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Nuus vir dope heads [boodskap #102323]

Wo, 06 April 2005 13:51

Ferdi Greyling
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Van New Scientist
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Cannabis: Too much, too young?

* 26 March 2005
* NewScientist.com news service
* Graham Lawton

AT THE end of Jim van Os's street in the pleasant Dutch city of
Maastricht there is a coffee shop. As with many such establishments in
the Netherlands, "coffee shop" is something of a euphemism: most of
its customers go there not to drink coffee but to buy and smoke dope.
Van Os isn't too keen on the place. He doesn't like the shady
characters it attracts. He doesn't like the fact that his children
have to walk past it. And most of all he doesn't like that fact that
the place breaks the law and sells marijuana to under-18s.

Van Os's fears are rooted in more than the usual parental angst. He is
a psychiatrist at the University of Maastricht who investigates the
effect of marijuana on people's brains - particularly adolescents'
brains. And the findings of his research make him worry about the
effects of all this dope smoking on the kids in his neighbourhood.

Over the past couple of years van Os and several others have been
building the case that, for some teenagers, smoking cannabis leads to
serious mental health problems in later life, including schizophrenia.
Van Os claims that marijuana is responsible for up to 13 per cent of
schizophrenia cases in the Netherlands. And with cannabis use among
teenagers on the rise, the age at first use falling (see Graphic), and
the strength of cannabis on the up, he says the figure can only
increase.

It is a frightening conclusion, and one that is already starting to
shape the debate over the legal status of cannabis. In the UK, van
Os's findings have been seized upon by politicians, tabloid newspapers
and mental-health lobby groups who want drug laws tightened up. But
their case is far from made. Some researchers say there are
potentially fatal flaws in the research, and that it would be a
serious mistake to change the law based on an as-yet unproven theory.
So who is right? The answer, it turns out, is more complex than it
first appears.

Compared with substances like heroin and crack cocaine, cannabis is
seen by many people as relatively harmless. Several European countries
take a lenient view of its use, and in the UK marijuana was downgraded
from a class B to a class C drug last year, meaning people caught with
small quantities are not usually arrested.

But doctors have long known that taking a lot of cannabis over a short
period can occasionally cause temporary symptoms of psychosis, one of
the hallmarks of schizophrenia (see "Psychosis explained"). The
question of whether the drug has long-term mental health consequences,
however, is much more contentious.

The first hints of possible long-term harm came from Jamaica in the
1960s, where doctors noticed that Rastafarians who were heavy dope
smokers seemed unusually prone to psychotic illnesses. The suspicion
grew in the 1980s, when studies led by Robin Murray of the Institute
of Psychiatry in London showed that patients with schizophrenia or
some other kind of psychosis, were twice as likely as those without
mental illness to be regular cannabis users.

But it wasn't until a major Swedish study was published in 1987 that a
link between cannabis and long-term mental health problems was
established. A team from the Karolinska Institute in Stockholm
analysed 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.
The records included details of the men's experiences with drugs
before being called up, including age at first use, what they had
taken and how often.

The team then checked out 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.

Case closed? Not at all. The study certainly showed a correlation
between cannabis use and psychosis, but, as many people pointed out,
it by no means proved that the former caused the latter. For one
thing, the analysis ignored several possible "confounding factors" -
other differences between users and non-users of cannabis that could
be the real explanation for the link with schizophrenia. For example,
dope smokers could plausibly be more likely to take other drugs such
as LSD, which is a hallucinogen. Perhaps it was these drugs that were
actually causing schizophrenia. Another possibility was that there was
some hidden factor - possibly genetic - that predisposed people both
to smoking cannabis and developing psychosis.

More importantly, even if there were a causal relationship between
cannabis use and psychosis, the researchers failed to establish in
which direction it lay. Sure, it was possible that cannabis led to
schizophrenia. But it was just as likely that schizophrenia was
causing people to smoke cannabis. Perhaps they were "self-medicating"
- taking the drug to alleviate their symptoms.

