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Table of
Contents
Title Page
Contents at a glance
Contents
Preface
1 Why I had to write this book
2 Is ecstasy more dangerous than
horse riding?
3 How can we measure the harms done
by drugs?
4 Why do people take drugs?
5 Cannabis, and why did Queen
Victoria take it?
6 If alcohol were discovered today,
would it be legal?
7 “Meow meow” – should mephedrone
have been banned?
8 What is addiction? Is there an
“addictive personality”?
9 Can addiction be cured?
10 Cocaine – from chewing to crack
(or, eats shoots and leaves)
11 Why was smoking banned in public
places?
12 Prescription drugs – Am I
addicted to Valium, Doctor?
13 Can drugs improve performance?
14 Psychedelics – should scientists
try LSD?
15 The War on Drugs, and drugs in
war
16 The future of drugs
17 What should I tell my kids about
drugs?
URLs
Index
A, B, C
D, E, F
G, H, I
J, K, L
M, N, O
P, Q, R
S, T, U
V, W, X
Y, Z
Copyright
Advertisement
Contents
at a glance
Preface
1 Why I had
to write this book
2 Is ecstasy
more dangerous than horse riding?
3 How can we
measure the harms done by drugs?
4 Why do
people take drugs?
5 Cannabis,
and why did Queen Victoria take it?
6 If alcohol
were discovered today, would it be legal?
7 “Meow meow”
– should mephedrone have been banned?
8 What is
addiction? Is there an “addictive personality”?
9 Can
addiction be cured?
10 Cocaine –
from chewing to crack (or, eats shoots and leaves)
11 Why was
smoking banned in public places?
12
Prescription drugs – Am I addicted to Valium, Doctor?
13 Can drugs
improve performance?
14
Psychedelics – should scientists try LSD?
15 The War on
Drugs, and drugs in war
16 The future
of drugs
17 What
should I tell my kids about drugs?
URLs
Index
Contents
Title Page
Preface
1 Why I had to write this book
Who this book is for
2 Is ecstasy more dangerous than horse riding?
Go compare
Equasy
What is ecstasy?
Does ecstasy kill?
What are the other harms of ecstasy?
Ecstasy in the media
Ecstasy: a moral issue
Why measuring drug harms frightens politicians
Ecstasy and post-traumatic stress disorder
3 How can we measure the harms done by drugs?
Why measure?
Sixteen different sorts of harm
Multi-criteria decision analysis
The expert panel
Which drugs did the expert panel consider?
Rating the drugs
Weighting the scores
Results
Limitations of the model
Critical reception
Conclusion
Reviewing a drug’s Class? The case of ketamine
4 Why do people take drugs?
How drugs evolved
Chemicals in the human brain
A typical day without drugs
What is a drug?
1. Opioids – opium, heroin, methadone,
2. Stimulants or “uppers” – cocaine, amphetamine,
3. Depressants or “downers” – alcohol,
benzodiazepines, GHB
4. Psychedelics – LSD, mushrooms,
Less easily-classified drugs
A typical day on drugs
A brief history of drug use
Why do people take drugs?
Why this matters
5 Cannabis, and why did Queen Victoria take it?
Cannabis as hemp
Cannabis as a drug
What are the benefits?
What are the harms?
Cannabis routes of use
Is skunk more harmful than hash?
Why did cannabis stop being seen as a medicine?
Medicinal cannabis use in the UK today
Conclusion
Does cannabis cause schizophrenia?
6 If alcohol were discovered today, would it be
legal?
How the drinks industry influences alcohol policy
How can we reduce the harm done by alcohol?
Conclusion
7 “Meow meow” – should mephedrone have been banned?
“Meow meow”
What is mephedrone and why is it called plant food?
The harms and benefits of taking mephedrone
Why was mephedrone banned?
The designer drug problem
Alternative approaches
The very least we ought to know
Conclusion
The original cathinone: khat
8 What is addiction? Is there an “addictive
personality”?
Addiction in history
The brain mechanisms of addiction
What is tolerance and why does it occur?
Withdrawal and craving
Diagnosing addiction
Is there an “addictive personality”?
Protective factors – why some people don’t get
addicted to drugs
Conclusion
How does neuroimaging work?
9 Can addiction be cured?
Introduction
Case study 1: Tony Adams and alcohol
Case study 2: Pete Doherty, heroin and crack
Case study 3: Amy Winehouse
Psychological treatments
Pharmacological substitutes
Other pharmacological treatments
What is heroin?
Why do people take heroin, and why can’t they stop?
Using heroin to treat heroin addicts
Advantages and disadvantages of methadone treatment
Buprenorphine – a better solution?
Evaluating treatments
The Portuguese experiment
Preventing addiction
Conclusion
10 Cocaine – from chewing to crack
Routes of use and main associated harms
Why are drugs used in different forms?
Kinetics and dynamics of addiction
From chewing to crack: the history of cocaine
Why is crack twice as addictive as cocaine?
Conclusion
The international damage done by cocaine
11 Why was smoking banned in public places?
The 2007 ban on smoking in public places in the UK
What is tobacco?
What are tobacco’s harms and benefits?
How do we know that smoking causes lung cancer?
Why is smoking so addictive?
Public-health responses and industry resistance
Consequences of the UK smoking ban
Freedom and choice
Conclusion
12 Prescription drugs
What are benzodiazepines and how do they work?
What are the benefits and harms of benzodiazepines?
Antidepressants and SSRIs
Painkillers
The pharmaceutical industry and science
The mental-health epidemic
Informed consent
Conclusion
13 Can drugs improve performance?
Muscle and power
Other drugs in sport
Improving mental performance – cognition enhancers
Conclusion
14 Psychedelics – should scientists try LSD?
How do psychedelics work?
The discovery of LSD
LSD and psychiatry
Set and setting
LSD leaves the laboratory
What are the harms of LSD and psychedelics?
What are the benefits of psychedelics?
Should scientists take LSD?
Mushrooms and other psychedelics
Why were magic mushrooms banned in the UK?
Conclusion
15 The War on Drugs, and drugs in war
The other “war on drugs”
Amphetamines and war
The aims of the War on Drugs
A. Has the War on Drugs reduced supply?
B. Has the War on Drugs reduced demand?
C. Has the War on Drugs minimised harm?
Why are we still at war?
What are the alternatives?
Comparing the harms of cannabis and prison
16 The future of drugs
Genetic sequencing
What are the risks of genetic sequencing?
Treating addiction
Learning and unlearning
New drugs research
The Brain Science, Addiction and Drugs Foresight
programme
What sort of future do we want?
17 What should I tell my kids about drugs?
Young people and drugs
1. Alcohol and tobacco are drugs
2. All drugs can potentially cause harm
3. Tell your kids about drugs from an early age
4. Never inject
5. Don’t use solvents
6. Don’t take drink and drugs at the same time
7. A criminal record could ruin your career
8. Find good sources of advice
9. If you do take drugs, be clear why
10. If you do get into trouble with drugs, get help
quickly
11. If you use drugs, don’t let them interfere with
school
Butane and other solvents
URLs
Index
Copyright
To
avoid interrupting the flow of reading, the book contains no footnotes.
Instead, there are detailed lists of sources and references at the end of each
chapter. In the text, a numbered link (e.g. 2) indicates the start of the text that the note relates to, and the
chapter’s endnote repeats the page number and the original text, followed by
the text of the note. For example, on page 1, “2 a lecture I’d given a few months before”, points to the note “2 a
lecture I’d given a few months before • Estimating Drug
Harms: A Risky Business?, David Nutt, URL-2, October
10th 2009”, which appears at the end of the chapter.
URLs and
web links
To
save space and duplication, URLs for webpages are shown like this: URL-2, with the
full text of the corresponding web link given in the list of URLs on page 317.
Acknowledgement
1Tom Brake MP: Does the Prime Minister
believe that once a healthier relationship is established between politicians
and the media, it will be easier for Governments to adopt evidence-based policy
in relation to, for instance, tackling drugs?
David Cameron: That is a lovely
idea.
In October 2009, 2a lecture
I’d given a few months before was released as a pamphlet on the internet. For
some reason – perhaps it was a slow news day – this got picked up by the media
and I was invited on to BBC Radio 4 for an interview. This generated more
interest and several more interviews. A few days later I got an e-mail from the
then Home Secretary Alan Johnson asking me to resign from my position as chair
of the Advisory Council on the Misuse of Drugs (ACMD). When I refused he
released a statement saying that I had been sacked.
The lecture that sparked
off this chain of events had covered a number of topics, but all the media
wanted to talk about were my views on cannabis. In January 2009, against the
recommendation of the ACMD, after four years in Class C, cannabis was
re-upgraded to Class B, indicating increased harmfulness. Jacqui Smith, who was
Home Secretary at the time, justified ignoring the recommendations of our
report because, she said, her 3“decision
takes into account issues such as public perception and the needs and
consequences for policing priorities…. Where there is … doubt about the
potential harm that will be caused, we must err on the side of caution and protect the public.” In the lecture, I discussed whether
this was a rational approach, and particularly whether putting a drug in a
higher legal Class in order to “err on the side of caution” would actually
protect the public and reduce harm.
I’d called the lecture Estimating Drug Harms: a Risky Business? because I knew
from experience that talking about the harm done by drugs in relative terms was
considered politically sensitive. This had been made very clear to me when a
scientific editorial I’d written the year before, comparing the harms of
ecstasy with those of horse riding, provoked questions in Parliament and an
unhappy personal call from Jacqui. (You can read more about this episode on
page 20.)
There had been a similar
reaction to a 4paper I
co-wrote in 2007, which tried to rank 20 drugs in order of harmfulness, taking
into account 9 different sorts of harm, including physical, psychological and
social factors. Politicians didn’t like the idea of some drugs being openly
acknowledged as “less harmful” than others (or even worse, less harmful than
legal drugs such as alcohol), in case it encouraged more people to use them, or
made the politicians seem less “tough” in the eyes of the tabloids. This is
despite the fact that the point of having different
Classes of drugs built into the Misuse of Drugs Act was to communicate to the public
a degree of relative harm 5(Table
1.1). Class B drugs should be less harmful than Class As, and Class C drugs
less harmful than Class Bs. Incidentally, many drugs that have medical uses are
both covered by the Misuse of Drugs Act, and regulated by the Medicines and
Healthcare products Regulatory Agency (MHRA) and the Medicines Act (Figure
1.1).
|
Class |
Includes |
Possession |
Dealing |
|
A |
Ecstasy, LSD, heroin, cocaine, crack, magic mushrooms, amphetamines
(injected) |
7 years |
Life |
|
B |
Amphetamines, cannabis, Ritalin |
5 years |
14 years |
|
C |
Tranquillisers, some painkillers, GHB, ketamine |
2 years |
14 years |
Which brings us back to
cannabis – the only drug in the history of the Misuse of Drugs Act ever to be
downgraded, following recommendations made by the 6Runciman
report in the year 2000. After the downgrading of cannabis, however, the media,
along with some politicians and medical professionals, became concerned that
stronger forms of the drug (known as “skunk”) were causing serious mental
illnesses such as schizophrenia.
Certainly,
nobody was calling cannabis safe. However, as my 2007 report had shown, across
a range of different sorts of harm it was by no means as damaging as many other
drugs, particularly alcohol. This was a point I made in my lecture, and which
got picked up in the radio interview: “surely you can’t be
saying alcohol is more harmful than cannabis?” I replied yes, that’s
exactly what I’m saying, it’s there in my 2007 paper, which at the time was reported
on the front page of the Independent and the Guardian so it was hardly a secret. But this question was
repeated in the other interviews that week – everybody wanted the quote that
alcohol was more harmful than cannabis. It seemed like an entirely defensible
thing to say, as it was based on my own scientific work, and backed up by a
similar study from Holland which had agreed that alcohol deserved to be ranked
among the most harmful of drugs. In these interviews I also observed that the
government had asked the ACMD to determine which Class cannabis belonged in,
and then hadn’t followed our advice.
7In a letter
to the Guardian a few days after he sacked me, Alan
Johnson explained that I “was asked to go because he cannot
be both a government adviser and a campaigner against government policy.”
8I responded
in The Times that I didn’t understand what he meant
when he said I had crossed the line from science to policy, and that I did not
know where this line was. The ACMD was supposed to
advise on policy, and indeed it was set up by the Misuse of Drugs Act because
even in the 1970s it was known that politicians liked to play party politics
with drugs regulation. Of course, politicians have to take into account issues
beyond “pure” scientific evidence in many of their decisions, but the legal
Class of a drug is supposed to inform the public about relative harm, and those
who designed the Act recognised this was best determined by a group of
independent experts. By acting against our recommendations, the Brown
government had themselves blurred the line between science and policy.
The subtitle of this book
refers to minimising the harm done by drugs. This has always been my primary
concern as a psychiatrist, and what I always hoped the ACMD was working
towards. The upgrading of cannabis to Class B was the third time we had been
ignored. (The other two were when magic mushrooms were made Class A without
consulting us, and when the government
refused to downgrade ecstasy to Class B despite our recommendation.) The longer
the government went on creating policies that conflicted with the scientific
evidence, the more harm those policies would do, not least because they
undermined our ability to give a consistent public-health message, especially
around the dangers of alcohol. The more hysterical and exaggerated any Home
Secretary was about the harms of cannabis, the less credibility they would have
in the eyes of the teenagers binge-drinking themselves into comas every day. If
we’re going to minimise harm, we have to have a way of measuring it, and a
policy framework that can respond to this evidence. Yet even comparing the
dangers of cannabis and alcohol was considered a “political” act that
overstepped my remit as a scientist and physician.
I am not the only
scientist to have suffered the displeasure of the Brown government. A couple of
years ago, the Chief Medical Officer (CMO) Sir Liam Donaldson warned of the
rapidly-growing medical costs of alcohol use and recommended 9a sensible
policy of increasing the price of the cheapest drinks. His report was dismissed
in an insulting manner by the Labour government, leading to his leaving the
post of CMO early. The past-president of the Royal College of Physicians 10Sir Ian
Gilmore was also ridiculed by much of the press and parts of government when he
shared his view that the current drug laws were not working, and that the
personal use of drugs should be decriminalised as in Portugal.
The day after I was
sacked, I received an email from Toby Jackson, a man with a keen interest in
science, who was in the fortunate position of being rather wealthy. He was
horrified by my treatment and offered to fund an alternative to the ACMD that
could carry out drugs research free from political interference. Together, we
founded the Independent Scientific Committee on Drugs (ISCD), and most of the
scientific experts who resigned from the ACMD as a result of my sacking have
joined us on the team. (A few members have also worked with both councils
simultaneously.) Being outside government has in many ways been a blessing, as
it has allowed us to be far more outspoken in our criticism of government
policies, notably during the mephedrone debacle. My hope is that this book can
put some of the ISCD’s work in context, and help contribute to a debate about drugs – including alcohol and tobacco – which is grounded
in objective evidence.
Who this book is for
You don’t need any
specialist knowledge to understand this book: it doesn’t assume you have any
prior experience in medical or drugs matters. At the back of the book there are
suggestions for further reading if you want to look into any of the topics in
more detail. There is also a full list of the webpages we reference; this list
is also on the book’s website (uit.co.uk/drugs) to make it easy to access the references online.
While everything in this
book is grounded in scientific evidence, drugs also have social and cultural
aspects. We can’t talk about reducing the harms drugs cause without examining
how they are used, how freely available they are, and their legal status. So
this is also a book about policies – the ones that reduce harms (like the
smoking ban), and the ones that increase them (like allowing cut-price alcohol
in supermarkets). Inevitably, the book is critical of the “War on Drugs”
(chapter 15), not just because this set of policies has caused enormous damage
to millions of people around the world, but
also because the evidence of the harm it has been causing hasn’t led to a
change of approach. Politicians must often make decisions with imperfect
knowledge, and sometimes those decisions don’t work or have unintended negative
consequences. The War on Drugs wasn’t so obviously the wrong thing to try in
the 1970s, but today it is clearly doing more harm than good, and the “drugs
problem” needs radical rethinking as a public-health crisis rather than a moral
crusade.
Notes
1 Tom Brake MP: Does the
Prime Minister believe •Phone Hacking Oral Answers to Questions – Prime
Minister, Tom Brake MP, URL-1, July 13th
2011. Follow the link at URL-1 to see Tom
Brake’s question in context.
2 a lecture I’d given a few months before• Estimating
Drug Harms: A Risky Business?, David Nutt, URL-2, October
10th 2009
3 “decision takes
into account issues such as public perception and the needs and consequences
for policing priorities.•URL-2 as above.
4 paper I co-wrote in 2007• Development of a rational scale to assess the harm of drugs of
potential misuse, Nutt et al, Lancet, 2007
5 (Table 1.1)• Class A, B and C drugs, Home
Office, URL-177.
6 Runciman report• Drugs and the law, Report
of the Independent Inquiry into the Misuse of Drugs Act, Chairman Viscountess
Runciman, URL-3, 2000
7 In a letter to the Guardian• Why Prof David Nutt was shown the door, Alan Johnson, URL-4, November
2nd 2009
8 I responded in The Times• Penalties for drug use must reflect harm, David Nutt, URL-5, November
2, 2009
9 a sensible policy of increasing the price of the cheapest drinks• Chief Medical Officer vows to press on with anti-alcohol campaign,
despite No. 10 rebuff, Sam Lister, URL-6, March
17th 2009
10 Sir Ian Gilmore was also ridiculed by much of the press and parts of
government• Top doctor Sir Ian Gilmore calls for drugs law
review, BBC news, URL-7, August
17th 2010
Every year in the UK around
110 people
die while horse riding, and there are over 2100 road
traffic accidents involving horses which often result in deaths as well. Falls
onto the neck and spine can lead to permanent spinal injuries, and head
injuries can lead to irreversible brain damage, as my patient experienced. In
some shire counties where the sport is very common, it is well-recognised as a
leading cause of early-onset Parkinson’s disease. Studies in the USA have
calculated there are approximately 11,500 cases of traumatic head injury each
year due to riding. In the UK, 3research
from the National Spinal Injuries Centre at Stoke Mandeville hospital shows a
rider can expect a serious accident once in every 350 hours riding. If we
assume that there are 42 million
riding episodes a year, that gives us about 5,700 serious accidents. And
although more experienced riders are probably more aware of the dangers, they
are also more likely to take risks and suffer injuries and take part in the
most dangerous forms of cross-country racing. (Eventing and fox-hunting are
more risky than other sorts of riding, because of the jumps.)
