Bak M, Hanssen M, Bijl R V, de Graaf R, Verdoux H, 2002, Cannabis Use and Psychosis: A Longitudinal Population-based Study, Am. J. Epidemiol. 2002; 156: 319 - 327
David Ferguson and John Horwood "Cannabis Use and Dependence in a New Zealand Birth Cohort" New Zealand Medical Journal 12/5/2000:
113 (1109): 1506-1508
Macleod J, Oakes R, Copello A, Crome I, Egger M, Hickman M, Oppenkowski T, Stokes-Lampard H, Davey Smith G. "Psychological and social sequelae of cannabis and other illicit drug use by young people: a systematic review of longitudinal, general population studies".
Zammit S, Allebeck P, Andreasson S, Lundberg I, Lewis G (2002) Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study. BMJ 325: 1199
Andreasson S, Allebeck P, Engstrom A, Rydberg U (1987) Cannabis and schizophrenia. A longitudinal study of Swedish conscripts. Lancet 2:1483-1486