MY BROTHER'S FIRST JOINT AND HIS DESCENT INTO A MENTAL WAR ZONE

With cannabis set to be recriminalised, Alexander Linklater, in this
moving report, tells how his brother Archie was sectioned, locked up
and consigned to a private hell of psychotic disorder for 20 years.
Now his family question whether Archie's teenage experiments with the
drug triggered his slow descent into depression and isolation

In the summer of 2005, there was nothing particularly new about the
onset of one of my brother's episodes. It was frustrating and sad,
because Archie had at that point been doing well for some time and
there is always the faint hope in manic depression that a remission
might somehow take root and become permanent. But the symptoms were
familiar enough: restlessness, the sudden announcement of grandiose
plans, bouts of rage - and then the wild paroxysms of mood and
personality that can lead to psychosis. Or madness, as Archie prefers
to call it.

What was slightly different was the recent appearance of news reports
on further studies into the links between cannabis and mental illness,
with the emphasis on a genetic vulnerability to the drug. It was a
subject that had gradually been worming its way into public
consciousness, and my family felt the potential implications acutely.
Living with extreme mental illness is a constant process of trying to
explain the inexplicable. In the 20 years or so of my brother's
bi-polar disorder, he has been sectioned many times and spent months
in locked wards; he has raged through doses of anti-psychotic
medication strong enough to knock out a horse; received both talk and
electroconvulsive therapies; and endured states of mind that can only
really be expressed in the theological vocabularies of hell. But there
has never been a precise explanation as to why this should have
happened to him - or to anyone suffering from one of the major
psychotic disorders.

The current psychiatric terminology that offers the most reliable
general explanation for the causes of mental illness is that of
'gene-environment interactions'. There may be various interacting
components in the causal chain, each of which can have varying degrees
of significance: hereditary, developmental, environmental (including
drug use), social and psychological. But this 'bio-psycho-social'
explanation comes to sound merely abstract when applied to the urgent
problem of understanding why a member of your family is going mad. So
when new evidence emerges that appears to point to something material,
specific and understandable, the temptation is to seize on it.

In my brother's case, he made the mistake of admitting that he had
been smoking a few spliffs before he also became 'high' in the
psychiatric sense. Momentarily, all sympathy for him vanished.
Marijuana was in the news and in the air, and my brother was doing it.
His furious psychiatrist, whom Archie had been lucky enough to have
had as his physician for 15 years, threatened to leave him if he did
it again. Our father, normally a man of consummate mildness, became
apoplectic with frustration. Harangued by everyone, and manic as a
burning tree, Archie was forced into a corner to explain himself.

Suddenly he blurted out something that none of us will forget. 'I
smoke dope,' he shouted, 'because I can't cope with staying well.'

That was a heart-stopper. Neither Archie, nor anyone, believes that he
consciously seeks out the terrible states of mania and depression that
have plagued his life. Yet there seemed to be some obscure truth in
this involuntary retort. One of the most gruelling challenges of
psychiatric illness is not just the pain of madness, but the strain of
adapting, between-times, to the drudgery of a normal existence.

It may sound a perverse thing to say of someone so profoundly
vulnerable to mental illness, but one of my brother's most remarkable
qualities is his psychological strength. He has been able to survive
and adapt himself to states of mind which - and I do not exaggerate -
would have killed me. For more than 20 years, the important dramas of
his life have been played out as a mental war zone, an admixture of
psychological trenches and apocalyptic firefights. When he emerges
from these states, he remains extraordinarily and movingly himself.
But, exactly like a traumatised veteran returning to a complacent home
country, he can find daily life a frightening impossibility.

Psychoanalysts of the Freudian tradition sometimes refer to psychotic
states as 'psychic retreats', as if they possessed some kind of dark
attraction to the sufferer. It's not an idea taken very seriously by
most of those working at the scientific and clinical front lines of
modern psychiatry, but the revolving door syndrome of patients leaving
hospital after they have improved, only to return soon afterwards, is
common enough. The mystery is why some patients should do so partly,
perhaps, as a result of their own actions.

Of course Archie had been warned many times that cannabis might be one
of the possible triggers (and interacting influences) in his episodes.
But what his outburst seemed to reveal was a tacit admission that he
was picking up a spliff not just despite the risks, but because of
them. 'The normal high from a joint was giving me the same level of
intense pleasure as a bout of hypomania,' he says now, referring to
the early, low-level high of an episode. 'During the smoking, it was
like riding a wave. The hypomania and the dope were working in tandem,
getting closer to full-blown mania. Some people get relaxed by it, but
for me mania and cannabis are like brother and sister.'

If, in cases like this where a patient is already ill, cannabis can
precipitate episodes of illness, is there a possibility that,
somewhere back in time, it was also the original cause?

When Archie was 14, and I was a couple of years older, I knew he was
smoking dope. He had started well before I smoked my first joint, and
we have often spoken about the possibility that it played a part in
what happened a year later, during his first, monumental breakdown.
Archie doesn't think it was particularly significant. He is a believer
in the hereditary, genetic predispositions of conditions such as
bi-polar disorder and schizophrenia. Yet the cannabis study that
appeared in 2005 was reported in the papers as suggesting that 'one in
four people carries genes that increases vulnerability to psychotic
illnesses if he or she smokes cannabis as a teenager'.

Was this the fundamental clue that we had all missed about the origins
of Archie's illness? And is it possible to draw any sensible
conclusions from his experience that might apply to others? Leaving
aside that first, beguiling question, the answer to the second one is,
at best, merely anecdotal. To some people, his story will sound
familiar; to others, it won't. And that's all that can honestly be
said of most personal accounts. The kind of studies that attempt to
look at risk factors across large numbers of people have very little
power to predict particular outcomes in individuals.