Go compare
I began by estimating the
number of people ecstasy kills each year. The numbers vary slightly depending
on where you get your figures from, but coroners’ reports list 5ecstasy as
the sole cause of death for 10–17 people a year, and it’s mentioned on the
death certificates of 33–50 others. Most people who take ecstasy are “poly drug
users” (meaning they take other things at the same time), and just because they
had ecstasy in their system when they died doesn’t mean it necessarily
contributed to their deaths. So I took a rough estimate of 10–50 deaths a year.
I then looked for data on
ecstasy and road traffic accidents. There didn’t seem to be much information on
this, perhaps because the police don’t test
for it very regularly, but I did find some laboratory studies where people
simulated driving while under the influence of ecstasy alone, and after taking
ecstasy and alcohol together. These showed that although the drug impairs some
aspects of driving performance, it actually improves things like attention and
concentration, and this was particularly marked when combined with alcohol.
Given the lack of clear data either way, I decided to omit ecstasy-related
traffic accidents.
To compare with the
number of head injuries from horse riding, I looked back at the report on
ecstasy we produced in 2008 when I was still chair of the ACMD, where we
estimated that the drug was in some way involved in a couple of thousand
hospital admissions every year. Most of these were pretty mild, or primarily
caused by co-ingestants (ie other drugs taken at the same time, such as alcohol
or GHB), but a few each year were serious, ecstasy-specific, injuries such as
liver damage. I picked a rough figure of 62,000
serious but non-fatal injuries from ecstasy every year, which was likely to be
an overestimate.
Of course, becoming
addicted is one of the biggest dangers posed by drugs, and while ecstasy doesn’t
cause a physical withdrawal syndrome, psychological dependence isn’t unknown.
About 71,000 of
those who seek specialist treatment for drug dependence every year say it’s the
main drug they’re abusing, which probably represents about half of those
addicted to ecstasy, as not everybody seeks professional help. (Although not
strictly an addiction, the pleasure of riding is so great that many people want
to continue the sport even after causing themselves harm. 8Melanie
Reid, the Times journalist who broke her neck falling
from a horse in 2010, has described her longing to ride again in terms very
reminiscent of drug use.)
Another big concern is
that people under the influence of drugs might behave antisocially. However,
aggression is very rare in ecstasy users, and if any do become violent it’s
almost certainly because of other drugs they’ve taken (such as alcohol). This
indirect association is similar to the relationship between horse riding and
the occasional violence when hunters clash with hunt saboteurs. Antisocial
behaviour doesn’t seem to be a significant source of harm for either activity.
|
Different sorts of harm
|
Ecstasy (60 m episodes/yr)
|
Horse riding (2 m episodes/yr)
|
|
Deaths |
10–50 deaths/yr |
10 deaths/yr, plus some fatal road traffic accidents |
|
Physical damage |
2,000 hospital admissions |
100 non-fatal road traffic accidents, 5,700 serious accidents |
|
Addictiveness |
1,000 seek treatment every year, 1,000 others are also addicted |
Not really applicable |
|
Psychological damage
|
Ecstasy can cause mild cognitive impairment for heavy users, memory
problems, occasionally people have visual hallucinations and panic attacks.
There’s a weak link to depression |
Memory loss, personality change, early onset Parkinson’s disease |
|
Loss of tangibles and relationships |
Rare cases |
Rare cases like my patient |
|
Injury to others |
Very little |
Road traffic accidents, occasional aggression between hunters and hunt
saboteurs |
|
Crime |
Not much, apart from dealing and supply of drug itself |
Illegal hunts |
|
Economic cost |
Treating injuries on the NHS |
Treating injuries on the NHS |
|
Total |
About 6,000/yr |
About 6,000/yr |
The total number of
“adverse events” for ecstasy and horse riding were very similar in the end –
perhaps about 6,000 cases every year (Table 2.1). Ecstasy pills, however, are
far more common than riding, with police estimating that about 960 million
tablets are taken every year. 6,000 out of 60 million means that ecstasy causes
roughly one case of 10acute harm
every 10,000 episodes: every 10,000th pill, someone is likely to get hurt. This
is obviously a very rough estimate, but was so much less
likely than getting hurt every 350 episodes that I felt confident saying that
horse riding was a more dangerous activity.
Equasy
In
2009, I wrote an 11editorial in
the Journal of Psychopharmacology comparing the harms
caused by ecstasy to those of a made-up affliction called “equasy”, short for
“equine addiction syndrome”. I pointed out how dangerous equasy was, and
suggested that we consider banning horse riding as a harm-reduction measure –
adding that this would be far more practical than banning drugs as it’s hard to
ride a horse in the privacy of your own home! Apart from a few readers of the Horse and Hound, most people understood that this was
tongue in cheek: I was making a point that criminalising risky behaviour is
only one way to reduce harm, and not always the most appropriate way. The
comparison with ecstasy was also intended to highlight the fact that the drug
debate takes place without reference to other causes of harm in society, which
tends to give drugs a different, more subjectively-worrying, status.
As chair of the Advisory
Council on the Misuse of Drugs at the time, I suppose I knew that this would
provoke a response from government, but I didn’t expect a personal call from
the then Home Secretary, Jacqui Smith, asking me to apologise, or for my
editorial to be mentioned in the House of Commons. In a speech shortly after
publication, she said that my piece 12“makes light of a serious problem, trivialises the dangers of drugs,
shows insensitivity to the families of victims of ecstasy and sends the wrong
message to young people about the dangers of drugs.” A Conservative MP joined in, saying that drug use and horse riding
were 13“completely
incomparable”, and that I was in the “wrong job”.
This seemed like
something of an overreaction. After all, I had only compared two sets of
figures already freely available, and suggested that they might help us to
think in a different way about our approach to drugs. I certainly didn’t mean
to trivialise the pain experienced by those who had lost family members to
ecstasy, and did make a public apology to that effect – although I maintain
that the suffering of my patient and her family as a result of her horse riding
accident was also very severe. But the fact that two thousand words in a
scientific journal could provoke so much hostility seemed to speak volumes
about our approach to the subject of
drug harms. To understand why people objected so strongly to the suggestion
that taking ecstasy might be a rational choice, comparable to the rational
choice of taking part in a risky sport such as horse riding, we need to look at
the history of the drug, learn more about its effects, and understand its
particular place in the media.
What is
ecstasy?
Ecstasy creates these
effects by releasing serotonin in the brain and central nervous system. Serotonin
is a naturally-occurring neurotransmitter – a chemical that sends messages
round the brain – which helps regulate sleep, appetite, muscle contractions,
intestinal movements and mood. (When people have clinical depression, we give
them Selective Serotonin Reuptake Inhibitors (SSRIs), which help to increase
the level of serotonin available to do its work.) Dopamine, a pleasure hormone,
is also released, contributing to the sense of euphoria. Users start feeling
the effects of the drug 30–60 minutes after taking a pill, and these effects peak after 1–2 hours. Some people prefer to buy the drug as a powder
and snort it, which produces faster and more short-lived effects. In recent
years this has probably become the most common form, as the purity of pills has
decreased.
Does
ecstasy kill?
Alongside these more
common causes of death, there have been the occasional cases of liver failure,
kidney failure and sudden cessation of heartbeat.
Serotonin is involved in regulating blood clotting, and some people have died
from blood clots followed by uncontrolled bleeding. Ecstasy raises the heart
rate and blood pressure, so heart attacks are not unknown, and some users have
also suffered brain haemorrhages. These rare but fatal reactions are similar to
allergies, and are probably the result of genetic susceptibilities or other
underlying conditions – it’s possible that one day we’ll be able to test for
particular genes that make these reactions more likely. Of course, these are
all tragedies for the families involved, but they’re considerably 14less common
than other allergies which can be fatal, such as peanut allergies.
What are the other harms of ecstasy?
As
time went by and deaths became less common, the focus of research and
public-health campaigns moved from the dangers of dying or long term physical
damage, to concerns about ecstasy’s psychological effects. In particular, a lot
of research has looked at the possible harm it might do to serotonin nerve
cells, a process called neurodegeneration. Studies which 15gave rats
and monkeys huge doses of the drug did find that it harmed their serotonin
cells, but despite a concerted effort to replicate this in humans when it was
being trialled for medical use, ecstasy has never been shown to cause
neurodegeneration at normal doses.
Heavy users have been
shown to have 16a degree of
cognitive impairment and memory loss, but this is mild and short term, and
almost always improves once they stop taking ecstasy. It’s hard to know with
poly drug users how responsible any individual substance is for causing
problems, and this impairment is probably caused by the other drugs and
activities people indulge in under the influence of ecstasy, such as dancing
for hours. An interesting study of 17Mormon teenagers,
who were taking ecstasy but no other drugs, and no alcohol, found no
differences between their mental functioning and those who took no drugs at
all.
Despite concerns that
ecstasy might interfere in the long-term with our serotonin systems, 18causing
depression, studies that have looked at this haven’t found a clinically
significant link. Although heavy ecstasy users,
particularly those with a specific genotype, score slightly worse on depression
rating scales overall, even the worst affected weren’t in the range for
clinical depression. A recent trial of treating post-traumatic stress disorder
(PTSD) with MDMA (ie ecstasy) has shown extremely encouraging results; as PTSD
has a strong relationship with depression, it may be that ecstasy can be used
to treat mood disorders. We simply don’t know, because the research has never
been done.
Ecstasy
in the media
The
media have an intense and often disproportionate interest in the harms of
ecstasy, in large part because of how the drug was introduced into the UK.
Ecstasy first appeared in dance venues in the USA in the early 1980s, and came
to Europe after being used by thousands of clubbers in Ibiza in the summer of
1986. The drug had a profound impact on the genre of dance music, and soon
large crowds were being pulled into clubs by the promise of the kind of
euphoric trance music that sounded particularly good if you were high on
ecstasy. Although extremely popular, this created 19two new
problems for the club owners. The first was that the dancers were inevitably
followed by the criminal gangs who were providing the illegal drug everyone
wanted to take; the second was that ecstasy users didn’t drink much alcohol,
which the dance clubs depended on for their profits. As clubs became too
expensive to hire, event organisers started looking for spaces they could use
without paying – open fields in summer and empty warehouses in winter. In the
days before the internet, the “rave” or “free party” organizer would announce a
meet-point over pirate radio, and then lead a convoy of cars to the secret
location which they’d occupy for the duration of their party.
These parties did pose a
genuine health and safety challenge: at big events, thousands of people were mixing
large quantities of drugs, in remote locations that were difficult for the
emergency services to reach if something went wrong, especially in the days
before mobile phones. Although the users themselves were unlikely to be
aggressive or behave antisocially, the drug dealers making money at the parties
were sometimes violent, and this was extremely
difficult to police. However, while these concerns were real, a lot of the
pressure on the government to respond to “rave culture” derived from several
other social issues which were then current, such as the protests against the
Conservative road expansion programme, squatter and traveller rights, and hunt
saboteurs. Since ecstasy was already illegal, John Major’s government took the
step of banning “free parties” in the Criminal Justice and Public Order Act of
1994, defining a rave as an event which played music with 20“repetitive
beats” in unlicensed venues. This essentially forced dancers back into clubs
which either charged high entrance fees or relied on clubbers consuming a lot
of alcohol. In fact, the only significant dip or levelling out in Britain’s
steady increase in alcohol consumption over the past five decades was from the
end of the 1980s to the mid-1990s 21(Figure
2.1), because so many people switched to ecstasy during that period.
Figure 2.1: Rise in estimated alcohol
consumption (in litres of alcohol per person over the age of 14).
The result of this social
and legal background was that ecstasy became a “story” for the media,
associated with anti-government protest and youthful counter-culture. As a
result, there has been the systematic 22over-reporting
of ecstasy-related problems compared with other drugs, giving
the impression that ecstasy is more harmful than it actually is. An
enlightening study of the Scottish press from 1990 to 1999 compared newspaper
reports of drug deaths with official coroners’ data. It found that media
interest varied considerably depending on the drug involved. Out of 265 deaths
from paracetamol, the media reported only one, but a third of deaths from
amphetamine (13 out of 36) made it into the news. Over the same time period,
there were 28 deaths from ecstasy, 26 of which were reported – a far higher
proportion than any other drug.
Of course, only stories
that fit with the narrative that “ecstasy is bad for you” receive this kind of
media coverage. An example of the contrast between the reaction to “good” news
and “bad” news about the drug took place in the USA in 2002. A scientist called
George Ricaurte published a 23paper in Science, which claimed to have found new evidence that
ecstasy caused “severe dopaminergic neurotoxicity” in monkeys. As this effect
hadn’t been found in previous studies at low doses, this surprised many other
scientists in the field, but if true it could mean that recreational ecstasy
users were putting themselves at risk of developing diseases like Parkinson’s
in later life. Ricaurte’s study was widely reported at the time, especially as
the Reducing Americans’ Vulnerability to Ecstasy (RAVE) Bill was going through
Congress at the time. Then, in September 2003, Ricaurte published a 24formal
retraction of his paper: somehow, two vials of drugs had got mixed up, and the
neurotoxicity he had found had actually been caused by methamphetamine (crystal
meth). The retraction received almost no attention from the media. “Ecstasy
causes Parkinson’s” is a story, whereas “ecstasy is no more harmful than we
previously thought” isn’t worth reporting.
In fact, rather than
causing Parkinson’s, ecstasy may actually be 25an
effective treatment for controlling its debilitating tremor. If the research that
is currently underway into this topic delivers positive results, this will be
evidence of yet another therapeutic use of the drug, alongside its beneficial
effects in reducing anxiety in terminal cancer patients and in treating
post-traumatic stress disorder (see box on page 24). These breakthroughs rarely
make headlines, and indeed ecstasy currently has no officially approved
medicinal uses at all.
All illegal
drugs have both a Class, which determines the penalties for possession and
supply, and a Schedule, which determines how they are regulated for medicinal
use. Ecstasy is in Schedule I, which means the government does not recognise
any medicinal uses, despite mounting evidence that it is much more effective than
current drugs for several chronic, treatment-resistant disorders. Part of the
reason ecstasy remains in an inappropriate Schedule is because the media are so
obsessed with its harmful qualities, making it very difficult for politicians
to consider any change in its classification. When the ACMD recommended that
ecstasy be downgraded to Class B in 2008, 26the
government made it clear that no matter what the evidence indicated, they were
not going to consider any reduction in the Class A status of Ecstasy.
Ecstasy:
a moral issue
Ecstasy
is a harmful drug – in no way should this chapter be interpreted as saying
anything different. But how harmful? As harmful as drinking five pints of beer?
As harmful as getting on a motorbike? David Spiegelhalter, a professor of risk
communication, has calculated that taking an ecstasy pill is 27as
dangerous as riding a motorbike for about 6 miles or a push-bike for 20 miles.
These sorts of comparisons are useful because they can help people make choices
about their behaviour based on a realistic assessment of the risks.
Politicians, however, are often highly resistant to them.
When Jacqui Smith called
me to ask me to apologise for my equasy editorial (page 13), we had the following
exchange:
Jacqui Smith: You can’t compare harms
from a legal activity with an illegal one.
Me: Why not?
Jacqui Smith: Because one’s
illegal.
Me: Why is it illegal?
Jacqui Smith: Because it’s
harmful.
Me: Don’t we need to
compare harms to determine if it should be illegal?
Jacqui Smith: You can’t
compare harms from a legal activity with an illegal one.
This is problematic for a
number of reasons. For a start, it shoots policy-makers in the foot somewhat,
since it’s 28not at all
clear that governments are especially influential on whether or not someone tries a drug, because experimentation is largely determined
by social norms and cultural trends. (Government policies can, however, be very
influential on whether or not an individual is harmed
by a drug.) In addition, if policies that aim for total abstinence do meet with
some success, this will primarily be among casual users (who will find it
easiest to give up altogether), rather than the heavy users and addicts who
suffer the most harm. If we focused solely on reducing the prevalence of
alcohol use, for example, it’s the 30 million British drinkers who stay within
the recommended daily limits who would be most likely to become teetotal, if
any did at all. It would be absurd to aim an alcohol-harm-reduction strategy at
those who suffer the least harm, rather than trying to help the 10 million
hazardous drinkers to reduce their intake.
In addition, the focus on
reducing prevalence can end up undermining measures that are
shown to reduce harm, in case these measures “encourage” people to experiment
with drugs. A case in point was the 29Reducing
Americans’ Vulnerability to Ecstasy (RAVE) Act which became law in the USA in 2003, supported by the misleading
evidence from Ricaurte’s neurotoxicity study. The Act put more responsibility
on venues to curb illegal drug use on their premises, citing features such as
selling bottled water and providing chill out rooms as evidence that a venue
was catering to the needs of ecstasy-users.
30Critics of
the legislation pointed out that these were precisely the public-health
measures that had helped to bring down the number of ecstasy-related deaths
from dehydration, and that if venues ceased to provide water or spaces to cool
down out of fear of prosecution this could lead to a rise in deaths. As I said
above, there is no clear relationship between policies like the RAVE Act and
levels of use, so the most likely effect would be that young people would
continue to take ecstasy in the same numbers under less safe conditions. But
even if a small number of people were dissuaded from using ecstasy by the RAVE
Act, it’s perverse that this would be charted up as a “success” if the harm
done to users had increased overall.
Why measuring drug harms frightens politicians
The
problems of the RAVE Act illustrate why governments are so nervous about
measuring drug harms. Being “tough on drugs” requires governments to reduce prevalence,
but prevalence alone is the wrong thing to measure – it’s only one factor among
many that make up the total effect of drugs on society; 31Figure 2.2
shows the USA’s estimated total costs in billions of dollars of legal and
illegal drugs, and of some other major causes of health problems. Prevalence
does have a relationship with harm, and reducing use (particularly among
specific target groups such as teenagers) might play a role in an effective
harm-reduction strategy, but it is also the area where we are most in the dark
about what works. What’s more, not only are policies aimed at reducing
prevalence unlikely to work, they often cause more harm than good in other
ways. Measuring these other sorts of harm would discredit governmental
policies, so often the data isn’t collected and this kind of analysis isn’t
done.