The self-medication hypothesis has proved a popular one, and was
virtually orthodoxy in the 1980s. For one thing, patients with
psychosis often report that cannabis makes them feel better. And
recent research suggests that one of the chemical ingredients of
cannabis, cannabidiol, exerts a powerful antipsychotic effect. Indeed
the UK firm GW Pharmaceuticals, which is awaiting approval for an
under-the-tongue cannabis spray for multiple sclerosis patients, plans
to investigate cannabidiol as a treatment for schizophrenia.

But the idea that cannabis caused psychosis didn't go away. One
prominent sceptic of the self-medication idea was Don Linszen, a
psychiatrist at the University of Amsterdam, the Netherlands, who, as
a mental-health practitioner in the cannabis capital of Europe, was in
daily contact with dope-smoking schizophrenia patients. He noticed
that the patients who used cannabis usually fared much worse than
those who didn't. Studies by Murray and others confirmed Linszen's
observations. If people with psychosis were self-medicating, it wasn't
working very well.
ÂThe more cannabis the young people smoked, and the earlier they
smoked it, the worse their risk of psychosisÂ

Meanwhile, several research groups were busy setting up long-term
studies that followed large groups of young people over many years,
keeping track of their drug use as teenagers and testing them for
signs of psychosis later in life. They were similar in principle to
the Swedish study, but were carefully designed to avoid its mistakes,
particularly on the question of self-medication.

In the past couple of years results from a number of these studies
have been reported, and together they make a decent case that the
Swedish research got it right first time. "I don't think we can deny
it any longer," says epidemiologist Mary Cannon of the Royal College
of Surgeons in Ireland, based in Dublin. "Cannabis is part of the
cause of schizophrenia."

Cannon helped carry out a study that followed 759 people born in
Dunedin, New Zealand, in 1972 and 1973 (British Medical Journal, vol
325, p 1212). After carefully controlling for self-medication and
other confounding factors, the researchers 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 - they had a 10 per cent chance compared with 3 per cent for the
general population. The team 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," says Murray, who
led the study. "But it's a risk factor."

Similar results have recently come in from a Greek study as well as a
re-analysis of the original Swedish research. And late last year van
Os and his team brought out further results. They followed a group of
nearly 2500 14 to 24-year-olds living in and around Munich, Germany,
over four years. After correcting for all the confounders they could
think of, they found that, overall, smoking cannabis as an adolescent
moderately raised the risk of developing signs of psychosis later on,
from 16 per cent to 25 per cent. But 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.

According to van Os, Murray and others, there can no longer be any
doubt that there is a small but significant minority of people who
have a predisposition to psychosis and who would be well advised to
steer clear of cannabis.

This message is already starting to filter out into society. In the
Netherlands, the findings have fuelled a growing clamour for reform of
the laws regulating drug use. In the UK, the mental-health charity
Sane has called for the reclassification of cannabis to be reversed.
And the British government recently acknowledged the link in its
strongest terms yet, when it said in a press release that cannabis was
an "important causal factor" in mental illness.

But for some researchers, such pronouncements are premature. "I'm not
convinced," says Les Iversen, professor of pharmacology at the
University of Oxford and a member of the UK Home Office's Advisory
Council on the Misuse of Drugs. "I think the jury is still out on this
one."
ÂDespite a steep rise in cannabis use among teenagers over the past 30
years, there has been no rise in schizophreniaÂ

He points out that epidemiological studies are notoriously bad at
proving cause and effect, in part because it is hard to identify all
the confounding factors. Scientists are particularly wary of such
research when the conclusions are based on small statistical
differences - as in this case. In the New Zealand study, the number of
people who had smoked dope on three occasions by the age of 15 was
just 29, and only three went on to develop psychosis. "I can't help
thinking that the conclusion is rather thin," says Iversen. "It makes
you wonder. If they found another confounder, where would that leave
them?" Van Os himself admits that his study does not eliminate all the
confounding factors.