That 2005 study, conducted by the Institute of Psychiatry, had tracked
803 men and women born in Dunedin, New Zealand, in 1972 and 1973, and
interviewed them at 13, 15, and 18 about their cannabis use, tested to
determine which type of genes they had inherited, and followed them up
at 26 for signs of mental illness. Rather than a definitive genetic
profile for those vulnerable to cannabis use, as newspaper reports had
stated, it revealed a loose genetic association that would take far
more intensive research to clarify. As Robin Murray, a professor of
psychiatry at the Maudsley hospital who has overseen several cannabis
studies says, the complex nature of mental illness means that
'probably a profile of around 10 genes would be necessary'.

But what has happened is that, since 2002, the year in which the then
Home Secretary, David Blunkett, announced the downgrading of the
classification of cannabis, several population studies have emerged
which have built on earlier evidence that consistently show an
increased risk of severe psychotic illness among cannabis users and
establish that it can play a causal role.

How significant this may be to the general population is, however,
still open for debate. Last year, a review of all the studies to date,
published in the Lancet, was able to assert that even having tried
cannabis once can be shown to increase the risk of developing
schizophrenia by 1.4 per cent. And it is estimated by Murray that at
least 10 per cent of all people with schizophrenia in the UK would not
have developed the illness if they had not smoked cannabis, which
means there are 25,000 people whose lives have been ruined
specifically by the drug. This is serious enough, but it is not an
epidemic; nor, statistically speaking, is it a powerful argument
against taking the drug.

Such studies have shifted the political debate, and in good part lie
behind the clearly stated intention of Gordon Brown and Jacqui Smith,
the current Home Secretary, to reverse the 2002 decision to downgrade
the drug when the Advisory Council on the Misuse of Drugs completes
its report in the next few months. Even if the council repeats its
recommendations of 2006 - against reclassifying cannabis as a class B
drug - there are signs that the government will proceed regardless.
One reason is simply that the government is responding to what it
believes are changing public perceptions about cannabis.

Another less convincing reason is the notion of increasingly powerful
forms of hydroponically produced 'skunk' taking over from less harmful
traditional forms of cannabis. Some groups have claimed that it can be
up to 15 times more powerful, though the likelihood is that it's more
like two or three times. But the same basic chemical agent,
Tetrahydrocannabinol, is involved, and all the studies to date are
based on traditional forms of cannabis. The drug may be stronger now,
but as Murray points out, you can be an alcoholic by drinking beer in
the same way as you can by drinking whisky; you simply need more of
it.

In terms of public perception, however, the government may well be
right. Cannabis has been more celebrated and excused, and less
scientifically studied, than any of the other major recreational
drugs. That is changing, and Murray points out that it is still early
stages in the research, especially if an interaction between
particular genes and cannabis are to be revealed. The elements of
population risk involved with cannabis are beginning to emerge more
clearly, but there is still no definitive way of describing the
neurochemical mechanism by which it might be seen to translate a
vulnerability into a disorder.

Of the idea of reclassifying cannabis back to class B, Murray says: 'I
didn't think it should have been classified C in the first place, so
I'm not going to object. But educating people is far more important.'

There is a long-standing psychiatric distinction between two ways of
approaching mental illness. First, there is the possibility, always
remote, of finding an actual explanation. In the case of cannabis,
this would mean identifying the extent to which it may actually cause
a mental illness, pinning down the chemical mechanism by which it
produces a psychotic disorder and the extent to which it threatens
users in the general population according to their genetic profile.
Epidemiological studies, though their techniques are ever more
refined, are not capable of doing this.

The other way, however, is through the distinction made by the great
philosopher-psychiatrist Karl Jaspers - between scientific explanation
on the one hand, and clinical 'understanding' on the other. When
psychiatrists such as Murray see patients, there is an entirely
different level of anecdotal evidence. And this is where the real
motor for changing perceptions about cannabis have originated.

First, there are patients who improve under care, leave hospital and
return, equally psychotic, after going off their medication and back
to the weed.

Then there are the increasing numbers of adolescents in wards
presenting with psychotic symptoms. There have been hints, but as yet
no firm evidence from the cannabis studies, that the earlier in
adolescence young people take cannabis, the greater the chances of
developing psychotic illnesses later in life. What Murray and others
want, before they make any claims, is more research. But it
nevertheless remains a phenomenon that many psychiatrists are
increasingly witnessing on the wards.

Despite the excitement of new research, there is no more certainty now
about the original causes of my brother's illness. Schizophrenia and
bi-polar disorder are ancient, complex diseases of the mind, as old as
consciousness itself. But if there is one thing that he and his family
would change, and can imagine changing, if we could - even if it
wasn't the primary cause - it would be to stop a 14-year-old boy from
taking that first toke.

[sidebar]

CANNABIS FACTFILE

. Cannabis is the name for products derived from the plant Cannabis
sativa. It contains over 400 chemicals, including THC
(delta-9-tetrahydrocannabinol), which determines its strength .

. It is most commonly found as grass, the dried flowering tops, leaves
and stems of the plant, or resin, a solid lump of compressed parts.
One modified strain, known as skunk, below, has a THC content of about
20 per cent.

. It is the UK's most popular drug, with 20.9 per cent of 16- to
24-year-olds using it, according to the 2006-07 British Crime Survey.
But between 1998 and 2006-07, use among 16- to 59-year-olds fell from
10.3 to 8.2 per cent.

. Cannabis was reclassified from a Class B to a Class C drug in 2004,
meaning smokers would not necessarily be arrested if found to be in
possession of small quantities. However, the sentence for possession
with intent to supply is two to 14 years compared with five to 14 for
class B drugs. The law in many European countries has been relaxed,
and although cannabis remains illegal it is tolerated in small quantities.