Drug harms are very
complex. My comparison of ecstasy with horse-riding was a
back-of-the-envelope calculation, trying to get a rough idea of the scale of
the harms caused by each activity rather than precise figures. Even so, I had
to take into account several different types of harm, some of which were to
individuals (such as deaths and addiction) and some of which were to other
people (such as crime and economic cost). This was not complete and I may have
missed out some important dimensions – for example, I didn’t take into account
the harm done to the horses themselves, who often 32die in big
races and jumping events. It’s important that our measurements are
comprehensive, or a policy which reduces harm in one area might be increasing
the negative consequences somewhere else in the system. In the next chapter
we’ll look at one way to think about harm much more systematically, comparing
drugs with each other across a range of different criteria.
Of course, if you truly
see illicit drug use as a moral problem, then it doesn’t matter if drug users
cause themselves harm, because they took a risk and any negative consequences
are their own fault. However, this is
illogical, since the level of risk in taking drugs is about the same as in
everyday activities like horseriding, which aren’t seen as immoral, and good
policies for horse-riding involve helmets and safety-conscious riding rather
than stopping people getting on horseback. It is also inhumane, going against
the principles of universal healthcare that the UK’s National Health Service
was founded upon, where even self-inflicted illness deserves compassionate
treatment. And it is misinformed, failing to understand how public health
works. The huge improvements in the nation’s health we have seen over the past
century have come about precisely because we started treating everybody: diseases are infectious, and everybody benefits
from helping those at most at risk of contracting and passing them on. Drug
users are part of society, and when we treat them as such the outcomes improve
for everybody, including non-drug users.
Ecstasy and post-traumatic stress disorder
Post-traumatic stress disorder (PTSD) is a
condition that sometimes occurs after a catastrophic life event or traumatic
experience, such as witnessing a murder or being mugged at gunpoint. The
patient suffers flashbacks, anxiety, fear, and nightmares, and may do anything
to avoid reliving the experience – by refusing to leave the house, for example.
PTSD is
surprisingly common – 337.7 million
people in Europe suffer from it each year. It’s very disabling and associated
with high rates of self harm and suicide. Rates are especially high among
soldiers, who are far more likely to experience violent events than civilians –
a study in 2004 found 3418% of
soldiers returning from Iraq and Afghanistan had PTSD, and more die from
suicide than from combat.
The best treatment is
trauma-focused therapy, where the memories are recalled in a safe setting, so
the patient can learn that they’re not in danger any more, and overcome the
fear of them. However, a problem with this approach is that re-engaging with
memories of trauma may be too stressful to contemplate. There are a number of
“traditional” drugs used to treat it, such as benzodiazepines (page 217) and SSRIs (page 221), but the condition is often
treatment-resistant and can last for years.
1.
Be short-acting enough for a
single session of therapy.
2.
Have no significant dependency
issues.
3.
Be non-toxic at therapeutic doses.
4.
Reduce feelings of depression that
accompany PTSD.
5.
Increase feelings of closeness
between the patient and therapist.
6.
Raise arousal to enhance
motivation for therapy.
7.
Paradoxically, increase relaxation
and reduce hyper-vigilance.
8.
Stimulate new ways of thinking to
explore entrenched problems.
Ecstasy has all these
qualities when used in a clinical setting, and is extremely effective. A recent
study of subjects with chronic, treatment-resistant PTSD resulted in an 3583% success
rate – 10 out of 12 subjects essentially no longer had the disorder after just
two sessions of ecstasy-assisted psychotherapy (Figure 2.3). The study also
found no adverse drug-related events or neurocognitive effects. Of course, rare
“allergic reactions” to the drug are still possible, but all medical treatments
are potentially harmful – if the risk is small and the benefit is large, then
the treatment can be justified. Within a clinical setting and under
medical supervision,
bad reactions to ecstasy are almost unknown, and the benefit is relieving
otherwise unremitting PTSD.
Notes
1 10 people die while horse riding• Equasy: an
overlooked addiction with implications for the current debate on drug harms,
David Nutt, Journal of Psychopharmacology 23 (1), 2009
2 100 road traffic accidents• As above.
3 research from the National Spinal Injuries Centre at Stoke Mandeville
hospital• Hazards of horse-riding as a popular sport,
JR Silver and JM Lloyd Parry, Br J Sp Med; 25(2), 1991
4 2 million riding episodes a year• Assume 200,000 riders, each of whom
rides 10 times a year for an hour each time, say.
5 ecstasy as the sole cause of death for 10–17 people a year, and it’s
mentioned on the death certificates of 33–50 others• MDMA
(“ecstasy”): a review of its harms and classification under the Misuse of Drugs
Act 1971, ACMD, URL-8, February 2008
6 2,000 serious but non-fatal injuries from ecstasy every year• As
above.
7 1,000 of those who seek specialist treatment for drug dependence every
year say it’s the main drug they’re abusing• As above.
8 Melanie Reid• Horse Sense, Melanie Reid, The Times, March 12th 2011
9 60 million tablets• MDMA (“ecstasy”): a review of its harms and classification under the
Misuse of Drugs Act 1971, ACMD, URL-8, February 2008
10 acute•An acute condition is one with a rapid
onset, or a short duration, or both. (Whereas in normal speech “acute” is often
used to mean “severe”, in the medical sense you can have a condition that is
acute but not severe.)
Chronic is the
opposite of acute – meaning a condition that lasts a long time. (Again, you can
have a condition that is chronic but not severe.)
11 editorial• Equasy:
an overlooked addiction with implications for the current debate on drug harms, David Nutt, Journal of Psychopharmacology 23
(1), 2009
12 “makes light of
a serious problem,• Drugs Adviser Criticised by Smith, BBC news, February 9th 2009
13 “completely incomparable”, and that I was in
the “wrong job”.• As above, the MP in question was
Laurence Robertson, MP for Tewkesbury.
14 less common than other allergies which can be fatal, such as peanut
allergies• Drugs drive politicians out of their minds,
New Scientist, URL-9, February 11th 2009
15 gave rats and monkeys huge doses of the
drug• MDMA(“ecstasy”): a review of its harms and
classification under the Misuse of Drugs Act 1971, ACMD, URL-8, February 2008
16 a degree of cognitive impairment and memory
loss• Dancing hot on Ecstasy: physical activity and
thermal comfort ratings are associated with the memory and other
psychobiological problems reported by recreational MDMA users, AC Parrott, J Rodgers, T Buchanan et al. Human Psychopharmacology: Clinical and Experimental 21: 285–98, 2006
17 Mormon teenagers• The harmful health effects of recreational ecstasy: a systematic review
of observational evidence, G Rogers et al, Health
Technology Assessment, January 2009
18 causing depression• MDMA(“ecstasy”): a review of its harms and classification under the
Misuse of Drugs Act 1971, ACMD, URL-8, February 2008
19 two new problems for the club owners• The Hacienda:
How Not to Run a Club, Peter Hook, Simon & Schuster Ltd, 2009
20 “repetitive beats”• Powers in relation to raves,
Criminal Justice and Public Order Act, URL-10, 1994
21 (Figure 2.1)• Popular
intoxicants: what lessons can be learned from the last 40 years of alcohol and
cannabis regulation?, Ruth Weissenborn and
David J Nutt, Journal of Psychopharmacology, September 17th 2011. Sources: British Beer and Pub Association Statistical Handbook 2008; Institute of Alcohol Studies Factsheet Trends in the affordability of alcohol in the UK, 2008.
22 over-reporting of ecstasy-related problems compared with other drugs• Distorted? a quantitative exploration of drug fatality reports in
the popular press, Alasdair JM Forsyth, International Journal of Drug
Policy (12), 2001
23 paper in Science•
Severe dopaminergic neurotoxicity in primates after a common recreational dose
regimen of MDMA, George Ricaurte,
Science, September 26th 2002
24 formal retraction of his paper• Retraction: Severe dopaminergic neurotoxicity in primates after a
common recreational dose regimen of MDMA, George Ricaurte, Science, September 12th 2003
25 an effective treatment for controlling its
debilitating tremor• MDMA (“ecstasy”): a review of
its harms and classification under the Misuse of Drugs Act 1971, ACMD, URL-8, February 2008
26 the government made it clear that no matter what the evidence
indicated• House of Commons, Minutes of Evidence, Science and Technology
Committee, URL-160.
27 as dangerous as riding a motorbike for about 6 miles or a push-bike
for 20 miles• Cambridge Ideas – Professor Risk, David
Spiegelhalter, URL-11, December 10th 2009
28 not at all clear that governments are especially influential on
whether or not someone tries a drug• Drugs Policy - Lessons learnt and options for the future,
Mike Trace, URL-12, February 23rd 2011
29 Reducing Americans’ Vulnerability to Ecstasy (RAVE) Act• RAVE Act, US Senate, URL-13, 2003. In
fact the original RAVE Act was never passed, but the Illicit Drug
Anti-Proliferation Act, which incorporated much of the orginal RAVE Act was
enacted in April 2003.
30 Critics of the legislation• Innocent club owners, young people vulnerable under rapidly moving
“Rave” Bill, Drug Policy Alliance, URL-14, July 11th 2002
31 Figure 2.2• Recent Findings on the Economic Impacts
of Substance Abuse, Henrick Harwood, URL-179, presented
to American Psychological Association, Science Leadership Conference, October
23, 2011
32 die in big races and jumping events• Race Horse
Deaths, URL-15, accessed December 10th 2011
33 7.7 million people in Europe suffer from it each year• The size and burden of mental disorders and other disorders of
the brain in Europe 2010, URL-164, HU
Wittchen, F Jacobi et al, European Neuropsychopharmacology (21) 655–679, 2011
34 18% of soldiers• Combat duty in Iraq and
Afghanistan, mental health problems, and barriers to care, Charles W
Hoge et al, The New England Journal of Medicine (351), 2004
35 83% success rate• The safety and efficacy of 3,4-methylenedioxymethamphetamine-assisted
psychotherapy in subjects with chronic, treatment-resistant post-traumatic
stress disorder: the first randomized controlled pilot study, Michael Mithoefer et al, Journal of
Psychopharmacology 25 (4) 439–452, 2010
Why measure?
In effect the ACMD was
formed to take party politics out of drug-harm assessments, because it was
known that politicians liked to vie with each other as to who could be the
“hardest” on drugs: even in the 1970s, this was seen as an easy way to score
political points and gain media support. So a group of experts were given the
responsibility for drug assessment – in much the same way as the Bank of
England has since been given responsibility for setting interest rates. And for
many years this worked. When the UK was facing a major problem with HIV/AIDS
arising from injected heroin use, the ACMD approached the then Prime Minister
Mrs Thatcher and 1recommended
needle exchange programmes. Even though this conflicted with her political
philosophy she agreed to go with the ACMD’s
recommendations, and the UK ended up with one of the lowest rates of HIV among
injecting drug users in Europe. This made the UK a beacon of preventative
policy for the world.
When I first joined the
ACMD in 1998, I thought that, broadly, government policy was going along the
right lines. As time went by, however, I began to see that there were serious
problems with the government’s approach. I became frustrated with politicians’
almost-religious aversion to comparing the risks posed by legal and illegal
activities, illustrated so clearly in the response to my equasy editorial (page
13). I began to question whether criminalisation
was ever an effective or appropriate moral response to drug use (which I’ll
talk about in more detail in chapter 15). But above all, in terms of my
specific role in the ACMD, I became deeply unhappy with the way the government
was ignoring the recommendations we were producing about the Classes that
should be allocated to certain drugs, notably ecstasy, mushrooms and cannabis.
The Misuse of Drugs Act may not be a perfect piece of legislation, but at least
the government could use it rationally, and do what the Act required by
listening to the expert Advisory Council it set up.
I started to think about
the whole purpose of classification. Clearly, some drugs are more harmful than
others, and people should have a broad understanding of the risks if they
choose to take them. Politicians sometimes invoke the precautionary principle
to argue that, if we’re not completely sure if something might do harm, we
should put it in as high a Class as possible. However, this may be unwise as it
can have perverse consequences. There was a very sad tale a few years ago of a 2young girl
in the Shetland Islands who wanted to try cannabis, but could only get hold of
heroin and died of an overdose; if cannabis and heroin are in the same Class,
indicating that they pose the same sorts of risks, this kind of tragedy may
happen more often. More generally, people aren’t stupid, and have access to
other sources of information about drugs apart from the government. If the
other evidence and the government response don’t seem to add up, it undermines
public confidence in what the government is doing and makes giving a credible
educational message impossible.
Having
different categories of drugs is sensible. Almost no ordinary member of the
public is going to read long scientific reports, and having a simple way to
assess relative harmfulness would be useful for a lot of people, regardless of
what criminal sanctions are attached to which Class. If a drug’s position in
the Class system was actually determined by how harmful it is on a number of
different measures, then people might understand the risks they were taking
better, and even choose to take substances in lower Classes which will do them
less damage.
Sixteen different sorts of harm
My first attempt to
compare drugs harms was in 3a paper I co-wrote in 2007,
where we looked at 9 different sorts of harm – 3 physical, 3 social and 3
associated with dependence. We received a lot of constructive criticism, and
once we had taken on board our critics’ comments we came up with a comprehensive list of 16 criteria of harm,
9 to users, and 7 to others. By this time I had been sacked by the government
and had set up the ISCD, so 4my second
paper, published in 2010, was under those auspices, although 5the initial
development of the 16 criteria was with the ACMD. These 16 criteria were:
Harms to
users
1. Drug-specific mortality – death from
poisoning. We measure how poisonous a substance is by comparing the amount
needed to give psychoactive effects and the amount that would be fatal; this
gives a safety ratio. For example, alcohol’s safety
ratio is 10. If 2 units of alcohol are enough to have a psychoactive effect on
a small female, 20 units will put her into a lethal coma. Some substances
rarely if ever cause death by overdose – cannabis and LSD, for example.
5. Dependence.
We discuss the concept of addiction in chapter 8.
7. Drug-related impairment
of mental functioning. While the previous criterion refers to the
effects of intoxication, drug-related impairment of mental functioning refers
to the psychological effects that continue once the drug has left the body. Heavy
use of some drugs is associated with psychotic symptoms, depression, memory
loss, increased aggression, and anhedonia (an inability to feel pleasure).
Addiction also often leads to depression from the stress and unpleasantness of
being a drug addict.
Harms to
others
10. Injury. Taking drugs usually impairs
motor control and judgement, increasing the likelihood of an incident that
damages someone else. This might be accidental, such as road traffic accidents,
or deliberate, like domestic violence, both of which are hugely influenced by
alcohol.
11. 6Crime outside of the Misuse of Drugs Act
(see endnote). Drug-related crime largely falls into two categories: (a)
acquisitive crime to fund a drug habit, and (b) crime committed when judgement
is impaired while under the influence, such as burglary and vandalism.
14. International damage. Although our main focus was on the
UK, we knew we needed to factor-in harms on an international level. These
include: the huge collateral damage of the War on Drugs; the brutality of the
international drug barons, who are making billions from the illicit trade and
have killed 25,000 people in Mexico alone; and the carbon emissions and other
environmental effects due both to the drug manufacturers and the measures taken
against them.
Multi-criteria decision analysis
Another
criticism of the 2007 paper was that we calculated the final score of harm by
giving each factor the same weight, when in fact some of them might be more
important than others. One of the people who approached us after reading our
paper was Professor Larry Phillips, from the LSE (London School of Economics),
an expert in 7Decision
Conferencing. He offered to help us design a new process for evaluating drug
harms, using multi-criteria decision analysis.
Multi-criteria decision
analysis (MCDA) is a technique often used in situations where a decision needs
to take into account different sorts of information, and where there are so many dimensions that conclusions
can’t easily be drawn from simple discussion. MCDA breaks down an issue into
different criteria, and then compares those criteria with each other to assess
their relative importance. These criteria can include both objective measures
and subjective value judgements, and can incorporate an element of uncertainty.
8Larry
Phillips had previously worked on a big public consultation about the options
for disposing of nuclear waste. Experts and members of the public considered
different criteria, such as cost, safety, and the impacts on future
generations, and then thought about how important each of these criteria was.
This created a model which could be tested under different scenarios and with
different interest groups; in the case of the nuclear consultation, they found
that it needed quite significant changes in the weight given to different
criteria for the most popular options for nuclear-waste storage to change.
Since the model was very stable, even across interest groups as diverse as the
nuclear industry and Greenpeace, it gave a great deal of legitimacy to the
final decision. It was also very transparent: by making clear which parts of a
decision are based on factual evidence and which parts are based on subjective
value judgements, it’s much easier to understand how a conclusion has been
drawn or a decision has been made.
The
expert panel
The panel included five
experts in addiction:
·
Colin Drummond, Professor of
Addiction Psychiatry at the Institute of Psychiatry (IoP). He has spent much of
his career studying alcohol problems, and chairs the group within the National
Institute for Clinical Excellence
(NICE), which develops guidelines for managing harmful alcohol use and alcohol
dependence.
We had
two experts in drug issues relating to young people:
·
Patrick Hargreaves, Durham County
Council Drugs and Alcohol Adviser, who has developed promising new approaches
to drugs education.
·
Eric Carlin, who specialises in
prevention and early intervention in drug use in young people.
The
panel included two chemists:
·
Les King, a former forensic
scientist and adviser to the Department of Health and the European Monitoring
Centre for Drugs and Drug Addiction.
Our
other five experts came from a range of backgrounds:
·
Phil Delgarno, a psychologist
based at Glasgow Caledonian University, who studies drug use in its social
context. Martin Frischer, Senior
Lecturer at the University of Keele, who conducted some of the key research
into the link between cannabis and schizophrenia that informed the ACMD’s 2008
cannabis report.
Which drugs did the expert panel consider?
·
Amphetamine (Class B): pills or
powder, mostly taken by clubbers.
·
Methamphetamine (Class A):
smokable crystal form of amphetamine, not common in the UK.
·
Anabolic steroids (Class C): pills
or powder, used to build up body mass.
·
Khat: a legal leaf which is
chewed, mostly used by people from the Middle East and East Africa.
·
Mephedrone (Class B) pills or
powder, popular with clubbers.
·
Cocaine (Class A): powder, which
is usually snorted.
·
Crack (Class A): smokable crystal
form of cocaine.
·
Butane (legal): gas that can be
inhaled, popular with teenagers.
·
Tobacco (legal): usually smoked in
cigarettes.
·
Alcohol (legal): comes in drinks
of different strengths.