Iversen also points out problems with how psychosis is defined in each
study. Van Os's results, for example, seem to show that psychosis is
relatively common in cannabis smokers. But he chose a very broad
definition - a single psychotic symptom, such as hearing voices or a
paranoid belief. That's not the same as schizophrenia. About 20 per
cent of the general population live with these symptoms: only 1 in 20
of them ever require treatment.

Iversen isn't the only doubter. Last year John Macleod of the
University of Birmingham, UK, carried out a systematic review of the
16 high-quality long-term studies that have looked at cannabis and
mental health and concluded that there was "no strong evidence" of a
link with psychosis (The Lancet, vol 363, p 1579). "I'm not saying
there is no causal association, but at the moment, by the conventional
standards of epidemiology, the evidence is not particularly strong,"
he says.

There are other reasons to doubt the reality of a link. If it were
genuine, schizophrenia should be becoming more common as teenage
cannabis consumption goes up. But it isn't. 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.
In the genes

The only study to find a rise in schizophrenia was carried out in the
inner London district of Camberwell, where continual demographic
changes make interpreting the result almost impossible.

It seems the question of whether cannabis use can indeed lead to
schizophrenia will be unresolved for some time yet. One research
avenue that may shed further light on the matter is to look at whether
genes are involved. One of the members of Cannon's group, Avsahlom
Caspi of King's College London, is an authority on gene-environment
interactions. A couple of years ago he made a splash by showing that a
genetic predisposition to depression could interact with a traumatic
experience such as bereavement to trigger the illness (New Scientist,
26 July 2003, p 15). "We thought, let's put this model to work on
cannabis and psychosis," says Cannon.

She and her colleagues reanalysed the data from the New Zealand study,
this time adding in another variable - genetic predisposition to
schizophrenia. The gene they investigated, called COMT, encodes an
enzyme (catechol-O-methyl transferase) that breaks down a signalling
chemical in the brain called dopamine. COMT comes in two forms, one of
which is marginally more common in people with schizophrenia and is
thought to be a risk factor for the disease.

The results were crystal clear. 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, cannabis
spelled trouble: smoking it as a teenager increased their likelihood
of developing psychosis by a factor of 10. The results have not yet
been published, and Cannon warns that they need replicating, but even
so she says "this is a very large effect, similar to the size of
smoking and lung cancer. This is a very significant finding." Case,
perhaps, closed.

What should be done about it, however, remains an open question. Van
Os advocates that teenagers with a personal or family history of
mental illness be urged to steer clear of the drug. He also advocates
legal changes: governments should focus on keeping cannabis out of the
hands of teenagers and outlawing extra-strong varieties of cannabis,
such as skunk and white widow.

For Iversen though, this is still stretching the evidence. "What the
data show is that the risk applies to a small minority of young people
who start smoking cannabis at a very young age," he says. "Are we
going to change the law for the benefit of a vulnerable minority? A
small minority of people are vulnerable to liver damage if they drink
even a small amount of alcohol, but we haven't changed the law to
protect them."
From issue 2492 of New Scientist magazine, 26 March 2005, page 44
Psychosis explained

WHAT IS PSYCHOSIS?

A symptom of mental health problems, not an illness in its own right.

WHAT DO THE SYMPTOMS INVOLVE?

Psychotic people often have delusional beliefs, such as that someone
is reading their mind or that they are immensely wealthy, powerful or
famous. Extreme disorganisation and auditory and visual hallucinations
are also common. Sufferers are usually unable to cope with daily life
yet most are unaware that their behaviour is abnormal.

WHAT CAUSES IT?

The main cause of psychosis is mental illness, principally
schizophrenia and manic depression but also depression and dementia.
Symptoms can follow infections, head injury, brain tumours,
intoxication, poisoning and even traumatic events. Some psychotic
episodes have no obvious cause.

WHAT'S THE OUTLOOK?

Some people have only one episode, others struggle with psychosis
their entire life.