·
Benzodiazepines (Class C): a type
of sleeping pills, mostly available on prescription (eg Valium).
·
Ketamine (Class C): powder which
is snorted, or liquid which is injected, popular with clubbers.
·
Heroin (Class A): brown solid
which can be smoked or “cooked up” into a liquid and injected.
·
Methadone (Class A):
pharmacological substitute for heroin; usually drunk as a liquid.
·
Buprenorphine (Class C):
pharmacological substitute for heroin; comes as a pill.
·
Ecstasy (Class A): pills or powder
containing MDMA which produce feelings of energy and euphoria, popular with
clubbers.
·
Mushrooms (Class A): eaten whole
or brewed as tea, and causing psychedelic experiences.
Rating
the drugs
The
first step of the MCDA process was to rate the 20 drugs according to each of
the criteria. Let’s take 9drug-related mortality as an
example. (Recall, we defined this as death caused by illnesses caused by
drug-taking and associated behaviour and activities.) Looking across the drugs
we decided that heroin was the worst for this criterion, mostly because of the
spread of blood-borne viruses, and health problems associated with addiction
and deprivation. Heroin was given a score of 100. The only drug that we thought
caused no drug-related mortality was LSD, so this was given a score of 0. For
drug-related mortality, this gave us a scale (Figure 3.1).
Our estimates of relative
harm were given an objective quality through the discussion and debate that
occurred during the rating process. We then corroborated our group judgements
by 10comparing
our scores with measurements such as official statistics on drug-related
deaths. We found strong relationships: for example, when we looked at fatality
statistics and drug-specific mortality, the correlation was around 0.98, and
looking at a USA survey on lifetime dependence and our own dependence scores we
found a correlation of 0.95. (A perfect correlation is a score of 1.)
The rating process for
other criteria did highlight a lack of objective data in many areas,
particularly social harms. Here the expert group approach is the best we can do
for now. While this is not perfect, it’s important we make a start on a
quantitative approach, and even approximate figures can give valuable insights,
as well as highlighting where it’s most important to concentrate future
research efforts. If we wait until perfect data is available for everything, we
paralyse the decision-making process and risk damaging or losing lives needlessly.
MCDA exploits the fact that people are generally good at making relative
judgements, particularly in well-informed groups, and using this method to
measure harms means we don’t have to wait until we have perfect information
before we can make decisions that have clear and transparent justifications. It’s also very easy to
incorporate new evidence as it comes to light. (See the section about ketamine
on page 47 as an
example.)
Weighting
the scores
Having
made scales (like those in Figure 3.2) for all 16 criteria, we then weighted
them against each other. This had to take into account two things: how big a
difference between 0 and 100 was, and how important we thought that difference
was between each of the 16 measures. An analogy for how someone might weigh up
different criteria like this in everyday life is if they’re looking to buy a
car. For most people, price is one of the biggest factors in choosing a
vehicle, but if you went to a dealer and the difference between the most
expensive and least expensive models was only £200, you would probably make your
decision based on other factors like size or fuel efficiency. Context is
important too – cost would probably be a much bigger issue if the price
difference was £2,000, unless you were very rich and
wouldn’t notice a few grand here or there. Figure 3.3 illustrates the software
we used to apply the different weightings when comparing the different drugs.
Results
Once
we’d rated all the drugs and weighted the criteria, each drug got a final score
out of 100. Alcohol came top with 72, followed by heroin and crack neck and
neck at 55 and 54, with quite a big drop after that to methamphetamine on 33.
At the very bottom were the empathogens and psychedelics, with ecstasy given a score
of 9, and LSD and mushrooms on 7 and 6. 11Figure 3.4
shows all 20 drugs ranked in order of total harms.
The first thing to note
is how little relationship there is between a drug’s current legal Class and
the position we ranked it in. The top six substances did include four Class As,
but there were also two drugs which are currently legal, which common sense
says you’d expect to find among the least harmful. At the bottom end of the
scale were another three Class As: ecstasy, LSD and mushrooms. In fact, when we
compared legal Class and overall ranking, we found a correlation of 0.04 – which means that there was effectively no relationship at all. By
contrast, the correlation between this paper and my 2007 paper was 0.7, and the
correlation with a similar Dutch study ranking drugs according to harm was
around 0.8. Although these figures show that there wasn’t perfect agreement
across the three studies, they do indicate that we’re all on a similar track,
and in fact many of the differences can be attributed to different
methodologies,
Note just how dangerous
alcohol is – it was ranked as the fourth most harmful drug to the user, and
most harmful drug to others (12Figure 3.5),
making it top overall. Over half of its score came from economic cost, injury,
family adversities and crime. While this is very worrying, we do at least have
a lot of evidence about ways to reduce the harms done by alcohol, and
implementing these should clearly be a priority in our policies relating to
drugs.
Limitations
of the model
No
model is perfect, and there were certain limitations to the approach we took.
Critical
reception
When
the report came out, the headline “Alcohol ‘more harmful
than heroin or crack’” appeared on the front page of the Guardian, and it was widely reported across the British press and beyond. 13The Daily Mail predictably called me a “dangerous
man”; it said the policies I was advancing “would
be a disaster for our society”. In fact I hadn’t
proposed any policies at all, but only a more rational approach to drug
classification.
The government’s response
was interesting. Although the design of the decision analysis process had been
publicly funded while I was still part of the ACMD, the Home Office’s
spokesperson said quite bluntly that they hadn’t read the report, and
continued: 14“our priorities are clear – we want to reduce drug use, crack down
on drug-related crime and disorder and help addicts come off drugs for good.”
This showed that much of the wrong-headedness of the Labour government in
relation to drugs was likely to continue with the new coalition. Getting
addicts off drugs for good is extremely difficult, as chapter 9 will show. Most
drug-related crime is caused by addicts stealing to fund their habit, most
drug-related disorder is related to people being drunk, and both addicts and
drunks tend to be unresponsive to “crackdowns”. And as I argued in chapter 1,
reducing drug use on its own is not a useful aim for drug policy: trying to
shift the focus away from reducing prevalence to reducing harm was exactly why
I wanted to measure drug harms in a more comprehensive way.
Conclusion
When
we wrote the 2007 paper, our primary aim was to examine whether or not the
classification of drugs under the Misuse of Drugs Act reflected the harms they
caused. The resounding conclusion of both that paper, and our later one in
2010, was that it didn’t. So, could we reconstruct a new classification system
out of our results? This would obviously depend on what set of harms – to self
or others – you were trying to reduce, but in terms of overall harm, alcohol,
heroin and crack are clearly more harmful than all the others, so perhaps drugs
with a score of 40 or more could be Class A, 39–20 could be Class B, 19–10 B
Class C, and 9–1 Class D. How widely available these should be and what
penalties they should entail is another conversation altogether, but
classifying in this way would
at least give a consistent public-health message.
Reviewing a drug’s Class? The case of ketamine
15Ketamine was
invented in 1963, as a substitute for phencyclidine, an anaesthetic agent.
Ketamine is a powerful anaesthetic, and very safe because it depresses
breathing very little and doesn’t stop the gag reflex, but it is rarely used in
mainstream medicine because of its psychoactive effects. It is commonly used on
animals, which is why it is often referred to as “horse tranquilliser”. The USA
saw a certain amount of ketamine abuse after the Vietnam war where it was used
in the combat zones. In the UK, until the 1990s recreational use of the drug
was limited to a small number of self-styled
“psychonauts”, who would inject medicinal supplies to explore the weird inner
worlds that ketamine can reveal.
A new sort of abuse
emerged in the 1990s, as the drug users associated with the dance scene started
to manufacture their own ketamine as a white powder, or to buy it in from India
in solution, mislabelled as “rosewater”. It was legal and relatively cheap, and
made a good “downer” at the end of a night on stimulants such as ecstasy and amphetamines;
it was also often mixed with cocaine and snorted in a concoction known as CK1.
The ACMD became concerned in the early 2000s, and recommended it become a Class
C drug in its 162004
report, advice which was acted upon by the government in 2006. The report still
thought that ketamine’s dependence profile was low and that it would primarily
be used in the poly drug setting: we thought the main harm it was doing was
interacting with other substances, making intoxicated people less aware of
their surroundings so they were more prone to accidents and misadventure. The
scores our expert panel gave ketamine over the 16 criteria in our 2010 paper
were largely based on our understanding of the drug from the ACMD’s 2004
report.
In the intervening years
however, new evidence had started to come to light, which was eventually
written up in the ISCD’s first drug report in 2010, about six months after we
went through the decision analysis process. Two new trends were causing concern
for drug workers and GPs: an increase in the number of people seeking help for
ketamine dependence, and an increase in young people (especially young men)
with urinary tract problems related to ketamine use, called “ketamine-induced
ulcerative cystitis”. This is a newly-identified condition, where the bladder
goes into spasm and its wall thickens, resulting in a small bladder capacity.
It’s not entirely clear why ketamine has this effect, but one theory is that it
activates the nerve fibres in the bladder, affecting its ability to expand and
contract as it fills and empties. Symptoms include needing to pee frequently
and urgently, incontinence, pain when peeing, and blood in the urine. In
extreme cases it’s irreversible, and patients need reconstruction or removal of
the bladder altogether, resulting in the need for lifelong medical care. New
evidence also emerged about kidney problems, abnormal liver function and severe abdominal pain (“k cramps”) probably
originating from the bladder. This new evidence showed that ketamine,
especially when taken daily in high doses, is more harmful than we previously
thought.
Notes
1 recommended needle exchange programmes• The role
and basis of drug laws, David Nutt, Prometheus, 2010
2 young girl in the Shetland Islands• Estimating Drug
Harms: A Risky Business?, David Nutt, URL-2, October
10th 2009
3 a paper I co-wrote in 2007• Development of a rational scale to assess the harm of drugs of
potential misuse, Nutt et al, Lancet, 2007
4 my second paper, published in 2010• Drug harms in
the UK: a multicriteria decision analysis, David Nutt et al, ISCD, URL-16, November
1st 2010
5 the initial development of the 16 criteria• Consideration of the use of Multi-Criteria Decision Analysis in drug
harm decision making, ACMD, URL-17, July 28th 2010
6 Crime outside of the Misuse of Drugs Act• We
did not consider crimes directly related to the production, supply and
possession of substances controlled under the Misuse of Drugs Act in this
criterion, or anywhere in our analysis. Since part of our aim was to make a
direct comparison between legal and illegal substances, it was felt that
including the harms stemming directly from legal status would skew the
calculation with Jacqui Smith’s circular logic that we outlined in chapter 2 –
because it is a crime to produce, supply or possess a substance it must be more
harmful than a drug which can be obtained legally.
7 Decision Conferencing• See URL-182 for a description
of decision conferencing.
8 Larry Phillips had previously worked on a big public consultation
about the options for disposing of nuclear waste• Committee
on Radioactive Waste Management Public Lecture, Larry Phillips, URL-18, October
11th 2006, a very informative and interesting podcast about Larry’s work on the
consultation, with the slides also available for download.
9 drug-related mortality• See Development of a
rational scale to assess the harm of drugs of potential misuse, Nutt et
al, Lancet, 2007, for more detail on how this is defined.
10 comparing our scores with measurements such as official statistics• Improving Data Input in the MCDA Model Based on Evidence, Y
Mu, MSc Thesis LSE, 2010
11 Figure 3.4• Drug harms in the UK: a multicriteria
decision analysis, David Nutt et al, ISCD, URL-16, November
1st 2010
12 Figure 3.5• Drug
harms in the UK: a multicriteria decision analysis, as above.
13 The Daily Mail predictably called me a “dangerous man”; it said the policies I
was advancing “would be a disaster for our society”• Why doesn’t
this dangerous man come clean and admit he wants to legalise drugs?, Stephen Glover, URL-19, November 3rd 2009
14 “our priorities
are clear – we want to reduce drug use, crack down on drug-related crime and
disorder and help addicts come off drugs for good.”• Alcohol “more harmful than
heroin” says Prof David Nutt, BBC news, URL-20, Nov 1st 2010
15 Ketamine was invented in 1963,• Ketamine: a
scientific review, Celia Morgan and Valeria Curran, ISCD, September 15th
2010
16 2004 report• Report on Ketamine, ACMD Technical
Committee, URL-21, Spring 2004
How
drugs evolved
Chemicals in the human brain
A neuron releases
neurotransmitters into the “synapse” (gap) between this and a neighbouring
neuron. The neurotransmitters move across the gap to
the other neuron, where they activate receptors
specifically designed to recognise the particular chemical (Figure 4.1), and so
create feelings – for example of hunger or fear. These neurotransmitters are
then reabsorbed at reuptake sites (Figure 4.2) when
the signal isn’t needed any more – for example, when a predator has gone. (At
the reuptake site, special transporter proteins in
the cell wall allow the neurotransmitter molecules, which are large, to pass
into the interior of the neuron. We’ll see later than some drugs work by
blocking the transporters and preventing the reabsorption of the
neurotransmitter.) 1
A typical day without drugs
The
brain is extremely complex, and there’s still a lot we don’t know, although in
the last two decades neuroimaging techniques have vastly improved our
understanding of how neurotransmitters work. The most important chemicals, and
a brief summary of what they do, are listed in Table 4.1 on page 54. As we’ll see shortly, drugs
target receptors designed to respond to these natural chemicals; the better we
understand natural chemicals, the better we’ll understand the effects of the
drugs that mimic them.
To illustrate how these
chemicals work, let’s meet Ben, a clean-living man who doesn’t like to take any
drugs at all – not even coffee. As he wakes up
and gets out of bed, glutamate is released, kickstarting his body’s transition
into being awake. He drives into work, getting stuck in traffic; it’s really
important he’s on time today, and his brain is flooded with noradrenaline as he
becomes angry and stressed at the thought of being late. When he gets to work,
it turns out his boss is late as well so he isn’t in trouble after all, and a
rise in serotonin levels makes him feel better. As lunchtime approaches,
there’s a dip in his cholecystokinin which makes him feel hungry, so he goes to
the canteen and his cholecystokinin level rises again as he eats.
After lunch he gives an
important presentation, which his boss is really pleased with, and his being
congratulated causes the release of the reward chemicals endorphins and
dopamine. On the way home he has an argument on the phone with his wife, and
his serotonin drops making him feel miserable, but after going for a run his
endorphin levels go up and he feels a lot happier. While making dinner to
apologise, he cuts his finger and endocannabinoids and endorphins help numb the
pain. As night falls, adenosine builds
up in the brain, glutamate falls and GABA levels rise, making him feel tired
and ready for sleep.
|
Type |
Chemical |
What it does |
|
On/off switch |
Glutamate |
Turns the brain on: builds memory, regulates alertness, movement,
sensation, and mood |
|
On/off switch |
GABA |
Turns the brain off: involved in sleep, sedation, relaxation, reducing
anxiety, decreasing muscle tension |
|
Lipids |
Endocannabinoids |
Regulate pain, appetite, coordination, learning |
|
Amines |
Serotonin |
Regulates mood and anxiety, appetite, sleep/wake cycle, body temperature |
|
Amines |
Noradrenaline (Norepinephrine in the USA) |
Creates feelings of alertness, attention, concentration, raises blood
pressure, lifts mood, can increase anxiety |
|
Amines |
Dopamine |
Creates feelings of motivation and drive, liking, attention, pleasure,
enjoyment of food |
|
Amines |
Acetylcholine |
Regulates sleep/wake cycle and alertness, builds memory |
|
Amines |
Adenosine |
Makes us feel tired and hungry |
|
Peptides |
Endorphins |
Create feelings of pleasure and reward, reduce pain |
|
Peptides |
Substance P |
Regulates pain, stress responses |
|
Peptides |
Cholecystokinin |
Tells us when to eat, possibly involved in managing anxiety |
What is a
drug?
In the
context of this book, the definition of a drug is a
substance that comes from outside the body, crosses the blood/brain barrier,
and has an effect similar to our natural neurotransmitters. (There are other
types of drugs – antibiotics, asthma inhalers, warfarin, cough mixture, etc,
but we’re not concerned with those here.) Sometimes a drug works by blocking
the reuptake sites on the synapses, so the brain experiences a surge of natural
chemicals; cocaine, amphetamines and MDMA all work in this way. Other drugs mimic neurotransmitters (Figure 4.3), communicating
with the receptors directly; alcohol and heroin both work like this, and heroin
is in fact a much better fit on our endorphin receptors than the natural
chemicals we produce, making it a much more effective painkiller.
1. Opioids – opium, heroin, methadone, buprenorphine, codeine
Carrying out normal
activities under the influence of opiates is pretty difficult, and even mild opiates such as codeine are not recommended
for people driving or operating heavy machinery. Some are highly addictive and
repeated use leads to physical dependence and powerful withdrawal symptoms. The
main harms they do to the body are causing nausea, vomiting and chronic
constipation, and of course the risk of death from stopping breathing in
overdose.
2. Stimulants or “uppers” – cocaine, amphetamine, methamphetamine,
caffeine, steroids, khat, mephedrone, tobacco
|
Stimulant |
Receptors targeted |
|
cocaine |
dopamine, and noradrenaline to a smaller extent |
|
amphetamine/methamphetamine
|
dopamine, and noradrenaline to a smaller extent |
|
mephedrone |
noradrenaline, dopamine, serotonin |
|
khat |
noradrenaline |
|
caffeine |
adenosine |
|
tobacco |
acetylcholine, dopamine |
Amphetamines have a
number of medicinal uses, such as treating attention deficit
hyperactivity disorder (ADHD) and narcolepsy, while cocaine is a useful
local anaesthetic. Soldiers, students and shift workers who need to stay alert through the night often rely on stimulants, and
clubbers use them to keep dancing for hours. For people in highly-competitive
environments, from street gangs to war zones to high finance, stimulants can
help them cope with the psychological stress. Forms that reach the brain very
quickly can be highly addictive, and regular stimulant use puts strain on the
heart.
3. Depressants or “downers” – alcohol, benzodiazepines, GHB
4. Psychedelics – LSD, mushrooms, ayuesca/DMT, peyote/mescaline,
ibogaine
“Psychedelic”
means “mind-manifesting”, and drug of this sort are still something of a
mystery to psychopharmacologists like myself. They seem to have an effect on serotonin receptors, which explains the
strong pro-social feelings of openness and talkativeness they create, but it is
unclear why this should be accompanied by intense visual and transcendental
experiences. They very rarely produce true hallucinations (ie which have no
basis in the environment), but they do produce intense visual distortions
inspired by the surroundings.
Less easily-classified drugs
Ketamine is another drug
that falls between the classes. You could call it a depressant as it blocks
glutamate, switching off the brain in a similar way that increasing GABA does
(Figure 4.5), which accounts for its medicinal usefulness as an anaesthetic.
Subjectively, many users liken it to a psychedelic, distorting time and space
and presenting them with new perspectives.
We seem to
have a particular liking for drugs that combine both sedation and stimulation.
Alcohol and cannabis are the most obvious examples, but Figure 4.6 shows some
others as well. One of the most popular drugs of the 20th century was Dexamyl
(commonly known as Purple Hearts), an early antidepressant which appeared in
the 1930s. Purple Hearts contained a combination of amphetamine (to raise mood)
and barbiturates (to counteract the side-effects of the amphetamine). Even more
potent were the “speedballs” invented by soldiers in Vietnam, where liquid
cocaine and heroin were injected in the same syringe. It was this combination
which famously killed actor River Phoenix in 1993.
A
typical day on drugs
Let’s
go back to our story about a typical day, but this time following Jen. She does
all the same things as Ben, except that she, like most people, regularly uses
(legal) drugs to change her brain chemistry. As she gets out of bed, her
glutamate levels naturally increase, but she also drinks a cup of coffee which
blocks the adenosine in her brain, making her feel more alert. When she’s
stressed about being stuck in traffic and her noradrenaline rises, she lights
up a cigarette; the nicotine activates her acetylcholine
receptors, calming her down. A glass of wine with lunch, (her cholecystokinin
levels falling and rising again as she eats), elevates GABA, lowering her
anxiety about presenting to an important client in the afternoon.
A brief history of drug use
The first stages were
back in prehistory. Plants developed drugs to avert predators by interfering
with their brains; some animals learned to overcome this aversion and to
experience the chemical changes as enjoyable. Humans, with our immense
curiosity, ability to remember and record experiences, and facility with tools,
developed new methods for consuming drugs to deliver them to the brain more
efficiently. Inhaling the smoke of the dried leaves of the tobacco plant,
roasting and grinding up coffee beans, milking opium poppies for their resin
and fermenting fruit and grains to make alcohol are not obvious things to do,
but once we’d discovered them we found
we could open up new realms of pleasurable experience. We also learned that we
could heighten the effects of drugs by combining them with other substances, or
encouraging the release of natural chemicals through creating euphoric or
relaxing environments.
It’s hard to know exactly
when different drugs came into use, but a thousand years ago a traveller would
probably have encountered a world like that shown in Figure 4.8. The traveller
would have found that each of the drugs shown had a specific cultural context,
and was loaded with social, religious and political meanings. The psychedelics
peyote, ayuesca, ibogaine
and fly agaric mushrooms were an essential part of religious rituals and
shamanic trances, just as wine had a prescribed role in many Jewish rituals.
Switching from one intoxicant to another sometimes accompanied major cultural
changes, such as the replacement of alcohol with coffee in the Arab world with
the rise of Islam. Kava drinking in the Pacific and smoking tobacco in peace
pipes in the Americas played important roles in maintaining social cohesion,
while also cementing gender divides, as women weren’t allowed to consume them.
Sometimes substances that we would consider drugs today were seen as food, and
vice versa: beer played an essential role in the diets of northern Europe in
the past, because water was usually contaminated with bacteria. In Latin
America, cacao was treated as a kind of medicine when Western explorers first
encountered it.
As travel became easier
and more common, medications and pleasure drugs were introduced to new places.
The empires that emerged in places like China and the Middle East spread
knowledge about the natural world, and most of the standard therapies available
in medieval England were derived from Greek or Islamic sources. European
expansion spread drugs and medicines as well as disease. Explorers brought back
tobacco and cacao (and probably syphilis too) from the Americas, and coffee was adopted in Europe with the expansion of the Ottoman
Empire. Over the course of a few centuries, the drugs available in many parts
of the world multiplied, creating new social contexts.
These new drugs were
powerful and immensely pleasurable, and humans are programmed to want to repeat
pleasurable experiences. We’ll look at the concept of addiction in detail in
chapter 8, but its defining feature is that the user has such powerful cravings
for the drug that they find it almost impossible to resist taking it, even if
it is destroying their relationships, their health, or their ability to lead a
normal life. Unfortunately, as we’ve developed more and more efficient ways of
delivering drugs to the brain we’ve inevitably made them more and more addictive. These leaps forward in medicine and our understanding of the
brain have had unintended consequences, and pharmacologists now spend a lot of
time researching substitutes for common drugs of abuse, in the hope of finding
less harmful ones.
Why
do people take drugs?
Let’s
go back to the opening question: why do people take drugs? Looking at how drugs
came to exist, it would be surprising if we didn’t
take them. Plants were producing chemicals especially designed to interfere
with animals’ brains long before humans existed, and humans have evolved to
respond to their effects just as we’ve evolved to digest certain foods.
Cultures that haven’t employed the psychoactive powers of plants have been in
the minority, and have used other methods to alter their states of
consciousness. From this point of view, taking drugs is entirely natural; as
Mike Jay puts it in his book 2High Society, “we were taking drugs long
before we were human”.
We use drugs for two main
reasons: to experience pleasure, and to relieve suffering. These could crudely
be referred to as “recreational” and “medicinal” drug use, but although the 3international
treaties of the 1960s created a strict legal division between the two, in
reality the line between them is very blurred. The most obvious examples are
drugs such as cannabis and LSD which are placed in Schedule I (with no
recognised medicinal value), so that any use at all is seen as “recreational”,
despite the fact that many people with conditions like multiple sclerosis (MS)
or cluster headaches are demonstrably reducing their suffering by taking them.
Other drugs which have recognised but limited medicinal uses, such as heroin
for extreme pain, may still be reducing suffering when taken outside of an
obviously therapeutic context. For people who have experienced serious trauma
(such as soldiers with PTSD) taking a drug like heroin might be the only thing
that makes their lives liveable. Alcohol is often used to self-medicate, as we
discuss below.
The use of drugs for
pleasure has a number of elements beyond their mechanical effects on our
brains. Indeed, we have to be expecting to experience pleasure: most of us would find taking a drug by accident
deeply unpleasant, and would think that we had been poisoned or were having a
psychotic episode. Actively choosing to take a drug is an essential part of the
effect it has, and even animals experience different effects depending on
whether or not they’ve chosen to consume it. 4Rats that
are passively given cocaine injections will become physically dependent on the
drug (experiencing withdrawal symptoms if they stop), but become much more
addicted – in terms of actively seeking out the drug – when they have to push a
lever themselves to self-administer it.
Drugs are social, and are
usually consumed in groups, where the feelings of disinhibition and
talkativeness that many drugs generate help promote social bonding. Using a
particular substance, or using it in a particular way, can become a strong
marker of identity, and can herald important social changes. 5Coca
chewing has become more popular in Bolivia since the election of an indigenous
president, for example, and 6greater
gender equality has often been accompanied by increased rates of smoking
amongst women. Refusing to participate in drug-taking can feel very
uncomfortable, as teenagers know when they struggle with peer pressure, and as
many adults experience if we refuse the offer of an alcoholic drink in the pub.
The use of some drugs,
especially psychedelics, can be heavily imbued with meaning. Taking
psychoactive substances in religious settings and rituals is called entheogenic drug use, and blurs the line between what is
recreational and medicinal. Sometimes these occasions are explicitly for
healing purposes, although it may be the shaman who takes the drug rather than
the patient. (This was how tobacco was used in some traditional Native American
ceremonies.) In other cases, the drug is used to access secret knowledge or divine
experience. It may be only the shaman who consumes the drug, or it may be the
entire congregation, as with 7the Native
American Church’s use of peyote. While entheogenic drug use may have
pleasurable moments of euphoria and ecstasy, these experiences are often
described as painfully intense, an ordeal to be struggled through rather than
an escapist “trip”. This makes them very different from,
for example, the use of LSD in a dance club setting, as was recognised in 1996
when the Native American Church was granted special dispensation to use peyote
in their services.
Sometimes people get
pleasure from taking drugs precisely because it is risky. This is particularly
noticeable when prescribed medicines get diverted: 8American
schoolchildren who take Ritalin illicitly have quite different reactions to
those who take it as directed by their doctor. (An illicit activity is illegal
in one context but might be legal under other circumstances – for example, if
your grandmother has a prescription for Valium she can take it legally, but if
you take her Valium that’s illegal/illicit drug use.) In recent years, a new
trend has emerged amongst young people in the UK, of deliberately trying to get
so intoxicated (usually on alcohol) that they have no memory of getting
“wasted” or “ended”. It can be hard to understand why this would be
pleasurable, but it probably relates to the social kudos of the things people
feel permitted to do while extremely disinhibited.
Finally, a minority of
drug users will take them because they are addicted, which we’ll explore in
greater detail in chapter 8. Addiction blurs the line between pain and
pleasure. It is quite common for someone to start
taking a drug for the enjoyable effects, but once they’re addicted it becomes
the only thing that can relieve the intense cravings and unpleasant physical
symptoms of withdrawal.
Why this
matters
When it comes to
minimising the harms of recreational drug use, there are several schools of
thought. One aims to eradicate the decadent use of drugs altogether – the
“drug-free world” that the 1961 UN Single Convention on Drugs aimed to create.
This plays well in the tabloids, but is very flawed in practice. For a start,
there are measurable benefits to a life which includes pleasure, so eradicating
pleasurable drug use could cause other sorts of harm, such as an increase in
stress-related health problems. This is understood with alcohol, and sociable
drinking or drinking to unwind after work is genuinely beneficial (although the
harms are also very real). The
government can certainly make it easier for people to enjoy the benefits of the
pub while doing themselves less damage, by making alcohol more expensive,
ensuring that non-alcoholic drinks are cheaper and more widely available, or
funding research into a safer alternative. But banning pubs altogether would
damage people’s health in other ways, as well as causing public outrage.
If we accept that people
are going to take drugs for pleasure, and that the important thing is to
minimise harm, then understanding the reasons behind drug use can give us
inspiration as to how this should be achieved. If part of the pleasure of the
drug is the positive social context it is consumed in, then it might be
possible to create similar contexts where the drug is not the focus, such as
the measures proposed above to make the pub less harmful. On the other hand, if
people are specifically looking for a risky experience, they are going to
expose themselves to harm whatever drugs they take. Challenging the culture of
extreme intoxication is one of the most difficult tasks we face, but it is
essential if harm is going to be reduced. One of the best protections against
this kind of risk-taking is allowing positive cultures to develop around drugs
that emphasise moderate consumption rather than bingeing – in a sense, creating
entheogenic-type social contexts similar to traditional uses of psychedelics
and other substances. This would help protect against the acute problems of extreme intoxication, and also against
addiction: 9Native
Americans avoided becoming addicted to tobacco for thousands of years by
surrounding its use with ritual and having strictly-observed restrictions on
when and how it was taken. While this kind of context is unlikely to develop in
the UK, a renewed sense of a social code of acceptable and unacceptable
behaviour when taking drugs like alcohol and cocaine would certainly help to
reduce harm.
Notes
1 •Recommended reading on neurotransmitters: The
Atlas of Psychiatric Pharmacotherapy, Roni Shiloh and David Nutt et al,
Taylor & Francis, 2006
2 High Society, “we were taking drugs long
before we were human”• High Society,
Mike Jay, Thames & Hudson, 2010
3 international treaties of the 1960s created a strict legal division
between the two• Single Convention on Narcotic Drugs,
UN, URL-22, 1961 (amended 1972)
4 Rats that are passively given cocaine
injections• Differences in extracellular dopamine
concentrations in the nucleus accumbens during response-dependent and
response-independent cocaine administration in the rat, SE Hemby et al, Psychopharmacology (Berlin)
133(1), September 1997
5 Coca chewing has become more popular in Bolivia since the election of
an indigenous president• The Wonders of the Coca Leaf,
Alan Forsberg, URL-23, 2007
6 greater gender equality has often been accompanied by increased rates
of smoking amongst women• Gender empowerment and
female-to-male smoking prevalence ratios, Sara Hitchman and Geoffrey
Fong, Bulletin of the World Health Organization, URL-24, January
5th 2011
7 the Native American Church’s use of peyote• American
Indian Religious Freedom Act, URL-25, 1996
8 American schoolchildren who take Ritalin
illicitly have quite different reactions to those who take it as directed by
their doctor.• Evidence-based guidelines for
management of attention-deficit/hyperactivity disorder in adolescents in
transition to adult services and in adults: recommendations from the British
Association for Psychopharmacology, David Nutt et al,
Journal of Psychopharmacology (21), 2006
9 Native Americans avoided becoming addicted to tobacco for thousands of
years• Tobacco use by Native Americans: sacred smoke and
silent killer, Joseph Winter (ed.), University of Oklahoma Press, 2000
Cannabis
as hemp
The
stem of the cannabis plant can be used to make hemp, which was an essential
commodity for making ropes in seafaring societies such as the ancient Greeks
and the British in times past. 1Henry VIII
even passed a law requiring farmers to grow it! Nowadays, hemp is used for
special paper, such as for banknotes and bibles, for fabrics, and for a
low-carbon building material called “hempcrete”, which is a mixture of hemp and
lime. The varieties grown for these purposes have only trace psychoactive
properties.
Cannabis
as a drug
The psychoactive
ingredient in cannabis is tetrahydrocannabinol (THC), 2and the receptors it acts on
are named cannabis receptors.
When scientists began looking for the naturally-occurring neurotransmitters
that these must have evolved to recognise, they found a control system that
helps regulate appetite, pain sensation, mood and memory. This is known as the endocannabinoid system, and the
naturally-occurring chemicals that activate it were named endocannabinoids,
from “endogenous cannabinoids”.
Cannabis usually makes
users feel relaxed, talkative and sociable – known colloquially as being
“stoned”. It can produce a distorted sense of time and
space, although not as severely as psychedelic drugs. Some people can also
experience paranoia. Although by no means safe, it is considerably less harmful
than alcohol, and rarely induces violence or antisocial behaviour.
What
are the benefits?
Cannabis
is probably the world’s oldest medicine, used mainly for treating pain and
spasm. It’s known as 3“ma” in Chinese medicine, a pun
on the word “chaotic”, and was historically used largely in a therapeutic
context, although a minority also used it as an intoxicant. While medical uses
have long been known in Indian medicine as well, where it’s known as 4“bhang”,
there is also a long history of widespread use for recreational purposes, and
the plant and its psychoactive properties are a common feature in Indian
legends and folktales. Even today it is used in certain festivals.
Although cannabis was
known to Western medicine in the middle ages, 5it was only
popularised in Britain in the 1840s, by an army surgeon who had served in
India. Cannabis became a common painkiller, alongside opium (laudanum). It is
thought that Queen Victoria’s physician JR Reynolds prescribed it to help her
with period pains and after childbirth. In the Lancet,
Reynolds wrote a paper entitled On the Therapeutic Uses and
Toxic Effects of Cannabis Indica, in which he said 6“when pure
and administered carefully, it is one of the most valuable medicines we
possess”. Queen Victoria was apparently very fond of it – perhaps getting
access to cannabis was one of the reasons she had so many children!
7The
condition that seems to benefit most commonly from the use of cannabis is
multiple sclerosis (MS), a disease characterised by fatigue, muscle weakness,
incontinence, muscle spasms and chronic pain. About 85,000 people in the UK
suffer from MS, and at least 1% of these self-medicate with cannabis. Sufferers
say that the drug helps with spasticity, pain, tremor and urinary bladder
control, and even though the drug is illegal many doctors do not discourage
their patients from self-administering it.
8Cannabis
also seems to have benefits in a number of other disorders, such as relieving
the pain from a phantom limb among amputees, and preventing seizures in
epileptics. There is anecdotal evidence that it may be useful in treating
glaucoma and bronchial asthma, as it lowers the pressure in the eye and dilates
the small airways of the lung.
Other therapeutic uses of
cannabis include helping underweight people, such as those with cancer and
AIDS, bulk up by increasing their appetite – wanting to eat after taking cannabis
is a common effect of the drug, known colloquially as “the munchies”. And
although cannabis can worsen psychotic symptoms, it does seem to have some
antipsychotic effects as well, which may account for its popularity with people
suffering from schizophrenia. (See box Does cannabis cause
schizophrenia? on page 85.)
Recreationally, cannabis
serves a similar role to alcohol as a social lubricant, particularly as there
is a long established culture of sharing the drug – it’s extremely rude not to
pass the spliff! It is also popular with artists and musicians, and there are 9many
accounts of its helping inspire people’s creativity. Some say that the whole
genre of jazz emerged as cannabis allowed musicians to break free of
conventional music structure and syncopate!
What
are the harms?
While
cannabis is considerably less damaging than alcohol, it still 10scored 20
on our harm scale. This might surprise some people, particularly those who are
experienced with the drug and view it as harmless. Over the 16 criteria, it
scored highest on drug-related damage and drug-related impairment of mental
functioning, mostly because of the harms associated with smoking, and the drug’s
links with depression and psychotic symptoms.
11Cannabis
dependence occurs in about 10% of users, and there is a physical withdrawal
syndrome with some unpleasant symptoms, such as decreased appetite, weight
loss, mood changes and insomnia. These are real and not just psychosomatic:
drugs like 12rimonabant,
which block the effects of cannabis, can
precipitate these withdrawal symptoms. (This distinction is explained more
fully in chapter 8.) Even without physical symptoms, many regular users
experience psychological craving if they stop. 13In the UK in
2007/8, around 17,000 people were treated for cannabis addiction, half of them
under 18, and the problem is probably much more widespread.
Often the biggest effect
that cannabis has on people’s lives is a general sense of demotivation and lack
of enjoyment of activities when not intoxicated, and if used regularly,
especially daily, it can disrupt school work or employment. 14A study of
US postal workers found lower levels of attainment among people who tested
positive for cannabis, and research has shown that long-term use can affect
cognitive skills, making it harder to learn and retain information.
Being illegal, there are
other harms associated with the production and distribution of cannabis. Most
of the drug used in the UK is now sourced domestically, often being grown on
farms run by criminal gangs who channel the proceeds into other sorts of crime,
such as people trafficking. In recent years, many of the farms have started
being run by 15Vietnamese
gangs, who use illegal Vietnamese immigrants (some of them children) as workers
in conditions of near-slave labour.
Cannabis
routes of use
1.
Spraying the medicinal form on the
back of your throat. The spray is the least harmful route, as you would expect
with a medically approved substance.
2.
Eating (usually cooked in sweet
foods like cookies) is probably the second least harmful as it also avoids the
health problems associated with smoking, but it can take up to 4 hours to reach
the brain (Figure 5.2), and this delayed effect does make it harder to judge the
dose.
4.
Smoking cannabis with tobacco in
cigarettes puts the smokers at risk of the same problems that smoking tobacco
alone does; smoking cannabis pure reduces these risks, but it doesn’t remove
them completely. Spliffs are usually passed around a group rather than smoked
by an individual, but users usually inhale more deeply than they do with
tobacco alone, and often hold the smoke for 10–15 seconds as they believe this
makes them more “stoned”. (16Tests have
shown that this doesn’t actually increase THC levels in the brain, so it is
probably just oxygen deprivation that causes the bigger effect.)
Figure 5.3: A bong.
Is skunk more harmful than hash?
Skunk is potentially more
harmful than hash because it contains less cannabidiol
(CBD), a psychoactive compound that reduces anxiety
and can minimise some of the negative effects of THC. Breeding more THC into skunk
has resulted in CBD being bred out. However, we don’t know whether people using
skunk actually take in more THC, because there’s some evidence that experienced
users vary how deeply they breathe to keep an even level of THC intoxication;
this is called “titrating the dose”. Other research has found that products
with higher THC levels are less well liked – tests on hash smokers have found
that they find skunk too strong, and that many people would rather smoke hash
if they could get hold of it. This seems to have been recognised by cannabis
producers, and although 17THC levels
were at one point as high as 21%, they soon dropped back down to 15%, which was
clearly a more pleasurable and saleable strength.
Why did cannabis stop being seen as a medicine?
When cannabis entered the
physician’s medicine chest in Britain in the 1840s, it was 18overshadowed
by the more potent painkilling properties of opium, partly because opium was
easier to convert into other forms such as laudanum, morphine and heroin.
Cannabis tinctures (extract dissolved in alcohol) were sold as cures for cramp,
opiate withdrawal, migraines and insomnia, and enjoyed a brief period of
popularity in Britain towards the end of the century. However, growing concern
about unregulated medicines led to the British Medical Association launching
its campaign against “Secret Remedies” in the early 1900s, after which cannabis
was removed from most of these medications, as were cocaine, morphine and
heroin.
Meanwhile,
some British governors in India were becoming worried that cannabis might be
causing widespread psychological problems in the colony. This led to the 19Indian Hemp
Drugs Commission report in 1894, which assembled seven volumes’ worth of
evidence on the medicinal and social uses of cannabis in the subcontinent. The
report concluded that the drug was not harmful, and should not be controlled.
Yet the report was largely ignored in the UK, despite having been commissioned
by the British Parliament and having collected a huge variety of testimony and
evidence, and it was not even mentioned in Parliament until 1967. The legal
status of cannabis, and its possible harms and benefits, were seen as a foreign
issue unrelated to everyday British concerns.
The 1925 treaty led to
the Dangerous Drugs Act in the UK, which came into force in 1928, banning the
recreational use of opium, cannabis and cocaine. (Opium and cocaine had already
been controlled for a decade by the 1916 Defence of the Realm Act.) All three
drugs were still available as medicines, and recreational use was rare, so this
passed without much comment. While the media featured occasional stories about
“dope fiends” – foreign men using drugs to corrupt white women – there was
nowhere near the same level of hysteria in Britain as in the USA (described
below), and cannabis was rarely mentioned in these tales. 20In 1945
there were a total of 4 prosecutions for cannabis offences, and it wasn’t until
1950 that the number of prosecutions for cannabis (86) outnumbered
those for opium and other manufactured drugs (83). There was no domestic
pressure to control cannabis alongside other hard drugs – and equally, no
organised effort to keep it legal.
21The
situation was very different in the USA. The Geneva International Convention
was convened by the League of Nations, which the USA never joined, so cannabis
in the USA was controlled later than elsewhere, with the Marijuana Tax of 1937.
This prohibited the sale or growth of cannabis without a tax stamp which,
although it only cost one dollar, was never made publicly available,
effectively outlawing production. This was the culmination of several decades
of increasing concern about the drug’s recreational uses, fuelled by exaggerated
reports in the media about its harmful effects.
The three lives of
cannabis now became dependent on the fate of its use as a recreational drug.
Although ordinary Americans were familiar with hemp, many didn’t realise that
it had anything to do with marijuana, just as many doctors didn’t realise it
was the same plant as cannabis indica,
which they considered a valuable medicine. By the time the USA was leading the
negotiations behind the 1961 UN Single Convention on Drugs, the view of
cannabis was so dim that, not only was it placed in the same category of
harmfulness as cocaine and opiates, but whereas those drugs were still allowed
some medical use, WHO (the World Health Organization)
declared that cannabis had no medical value at all.
In Britain, cannabis
continued to be available on prescription throughout the 1960s. However, this
was the decade in which recreational use became common, with some people buying
it on the black market, and others 22diverting
prescriptions from their doctors. Although cannabis users and medical
professionals had become more organised by this point, and were trying to get
the drug decriminalised for all uses, some of the moral panic from the USA had
been imported, and there was a lot of political pressure to control the drug
still further. After the 1971 UN Convention on Psychotropic Substances, the
British government decided 23not to
renew the medical licence on cannabis, in part because of concerns about the
drug being diverted from medical sources. This was an odd way to have dealt
with the problem. Doctors have access to a wide range of other drugs with abuse
potential, and we stop those supplies being diverted by having strict rules and
regulations around what doctors can prescribe, and by disciplining them through
the General Medical Council if they break those rules. It was the doctors’
practice that needed to be banned, not the drug.
Medicinal cannabis use in the UK today
The
criminalisation of cannabis (Figure 5.4) for recreational use has resulted in a
great deal of harm from imprisonment, as we’ll discuss in chapter 15. However, the most inhumane result of the legal status of
cannabis has been the criminalisation of very sick and disabled people who rely
on the drug as a medicine. A middle-aged ex-teacher with MS wrote to me
recently detailing how the police have broken down her front door in dawn raids
on three occasions in the last six years to combat her use of cannabis for
medical purposes. This kind of aggressive law enforcement is devastating for
the patients and their families and distasteful for the courts – many magistrates
will privately admit their extreme dislike of having to criminalise users. And
that’s not to mention its being a complete waste of public money.
In 1998, 24the House
of Lords Select Committee produced a report into the medical uses of cannabis
and the effects of criminalisation on its users. They recommended that all
criminal sanctions against such users be dropped, and that a cannabis-based
medicine should be approved for prescription within three years. In fact, it
took until 2010 for the cannabis spray Sativex to receive approval in Britain;
even this doesn’t meet the needs of all patients,
and is available only if the doctor is willing to prescribe it, which most
still aren’t. If anything, 25the legal
situation has become even more draconian in recent years. In 2005, the Court of
Appeal ruled that the Defence of Necessity was no longer admissible in cases
where patients have been found growing or possessing cannabis to treat a
medical problem for which other treatments were ineffective.
This terribly unjust
situation surely cannot be allowed continue, especially once Sativex has been
rescheduled to make the law consistent. At the time of writing, the medicine
has been approved under a general licence, avoiding the fact that the drug it
contains is in Schedule 1, with no recognised medical use. The ACMD has
recommended that Sativex be rescheduled to Schedule 4, along with other
medicines such as benzodiazepines and anabolic steroids. However, any such
legislation will have to name the active components rather than use the trade
name Sativex. It has been suggested that it be described as an extract of THC
and CBD, but this is inadequate as Sativex also contains dozens of other
cannabinoids which occur naturally in the plant. It is very hard to get around
the fact that the only accurate description for the medicine is “cannabis”.
This will be quite a conundrum for politicians such as Minister for Crime
Prevention 26James
Brokenshire, who has insisted in Parliament that cannabis in its “raw form” is
a harmful drug with no medical purposes, and then asserted in the same breath
that Sativex is a “safe and effective” treatment for MS.
Conclusion
The
three stories of the cannabis plant – as pleasure drug, medicine and plant
fibre – show that many different factors have contributed to the legal situation we have today. Rather than being based on a rational
assessment of the harms and benefits of the drug, the current legal status of
cannabis in the UK is the result of factors such as Egyptian domestic politics
in the 1920s, a handful of British doctors misprescribing medicinal cannabis in
the 1960s, and industrial interests in the USA who wanted to stop hemp
production. To this day, 27no
varieties of hemp can be grown in the US, not even the versions that are used
in Europe, which have no psychoactive properties.
Does cannabis cause schizophrenia?
In
2007, the Home Secretary 28requested
the ACMD to review the status of cannabis for the third time in six years
because 29“Though
statistics show that cannabis use has fallen significantly, there is real
public concern about the potential mental-health effects of cannabis use, in particular the use of stronger forms of the drug,
commonly known as skunk.” The ACMD’s resulting report looked at this question
in depth.
If we err on the cautious
side, we can say that if you take cannabis, particularly if you use a lot of
it, you will be more likely to have psychotic experiences. That includes
schizophrenia, but the rarity of the condition, and the confounding factors
discussed above, make it very hard to be sure about its causation. The analysis
we came up with was that smokers of cannabis are about 2.6 times more likely to
have a psychotic-like experience than non-smokers. To put that figure in
proportion, you are 20 times more likely to get lung cancer if you smoke
tobacco than if you don’t: there is a relatively small risk that smoking
cannabis will lead to psychotic illness compared with quite a substantial risk
for smoking tobacco and developing lung cancer.
Another confounding
factor is that schizophrenia seems to be reducing in the general population
even though cannabis use has increased 20-fold in the last 40 years (30Figure
5.5). Figures from the General Practice Research Database in the UK
consistently and clearly 31show that
psychosis and schizophrenia are still on the decline. So, even though skunk has
been around now for ten years, there has been no upswing in schizophrenia. In
fact, where people have looked, they haven’t found any evidence linking
cannabis use in a population and schizophrenia.
Another interesting
finding of our analysis is what it would take to reduce the number of people
being diagnosed with schizophrenia by targeting cannabis use. Our research
estimates that, to prevent one episode of schizophrenia, 32we would
need to stop 5,000 men or 7,000 women aged 20 to 25 years from ever using the
drug. This is obviously an impossible public-health challenge, and not a viable
route towards reducing schizophrenia.
All of this was outlined
in the ACMD’s report. However, the government then summarily ignored it, which
I believe has reinforced a popular
impression that there is a far stronger causal relationship between cannabis
and schizophrenia than there probably is. Many people with schizophrenia
continue to take cannabis (even though they admit that it makes some symptoms
worse), because it helps them to cope with major aspects of the disease like
anxiety and tension, and lets them think more clearly; as with any medication,
people decide whether the side effects are worth the benefit they gain. The
situation we are seeing now is parents and doctors effectively blaming patients
for their condition, sometimes even going so far as to claim they’ve brought
the disease on themselves through their drug use. For most people this is
highly unlikely to be true, and constitutes a hurtful new form of
stigmatisation for a very distressed and damaged group.
Notes
1 Henry VIII even passed a law requiring farmers to grow it!• Marijuana - the first twelve thousand years, Ernest Abel,
Plenum Press, 1980. The decree stipulated that “for every 60 acres of arable
land a farmer owned, a quarter acre was to be sown with hemp”.
2 and the receptors it acts on are named cannabis
receptors• The Science of Marijuana, Leslie I
Iverson, Oxford University Press, 2000
3 “ma” in Chinese medicine• As above.
4 “bhang”• As above.
5 it was only popularised in Britain in the 1840s, by an army surgeon
who had served in India• Science and Technology - Ninth
Report, House of Lords Select Committee, URL-26, November
4th 1998
6 “when pure and administered carefully, it is one of the most valuable
medicines we possess”• On the therapeutic uses and toxic
effects of cannabis indica, JR Reynolds, The Lancet (1), March 1890
7 The condition that seems to benefit most commonly from the use of
cannabis is multiple sclerosis (MS)• Science and Technology
- Ninth Report, House of Lords Select Committee, URL-26, November
4th 1998
8 Cannabis also seems to have benefits in a number of other disorders,
such as relieving the pain from a phantom limb among amputees, and preventing
seizures in epileptics• As above.
9 many accounts of its helping inspire people’s creativity• The Effects of Cannabis Use on Creativity, The Beckley
Foundation Research Projects, URL-27, accessed
December 12th 2011
10 scored 20 on our harm scale• Drug harms in the UK:
a multicriteria decision analysis, David Nutt et al, ISCD, URL-16, November
1st 2010
11 Cannabis dependence occurs in about 10% of users• Cannabis:
classification and public health, ACMD, April 2008
12 rimonabant, which block the effects of cannabis, can precipitate these
withdrawal symptoms• Antagonist-elicited cannabis withdrawal
in humans, DA Gorelick et al, Journal Clinical Psychopharmacology 31(5),
2011
13 In the UK in 2007/8, around 17,000 people were treated for cannabis
addiction, half of them under 18• Cannabis: classification
and public health, ACMD, April 2008
14 A study of US postal workers• As above.
15 Vietnamese gangs, who use illegal Vietnamese immigrants (some of them
children) as workers in conditions of near-slave labour• As above.
16 Tests have shown that this doesn’t actually increase THC levels in the
brain• The Science of Marijuana, Leslie I. Iverson,
Oxford University Press, 2000
17 THC levels were at one point as high as 21%, they soon dropped back
down to 15%• Cannabis: classification and public health,
ACMD, April 2008
18 overshadowed by the more potent painkilling
properties of opium• Indian Hemp and the Dope
Fiends of Old England: A sociopolitical history of cannabis and the British
Empire 1840–1928, Sean Blanchard and
Matthew J Atha, URL-28, 1994
19 Indian Hemp Drugs Commission report in 1894• Indian
Hemp Drugs Commission report in 1894, Indian Hemp Drugs Commission,
available online on the Medical History of British India website, URL-29, accessed
December 7th 2011
20 In 1945 there were a total of 4 prosecutions for cannabis offences,
and it wasn’t until 1950 that the number of prosecutions for cannabis (86)
outnumbered those for opium and other manufactured drugs (83).• Indian Hemp and the Dope Fiends of Old England: A sociopolitical
history of cannabis and the British Empire 1840–1928, Sean Blanchard and
Matthew J Atha, URL-28, 1994
21 The situation was very different in the USA• Illegal
drugs: a complete guide to their history, chemistry, use and abuse, Paul
M Ghalinger, Plume, 2003
22 diverting prescriptions from their doctors• Necessity
or nastiness? The hidden law denying cannabis for medicinal use, David
Nutt, URL-30, December 13th 2010
23 not to renew the medical licence on cannabis• Science
and Technology - Ninth Report, House of Lords Select Committee, URL-26, November
4th 1998
24 the House of Lords Select Committee produced a report• As above.
25 the legal situation has become even more draconian in recent years• Necessity or nastiness? The hidden law denying cannabis for medicinal
use, David Nutt, URL-30, December 13th 2010
26 James Brokenshire, who has insisted in
Parliament• Cannabis Question in the House, URL-33, May 9th 2011, “We
do not recognise cannabis in its raw form to have any medicinal purposes;
cannabis is a harmful drug. However, Sativex, a cannabis-based medicine, has
been approved by the Medicines and Healthcare products Regulatory Agency as a
safe and effective medicine for patients with multiple sclerosis.”
27 no varieties of hemp can be grown in the US• Industrial
Hemp in the US: Status and Market Potential, United States Department of
Agriculture Economic Research Service, URL-34, January
2000
28 requested the ACMD to review the status of cannabis for the third
time• Cannabis: classification and public health,
ACMD, April 2008
29 “Though statistics show that cannabis use has fallen significantly,
there is real public concern about the potential mental-health effects of
cannabis use, in particular the use of stronger forms of the drug, commonly
known as skunk.”• Estimating Drug Harms: A Risky Business?,
David Nutt, URL-2, October 10th 2009
30 Figure 5.5• after Cannabis and schizophrenia: model projections of the impact of the rise
in cannabis use on historical and future trends in schizophrenia in England and
Wales, URL-175, Matthew Hickman, Peter Vickerman, John
Macleod, James Kirkbride and Peter B. Jones, Addiction, (102), 2007. Source:
OCJS survey.
31 show that psychosis and schizophrenia are still on the decline• Assessing the impact of cannabis use on trends in diagnosed
schizophrenia in the United Kingdom from 1996 to 2005., M Frisher, I
Crome, O Martino and P Croft, Schizophr Res 113: 123–128, 2009. And Popular intoxicants: what lessons can be learned from the last 40
years of alcohol and cannabis regulation?, Ruth Weissenborn and David J
Nutt, Journal of Psychopharmacology, September 17th 2011
32 we would need to stop 5,000 men or 7,000 women• Michael Rawlins et al,
Cannabis: Classification and Public Health, Home
Office, URL-161, 2008
A TERRIFYING new “legal high” has hit our streets. Methylcarbonol,
known by the street name “wiz”, is a clear liquid that causes cancers, liver
problems, and brain disease, and is more toxic than ecstasy and cocaine.
Addiction can occur after just one drink, and addicts will go to any lengths to
get their next fix – even letting their kids go hungry or beating up their
partners to obtain money. Casual users can go into blind RAGES when they’re
high, and police have reported a huge increase in crime where the drug is being
used. Worst of all, drinks companies are adding “wiz” to fizzy drinks and
advertising them to kids like they’re plain Coca-Cola. Two or three teenagers
die from it EVERY WEEK overdosing on a binge, and another TEN from having
accidents caused by reckless driving. “Wiz” is a public menace – when will the
Home Secretary think of the children and make this dangerous substance Class A?
In the
days following the publication of our harms paper, several newspapers ran
headlines along the lines of “Professor Nutt says Alcohol Worse than Drugs”, as
though alcohol weren’t a drug itself. This false distinction is a large part of
the communication problem I encounter whenever I try to emphasise how harmful
alcohol is. It has a separate language – you get “high” on drugs, but “drunk”
on alcohol, drug addicts need a “fix” but alcoholics need a “drink”. As I hope
the satirical article above about alcohol shows (methylcarbonol is another
chemical name for ethanol, which is the psychoactive part of alcohol), to think
rationally about drugs policy we have to see alcohol in the same context as
other drugs, not separately. Alcohol also has a lot to teach us about what not to do when a
potentially lethal, habit-forming substance is legal.
·
1Up to 40,000 alcohol-related
deaths, including 350 just from acute alcohol poisoning and 8,000 from
cirrhosis of the liver. More than a million hospital admissions in 2007/8
(including 13,000 under-18s), costing the NHS £2.7 billion.
·
27,000 road
traffic accidents, including 500 deaths.
·
31.2 million
violent incidents and 500,000 crimes, costing the police £7
billion.
·
440% of domestic violence cases
involve alcohol, as well as 550% of child protection cases.
·
63.5 million
adults in the UK are addicted, and 7up to
700,000 children live with a parent with a drink problem. 86,000
children a year are born with foetal alcohol syndrome each year.
·
Globally, 9the main
burden of disease in 15–24 year-old males is due to alcohol, outweighing unsafe
sex, illicit drug use, and physical accidents combined.
·
The total economic cost has been
calculated as 10£30 billion
a year – though some calculations estimate it may be as high as £55 billion.
Figure
6.1 11compares the
death and disability burden in the EU, due to several causes, showing alcohol
as the second most damaging.
The drinks industry
responds to critiques like mine by saying that alcohol misuse affects only a
“minority”. Clearly, alcohol harms don’t affect just a minority: they affect
all of us – as victims of car crashes and street violence, as patients, as
families of hazardous drinkers, and as taxpayers. Reducing these harms and
associated costs is a huge public-health challenge that ought to be a top
priority for our policy makers. Unfortunately, while the Labour government was
talking “tough on drugs”, trying to score political
points by making cannabis Class B, banning mephedrone and exaggerating the
harms of ecstasy, they missed the growing epidemic around the most harmful drug
of all – or more accurately just looked the other way.
How the drinks industry influences alcohol policy
The
drinks industry is one of the most powerful industrial groups in the UK today,
and spends huge sums of money on maintaining its privileged relationship with
our lawmakers. Political lobbying takes place largely in secret. Even so, the 12Labour
government’s 2004 Alcohol Harm Reduction Strategy shows clear evidence of the
influence of the drinks industry, because it focused on the measures the
industry had recommended (such as information campaigns and education) and
ignored the measures recommended by the Chief Medical Officer (such as minimum
pricing). In fact, the House of Commons Health Committee itself commented on
this in its 2009–2010 report on alcohol: 13“we are concerned that Government policies are much closer to, and
too influenced by those of the drinks industry and the supermarkets than those
of expert health professionals such as the Royal College of Physicians or the
CMO [Chief Medical Officer]”.
1.
Consuming alcohol is normal,
common, healthy and very responsible.
2.
The damage done by alcohol is
caused by a small group of deviants who cannot handle alcohol.
3.
Normal adult non-drinkers do not,
in fact, exist.
5.
Alcohol problems can only be
solved when all parties work together.
7.
Education about responsible use is
the best method to protect society from alcohol problems.
1a. Consuming alcohol is normal
It’s
certainly true that most societies throughout history have brewed some sort of
alcoholic drink, and that this has been part of the human diet for so long that
many of us are genetically adapted to consume alcohol. When ethanol breaks down in the body it produces acetaldehyde, a
substance even more toxic than alcohol, which needs to be oxidised to avoid
unpleasant and dangerous effects. People from ethnic groups who don’t have a
history of alcohol use – such as Native Americans, Inuit, and many Chinese –
often have a form of the ALDH2 enzyme (the enzyme that breaks down
acetaldehyde) which is less effective at this oxidation process, leading to
high levels of acetaldehyde in their system when they drink. The resulting
facial flushing, nausea, headaches and general discomfort largely outweigh the
pleasant effects of intoxication, and by and large these groups drink less
alcohol than groups who have a more active form of the enzyme (as most
Europeans, Africans and South Americans do), and suffer less alcohol addiction
and liver disease.
1b. Consuming alcohol is healthy
Physiologically,
alcohol’s benefits have never been proven, but the idea that low levels of drinking
are protective is a pervasive myth – and a very useful one for the industry. We
know that, 14for a
particular group of people (middle-aged men), those that drink small amounts,
particularly of red wine, have slightly lower levels of heart disease than
those who don’t drink at all. However, this may be because this group have
more-healthy lifestyles, or because of the “sick teetotaller effect” – where
many people give up alcohol because they are ill (perhaps from some other
disease); their worse health outcomes may have nothing to do with whether or
not they drink, but do make the health statistics of non-drinkers appear worse.
To know for sure if alcohol is actually preventing heart disease, we would need
to do a randomised trial where some of this group
drink no alcohol, others drink it in small amounts and others drink more
heavily. Until this experiment has been done we don’t have proof
that alcohol has health benefits.
As I’ve written before,
there is 15no such
thing as a safe level of alcohol consumption. Alcohol is a toxin that kill
cells and organisms, which is why we use it to preserve food and sterilise
needles. Acetaldehyde, produced when the body breaks down alcohol, is even more
toxic, and any food or drink contaminated with the amount of acetaldehyde that
a unit of alcohol produces would immediately be banned as having an
unacceptable health risk.
Although rare, alcohol
addiction after a single drink does happen in a small proportion of cases, as
you can read in Case Study 2; since we can’t predict who those people will be,
any exposure to alcohol runs the risk of producing addiction in some users. And
apart from the possible cardiovascular benefits of low intake for some
middle-aged men, for 16all other
diseases associated with alcohol the risks rise inexorably with intake. This
isn’t to say that I think nobody should ever drink at all – I drink myself, and
enjoy it. But I understand that there are always risks involved, and I
certainly don’t drink for the good of my health.
1c. Consuming alcohol is responsible
“Responsible
drinking” is another industry favourite. It’s a very curious phrase,
considering the drug’s actual effects. Alcohol is a depressant (similar to GHB,
and benzodiazepines like Valium) which, if taken at high enough doses, will
produce amnesia, sedation and eventually death. It stimulates the GABA receptors
in the brain, reducing anxiety and motor coordination, and blocks 17specific
glutamate receptors, switching off the parts of your brain that keep you alert
and awake, and switching on the parts that make you drowsy and tired.
Alcohol also indirectly
stimulates the noradrenaline circuit, producing some stimulating effects. This
is what creates the noisy energy we associate with drunkenness, even though the
drug is a depressant. Some interesting recent research showed that 18alcohol
interferes with our ability to recognise emotions in facial expressions, which
may be part of the reason drunk people are so quick to take offence and start
fights. The overall effects of increasing GABA and noradrenaline in the brain
are disinhibition, decreased concern for social codes and standards of
behaviour, an increase in risk taking and disregard for long-term consequences.
I’m sure the majority of the 40 million drinkers in this country are people who
take their responsibilities seriously in everyday life, but almost all of them
– with the possible exception of addicts in withdrawal – will be more
responsible when they’re sober!
2. The damage done by alcohol is caused by a small group of deviants
who cannot handle alcohol
The
statistics on page 92 show that millions of people, not a tiny
minority, suffer harm from their own alcohol consumption, or cause harm to
others. Alcohol dependence is on the rise, with the attendant social damage and
ruined lives, and binge drinking is killing hundreds of people a year as well
as causing cirrhosis in patients as young as their early 20s. But it’s very
important to understand that much of the surge in harms is actually among
people who don’t engage in these extreme behaviours. It is the everyday
drinking of people who have come to see alcohol as an essential
part of life rather than the luxury it used to be, that has created a spike in
cancers and stomach problems, and will see 19liver
disease match heart disease as the leading cause of death in the UK by 2020.
This new habitual daily consumption has been made possible because alcohol is
now only a third the cost relative to income than it was in the 1950s, and particularly
because of the availability of cheap liquor in supermarkets.
3. Normal adult non-drinkers do not, in fact, exist
4a. Ignore the fact that alcohol is a harmful substance for the body
Far
from being safe, there is no other drug which is so damaging to so many
different organ systems in the body. Figure 6.2 illustrates how alcohol can
harm almost every part of the body through its toxicity alone. (The Figure
doesn’t show the other physical damage caused by falls, road traffic accidents
and violence). Most other drugs cause damage primarily in one or two areas –
heart problems from cocaine, or urinary tract problems from ketamine. Alcohol
is harmful almost everywhere.
4b. Ignore the fact that alcohol is addictive
Alcohol
is not the most addictive drug, but its widespread availability and social
acceptability make becoming dependent more likely. This social context also
makes relapse after treatment highly likely, as Case Study 3 shows. It can be
hard for anyone, let alone an addict, to refuse a drink when it’s offered
socially. 20About a
quarter of the adult population of the UK drink more than the recommended
weekly limit; 6% of men and 2% of women are “harmful drinkers”, where damage to
health is likely, and levels are higher still in Scotland. As with many other
drugs, dependent users suffer withdrawal symptoms when they stop. The
withdrawal syndrome for alcohol is characterised by tremors, nausea, extreme irritability, and sometimes fits
and delirium, which can be life-threatening.
5. Alcohol problems can only be solved when all parties work together
The
drinks industry wants to portray itself as having the same aims and interests
as people who want alcohol policy to be guided by a concern for public health.
But there is a fundamental conflict of interest: however much the industry
wants to pretend otherwise, you can’t reduce harm without reducing the amount
people drink, whereas companies looking to maximise profits need to sell as
much alcohol as possible. There is a lot of evidence that the drinks industry
relies upon hazardous drinking as a major source of income. In fact, it has
been calculated that if everyone who drinks more than the recommended daily
limit started drinking moderately there would be a 21drop in
total alcohol consumption of 40% – equivalent to over £13
billion in sales. However much the industry talks about taking the harms
seriously, nothing can change the fact that their success is indirectly related
to the amount of damage they inflict on society at large.
This is not to say that
they bring no benefit to society at all – brewers contribute billions every
year in tax revenue, and the industry does provide a lot of jobs. Pubs in
particular are important social spaces and local
employers, but they’ve seen their profits plummet in recent years as a result
of the cut-price alcohol available from supermarkets and off-licences. “Working
together” implies that everyone can win, when in fact politicians need to weigh
up the different interests involved, and bring in policies that will produce
the best outcomes for society as a whole, even if that means that some parties
have to lose out.
In practice, what the
industry means by “working together” is bringing in voluntary codes rather than
statutory regulation – solving problems through rules that the industry chooses to comply with, rather than laws which they must comply with. These are supposed to be easier to
implement and more flexible than going down the legal route. However, evidence
from across the world shows that the 22voluntary
codes adopted by drinks industries are essentially ineffective at reducing
alcohol harms – they tend to focus on the wrong sort of interventions, and are
routinely ignored by signatory companies anyway. This was recognised with
smoking and the tobacco industry, and is equally true of those who profit from
alcohol.
6. Alcohol marketing is not harmful. It is simply intended to assist
the consumer in selecting a certain product or brand
The
drinks industry spends around 23£800
million a year on advertising, marketing, sponsorship, contests and special
promotions. While the most important factors determining consumption are price
and availability, marketing does have a demonstrable impact on levels of drinking, not just the brands people choose to
drink.
This is particularly true
with young people and a number of studies have concluded that marketing
communications do have a marked effect on consumption. A recent British Medical
Association (BMA) publication, 24Under the Influence, revealed many of the
techniques the drinks industry employs to target a younger audience, including
email campaigns with embedded film clips advertising alcohol, Facebook links
and texts going direct to people’s phones.
The industry claim that
their advertising is aimed at providing information and choice, but there is a
powerful symbolism to the sheer volume of
advertising that people are exposed to on a daily basis. To quote the BMA: “the fact that promotion is allowed, ubiquitous and heavily linked
to mainstream cultural phenomena, communicates a legitimacy and status to
alcohol that belies the harms associated with its use. It also severely limits
the effectiveness of any public health message.” There’s a lot of
evidence that the more common and acceptable consuming alcohol is seen to be,
the more people will drink, and this cultural context is especially influential
on young people. All this further entrenches the false division between alcohol
and illegal drugs, persuades people that consuming alcohol is safe, and makes
realistic discussions of the harm alcohol causes very difficult.
7. Education about responsible use is the best method to protect
society from alcohol problems
It is
useful for the drinks industry to emphasise the value of education, because it
takes the focus off regulation: if how much a person drinks is just their
individual choice, then there’s no need to control how much alcohol they have
access to. As well as being implausible with a drug like alcohol that dissolves
one’s self-control, there is also extensive evidence gathered by the WHO from
around the world, showing that 25merely
providing information and education without bringing in other policy measures
doesn’t change people’s drinking behaviour. At best, they are a waste of money
– though in the UK the sums involved (a few million pounds a year) are
pitifully small anyway. At worst, especially when these education programmes
are funded by the industry, they can reinforce heavy drinking by improving
people’s opinions of the industry. This is especially worrying in the UK, as
from 261989 to 2006 the
drinks-industry-run Portman Group was funding and delivering many of the
alcohol-awareness campaigns in this country.
Of course I believe that
informing people about the harms done by drugs has an important role to play in
reducing those harms – that’s why I’ve written this book – but it’s not enough
on its own. When it comes to an addictive substance that impairs our judgement,
we can’t rely on people cutting down the amount they use, just because they
have a rational understanding
of its harms. If the product is freely available, being aggressively marketed
all around them, and changes their brain to make self-control nearly
impossible, they need other sorts of interventions too.
How can we reduce the harm done by alcohol?
So what
can we do? As the title of this chapter suggests, one
approach would be to ban alcohol altogether. While this would be consistent
with policies towards other drugs, we know from historical examples that it
would be laden with perverse consequences. Where prohibition has been tried in
the West, most famously 27in the USA from 1920 to 1933,
medical harms such as deaths from liver cirrhosis were reduced over the
population as a whole, but the policies were considered failures. This was
because the social harms of the resulting “bootleg” alcohol market put so much
money and power into the hands of criminal gangs that law and order broke down.
The effects were so severe they led to the repeal of prohibition. Even in the
Islamic world, where the religion’s long-standing ban on the drug makes
prohibition politically possible, the use and abuse of alcohol is well known.
C. Make alcohol a
national health priority.
D. Make alcohol
dependence a priority for the National Treatment Agency.
E. Stop people binge
drinking.
A.
Increase the price
In the
1950s, alcohol was three times the price relative to income as it is now, and
we drank half as much. Evidence from across the world shows that the 28price of
alcohol determines use for almost everyone, with the possible exception of
severely-dependent drinkers. The government should triple the cost of alcohol
progressively over five years, through a minimum price per unit, or through
increased taxation. I prefer the second option because it delivers more money
back to the public purse, helping to offset the costs of the harm caused by the
drug. If we did go down the minimum pricing route, a simple way to calculate it
would be to charge the same amount in a shop as the average price in a pub.
Some people might argue
that increasing the price of alcohol will unfairly affect the poor – but many
of the poor are poor because they’re addicted to alcohol and tobacco.
Increasing the price of cigarettes has significantly reduced demand, and there
is every reason to think this would be the case for alcohol as well. Since
alcohol-related damage already costs each taxpayer £1,000
a year, tripling the price and reducing the harm by two thirds would save
everyone £666, making up for the price increase over
the bar. Anyone that would be financially worse off under this plan is drinking
at a dangerous level anyway. It’s possible that this could lead to higher
levels of smuggling, although with tobacco there is 29no clear
relationship between levels of taxation and levels of smuggling (in fact,
countries with the lowest levels of taxation have historically had the most
smuggling). Effective border controls have substantially reduced the amount of
contraband tobacco coming into the UK, even as the price has been rising, and there’s no reason to think
that this couldn’t work just as effectively for alcohol.
B.
Restrict availability
C. Make alcohol a national health priority
We
know that public-health campaigns really do work: when the current Health
Secretary Andrew Lansley cut the funding on anti-smoking campaigns in 2010, 30the number
of people contacting the NHS to help them quit fell noticeably. Public
campaigns, to make people aware of the damage alcohol does, and make excessive
drinking unfashionable, would help people reduce their intake. All alcohol
advertising should be banned, and drinks containing alcohol should have warning
notices similar to those on cigarette packets, containing information about its
physical risks and social and economic costs.
Education about the
dangers of alcohol should start in primary school. However, we already know
from research that, 31on its own,
lecturing teenagers about drug harms is not very
effective, and may do more harm than good. A more creative approach is a 32model that
has been tested successfully in East Sussex. This focuses on the drinks
industry itself. Students are given information about the way the industry
ignores its own voluntary codes, the influence it has on the public-health
message around alcohol, and the political agendas surrounding alcohol
consumption, along with the costs of drinking to users and society. The
students are then asked to make up their own minds about the issues. We should
encourage wider use of this sort of education.
D. Make alcohol dependence a priority for the National Treatment Agency
There
are a number of promising lines of research into pharmacological substitutes
and therapies, which can work well alongside psychological treatments like
cognitive behavioural therapy (CBT) and Alcoholics Anonymous. The pleasant
effects of alcohol are caused by the release of natural opioids; substances
such as acamprosate and naltrexone block these, making the experience less
pleasurable, and so might help in treatment. Some recent research has found
that building up tolerance to alcohol also results in a 33huge
increase in tolerance to GHB: where an alcoholic might be able to take three
times as much as a non-alcoholic without overdosing, they can tolerate much
more GHB. Although the mechanism is unclear, it may be that GHB could act as a
safer alternative for those severely dependent on alcohol, as they’d be less
likely to kill themselves. (But it is important to note that for people who are
not tolerant to alcohol, GHB/GBL taken with alcohol
is very dangerous – because the two drugs reinforce each other’s
respiratory-depressant effects.)
GHB is used in Italy and
Austria to treat alcoholism. The potential as an alcohol treatment of another
drug, baclofen, that acts on GABA receptors, has been discussed by a recovering
alcoholic, Olivier Ameisen, in his book The End of My
Addiction, and 34a number of
doctors are now using this drug to treat alcoholics, particularly those with liver
disease. There should be more funding for research in this area.
E. Stop people binge drinking
To
stop binge drinking we need a cultural change. It’s very difficult to achieve
this through regulation, but we could start by banning companies who run events
at which reckless levels of drinking routinely occur, such as the student event
promoter, Carnage UK. The dangers of these events are well-recognised by public
services; as the National Union of Students’ vice-president for Welfare said, 35“Any
organised bar crawl that has an ambulance following behind it clearly has
something deeply wrong.” While it would be hard to regulate private groups,
drinking games and pub crawls should be banned in government-supported
organisations like university sports and social clubs, and financial support
removed if they continue to host them.
F. Save lives on the road
Decrease
the drink-driving limit to 40 mg/100 ml in blood, assess people properly when
they’re caught, and revoke their licence if they flout DVLA guidance to be
assessed as fit to drive again. Encourage the wider use in cars of alcohol
detectors that won’t allow the car to start if the driver is over the limit. 36A large
number of road deaths are among young people, and raising the drinking age to
21 would almost certainly reduce them. Road deaths 37declined by
11% after the USA did this in the 1990s.
G.
Provide alternatives
Conclusion
Realistically
this kind of policy-making is probably a long way off. Many of the measures
I’ve suggested would be profoundly unpopular, and would require real leadership
from government – and a willingness to stand up to criticism from both the
drinks industry and the tabloids. The House of Commons Health Committee
summarised the failures of many different areas of government to take action on
alcohol harms in stark terms in its 382009–10
report:
“DCMS [Department of Culture, Media and Sport] has been particularly
close to the drinks industry. The interests of large pub chains and the
promotion of the “night-time” economy have taken priority; Ofcom, the ASA
[Advertising Standards Authority] and the Portman Group preside over an
advertising and marketing regime which is failing to adequately
protect young people. OFT [The Office of Fair Trading] shows a blinkered
obsession with competition heedless of concerns for public health. The Treasury
for many years has pursued a policy of making spirits cheaper in real terms.
Collectively, government has failed to address the alcohol problem.”
Notes
1 Up to 40,000 alcohol-related deaths, including 350 just from acute
alcohol poisoning and 8,000 from cirrhosis of the liver. More than a million
hospital admissions in 2007/8 (including 13,000 under-18s), costing the NHS
£2.7 billion• Alcohol: First Report of Session 2009–10,
House of Commons Health Committee, December 10th 2009
2 7,000 road traffic accidents, including 500 deaths• Chief Medical Officer 150th annual report, Liam Donaldson,
2008
3 1.2 million violent incidents and 500,000 crimes, costing the police
£7 billion• Alcohol: First Report of Session 2009–10,
House of Commons Health Committee, December 10th 2009
4 40% of domestic violence cases involve alcohol• As above.
5 50% of child protection cases• Swept under the carpet: children affected by parental alcohol misuse, Alcohol Concern, URL-35, October 2010
6 3.5 million adults in the UK are addicted• Alcohol:
First Report of Session 2009–10, House of Commons Health Committee,
December 10th 2009
7 up to 700,000 children live with a parent with a drink problem• Swept under the carpet: children affected by parental alcohol
misuse, Alcohol Concern, URL-35, October
2010
8 6,000 children a year are born with foetal alcohol syndrome• Alcohol: First Report of Session 2009–10, URL-162, House of
Commons Health Committee, December 10th 2009
9 the main burden of disease in 15–24 year-old males• Global burden of disease in young people aged 10–24 years: a
systematic analysis, URL-163, Fiona M
Gore, et al, Lancet, June 2011
10 £30 billion a year – though some calculations estimate it may be as
high as £55 billion• As above.
11 compares the death and disability burden in
the EU,• The size and burden of mental disorders
and other disorders of the brain in Europe 2010, URL-164, ECNP/EBC Report 2011
12 Labour government’s 2004 Alcohol Harm Reduction Strategy shows clear
evidence of the influence of the drinks industry• As above.
13 “we are concerned that Government policies are much closer to, and too
influenced by those of the drinks industry and the supermarkets• Alcohol: First Report of Session 2009–10, URL-162, House of
Commons Health Committee, December 10th 2009
14 for a particular group of people (middle-aged men), those that drink
small amounts, particularly of red wine, have slightly lower levels of heart
disease• Alcohol: no ordinary commodity, Thomas Babor
et al, Oxford University Press, 2003
15 no such thing as a safe level of alcohol consumption• There is no such thing as a safe level of alcohol consumption,
David Nutt, URL-36, March 7th 2011
16 all other diseases associated with alcohol the risks rise inexorably
with intake• Alcohol: no ordinary commodity, Thomas
Babor et al, Oxford University Press, 2003
17 specific glutamate receptors• These are the NMDA glutamate receptors.
18 alcohol interferes with our ability to recognise emotions in facial
expressions• Effects of acute alcohol consumption on
processing of perceptual cues of emotional expression, AS Attwood, C
Ohlson, CP Benton, IS Penton-Voak, MR Munafò, Journal of Psychopharmacology
23(1), 2009
19 liver disease match heart disease as the leading cause of death in the
UK by 2020• I am not a Prohibitionist, David Nutt, URL-37, November
5th 2010
20 About a quarter of the adult population of the UK drink more than the
recommended weekly limit• Statistics on Alcohol: England
2010, NHS Information Centre, URL-38, 2010
21 drop in total alcohol consumption of 40%• Alcohol:
First Report of Session 2009–10, House of Commons Health Committee,
December 10th 2009
22 voluntary codes adopted by drinks industries are essentially
ineffective at reducing alcohol harms• As above.
23 £800 million a year on advertising, marketing, sponsorship, contests
and special promotions• The seven key messages of the
alcohol industry, European Centre for Monitoring Alcohol Marketing, URL-39, February
2011
24 Under the Influence• British Medical
Association, URL-40, September 7th 2009
25 merely providing information and education without bringing in other
policy measures doesn’t change people’s drinking behaviour• Alcohol:
First Report of Session 2009–10, House of Commons Health Committee,
December 10th 2009
26 1989 to 2006 the drinks-industry-run Portman Group was funding and
delivering many of the alcohol-awareness campaigns in this country• As above.
27 in the USA from 1920 to 1933, medical harms such as deaths from liver
cirrhosis were reduced over the population as a whole, but the policies were
considered failures• Lessons from Alcohol Policy for Drug
Policy, Harry G. Levine and Craig Reinarman, URL-41, 2004
28 price of alcohol determines use for almost everyone• Alcohol: First Report of Session 2009–10, House of Commons
Health Committee, December 10th 2009
29 no clear relationship between levels of taxation and levels of
smuggling• Cough Up, Policy Exchange, URL-42, March
18th 2010
30 the number of people contacting the NHS to help them quit fell• Andrew Lansley forced to make U-turn on public health campaign
cuts, Daniel Boffey, URL-43, May 28th
2011
31 on its own, lecturing teenagers about drug harms is not very
effective, and may do more harm than good• Alcohol: First
Report of Session 2009–10, House of Commons Health Committee, December
10th 2009
32 model that has been tested successfully in East Sussex• Teaching the tricks of the liquor trade, Paul Myles, URL-44, January
19th 2011
33 huge increase in tolerance to GHB• Cross-tolerance
to ethanol and γ-hydroxybutyric acid, Giancarlo Colombo et al,
Alcoholism: Clinical and Experimental Research, Volume 23 (10), October 1999
34 a number of doctors are now using this drug to treat alcoholics,• Substitution therapy for alcoholism: time for a reappraisal?,
URL-165, J Chick and DJ Nutt, Journal of Psychopharmacology, July 8th, 2011
35 “Any organised bar crawl that has an ambulance following behind it
clearly has something deeply wrong.”• Student pub crawls
face ban amid backlash over drunken disorder, Amelia Hill, URL-45, November
8th 2009.
36 Alarge number of road deaths are among young people• Drinking and Driving, Institute of Alcohol Studies Fact
Sheet, URL-46, October 19th 2010
37 declined by 11% after the USA did this in the 1990s• Minimum drinking age of 21 cuts road deaths, Reuters, URL-47, July 1st
2008
38 2009–10 report• Alcohol: First Report of Session
2009–10, House of Commons Health Committee, December 10th 2009
“Meow meow”
From the beginning, it
seemed unlikely that mephedrone was responsible. The boys had been drinking
heavily, and had died when they stopped breathing; if anything, taking a
stimulant would have been protective. But as it turned out, 1they hadn’t
taken mephedrone at all. As the toxicology report eventually showed, they had
actually mixed alcohol and the heroin substitute methadone – possibly by
mistake, because of their similar sounding names. As the boys tragically
discovered, mixing depressants like alcohol with opiates is extremely dangerous.
(This also turned out to have been the cause of death for 18-year-old 2Joslyne
Cockburn, who died the weekend after.) The fact that the new legal high had
nothing to do with either case didn’t stop the police, the media, or politicians
from using them as evidence for why it needed to be banned.
The media
storm around mephedrone had begun with the death of Gabrielle Price, a
14-year-old from Brighton who collapsed after allegedly taking it at a party,
although she was eventually found to have 3died from
bronchopneumonia caused by a streptococcal A infection and hadn’t taken any
drugs at all. Extreme stories of mephedrone’s harmful effects began to fill the
papers. The Sun reproduced an account from a message
board in which someone claimed to have 4ripped off
his own scrotum while high on mephedrone, 5though this
turned out to have been made up. More and more deaths were linked to it, long
before confirmation from coroners that it was responsible, or had even been
taken by the person who died. Quite aside from the ethical issues of whipping
up hysteria with fictional articles, an analysis of internet activity clearly
shows that every time a big story was published, interest in the drug increased
– more people searched for information, and sales went up. Far from protecting
people by exposing the truth, 6the media
through publicising the drug were contributing to its astronomical rise in use
(Figure 7.1).
What is mephedrone and why is it called plant food?
Mephedrone
is the common name for 4-methylmethcathinone. This is a synthetic derivative of
cathinone, which is the active ingredient in the East African plant khat. (See
box The original cathinone: khat on page 126.) Mephedrone was first
synthesised in 1929, and largely forgotten until the early 2000s, when some 7Israeli
scientists working for an insecticide company started experimenting with
cathinones. They were looking for a more ecological way to protect plants and
searching for a chemical that would disrupt the brain activity of greenfly and
make them easier for ladybirds to catch. Mephedrone did this to some extent,
and so was used for a few years as a horticultural product. However, third-party
companies soon discovered its psychoactive effects and started buying up
hundreds of kilos to sell as a party drug in Israel, where it became widely
used. Because of mephedrone’s origin as a plant protector, it got the nickname
“plant food”, although calling it that and labelling it “not for human
consumption” also proved useful for avoiding food safety standards. As well as
its media nickname “meow-meow”, mephedrone has many other street-names,
including Drone, M-cat, and bubbles.
The drug was widely used
in Israel until it was banned in 2007. It was banned partly because the
authorities were concerned about conscripts taking it while they were doing
their time in the army, though in the years that it was legal and popular no
deaths were reported. It caught people’s attention in the UK in 2009, and there
was an extremely rapid increase in the number of users over the second half of
the year. A 8survey of
Tayside schoolchildren and university students in February 2010 showed that 20% of them had tried it, and in late 2009 a
survey of readers of Mixmag magazine found it was the 9fourth most
popular drug amongst clubbers (cannabis, ecstasy and cocaine being the most popular).
Its subjective effects seem to be partway between ecstasy and cocaine – users
say it increases their self-confidence and makes them more talkative (like
cocaine), but also report feeling a greater sense of openness, appreciation of
music and desire to dance, (similar to ecstasy). As well as being legal, it was
widely available, and cheap, costing about 10£10 a gram
or £1–2.50 a dose.
The harms and benefits of taking mephedrone
Of the
dozens of deaths in 2009 that the media attributed to mephedrone, only two have
been confirmed as being directly and solely caused by the drug. One of these
was a 1146-year old
man with underlying health problems who repeatedly injected large doses
intravenously. Mephedrone was also recorded: as a factor in a handful of other
cases; as part of the cocktail in a few mixed-drug deaths; and as having
contributed to the mental states of two people who committed suicide. There
have been some cases of people with hyponatraemia after taking mephedrone,
where low sodium levels lead to swelling in the brain, as happened to Leah
Betts when she took ecstasy
Each of these deaths is
extremely sad, and anyone would wish they hadn’t happened. However, because
many people switched to using mephedrone from cocaine, which is a more harmful
drug, it may actually have saved lives overall. Statistician Professor Sheila
Bird has suggested that the drop in deaths from cocaine, from 95 in the first
six months of 2008, to 66 in the first half of 2009, may have been due to this
switch, and she calculated that 12about 40
deaths have been avoided. There was also a 13drop in
soldiers testing positive for cocaine in the army so far fewer were kicked out,
so that many careers and lots of taxpayers’ money were saved. In addition, the
British government gained 14£600,000 in
import tax.
We now know a little
about the harms of mephedrone. Users report negative effects such as jaw clenching, nausea, anxiety, insomnia,
paranoia and hallucinations, related probably to lack of sleep. Heavy users may
well experience insomnia, and there is also the danger of paranoia or even
triggering a psychotic episode. Most of these negative effects are relatively
mild and short-lived, but some users end up in hospital, usually presenting
with a fast and irregular heartbeat, tightness in the chest, agitation,
excessive sweating and headaches. Most worryingly, 15up to 85%
of users have reported experiencing cravings for the drug, making it likely
that some are using it compulsively and becoming dependent. The desire to
redose rapidly seems to be more acute when people snort the powder rather than
eating it, which makes sense, as the faster a drug hits the brain, the more
addictive it is.
Because use of the drug
is so recent, we have very little knowledge about its long-term effects. A lot
of people were taking it in Israel for a number of years, and there doesn’t
seem to have been a large increase in harms as a result. There’s now a lot of
research taking place around the world into its effects. An Australian survey
of ecstasy users found that those also using mephedrone were 16more likely
to have engaged in risky sexual behaviour, which may be related to the fact
that it seems to increase sexual drive more than ecstasy.
Why was mephedrone banned?
Louis
Wainwright and Nicholas Smith were found dead on March 16th, three weeks before
the 2010 UK general election was called. With the dangers of “meow meow” making
headlines and an election looming, it was almost inevitable that Home Secretary
Alan Johnson would push for mephedrone to be made illegal as soon as possible.
The ACMD, who were in the midst of producing a report on cathinones, were asked
to speed up the process, and on March 31st published their recommendation that
all the synthetic cathinones be placed in Class B. According to one member, 17the report
was only in draft form and still under discussion when the chair rushed off to
give Alan Johnson their recommendation in time for him to brief the press.
The period
after a general election has been called is known as the “wash up”, where
legislation that the government wants to push through with the minimum amount
of consideration can get fast-tracked into law. In this case all three parties
agreed with the amendment to the Misuse of Drugs Act banning the cathinones, so
it was debated for an hour and passed without a vote. At such a politically
sensitive time, it was highly unlikely that any politician would have stood up
and pointed out that at this stage 18we had
almost no evidence (Figure 7.1) that the drug actually caused harm.
|
|
Dopamine |
Serotonin |
Noradrenaline |
|
Amphetamine |
••• |
• |
•••• |
|
MDMA |
•• |
••• |
••• |
|
Cathinone |
••• |
•• |
••• |
|
Methcathinone |
••• |
• |
••• |
|
Methylone |
•• |
••• |
•••• |
|
Mephedrone |
? |
? |
? |
Two of my former
colleagues quit the ACMD in protest: 19Eric Carlin
said the decision to ban mephedrone was “unduly based on
media and political pressure”, and 20Dr Polly
Taylor said that she “did not have trust” in the way
that the government would use the council’s advice. Those who stayed were also
vocal in their criticism. Criminologist Fiona Measham described the media’s
portrayal of the unconfirmed deaths as involving 21“the usual cycle of exaggeration, distortion, inaccuracy and
sensationalism” we’ve come to expect in the reporting of recreational
drug use. Alan Johnson himself admitted in interview a few months after the
election that the 22media’s
obsession with the drug sped up the decision to ban it yet he still made the
ridiculous assertion that there had been a high-quality scientific review of
the evidence: 23“The unanimous recommendation to ban the drug made by the scientists,
clinicians and other experts on the Advisory Council on the Misuse of Drugs to
prevent tragedies in the future was based on painstaking evidence.”
The immediate consequence
of the ban was that the price went up. The cost per gram has now quadrupled to 24about £50,
which may have helped to reduce use, although this money is now entirely in the
black market, untaxable and being channelled into other sorts of criminal
activity. Surprisingly, mephedrone’s purity does not seem to have significantly
declined, which is probably part of the reason it has stayed so popular since
it was criminalised.
The designer drug problem
There
are many reasons why mephedrone rose meteorically from little-known pest
control agent to household name. In 2009–10 there was definitely a gap in the
market for a substitute for cocaine and ecstasy, because at the time these were
of exceptionally poor quality. The average purity of cocaine dropped 25as low as
22% in 2009, and may of the 26ecstasy
pills seized in mid-2010 contained no MDMA at all. (27A huge
seizure of sassafras oil in Cambodia in June 2008, which could have made 245
million doses of MDMA, was probably responsible for this.) In contrast, before
the ban 28most
mephedrone was at least 95% pure.
But even if mephedrone
had had quite different effects, the appearance of a new “legal high” was
inevitable. Since 2005 we’ve had GBL, spice and benzylpiperazine (known as BZP) being produced in vast quantities
and sold over the internet for a brief period until being banned. This is the
designer drug problem: as fast as government can legislate against known drugs,
chemists around the world design new compounds specifically to get around the
law. This process is speeding up, and the internet is the perfect marketplace
for new designer drugs. Mephedrone’s appearance on the scene has been
specifically 29linked to
the banning of BZP at my recommendation as chair of the ACMD. Perhaps the Daily Mail will say the entire episode was my fault!
Alternative
approaches
So what
can governments do? One approach is to copy the USA, and make analogues of
existing controlled substances illegal automatically. This approach is now
being suggested by the ACMD, despite the fact that the USA drug enforcement
agency has concluded that this is a failed policy, because they find it almost
impossible to prosecute under it. And, it would be disastrous for medical
research: we know from experience that the use of MDMA as a tool for
psychotherapy has been held back for the 40 years since the drug was banned.
Already, another cathinone called naphyrone has been made illegal, owing to its
chemical similarity to mephedrone, although there is no evidence of widespread
use or harm. It was developed as a possible treatment for addiction, and that
whole line of research will now suffer as a result of its legal status. And
while chemically close to mephedrone, it is also similar to antidepressants
such as bupropion, sold under the trade name Wellbutrin. Once you start
banning analogues of illegal substances, where exactly do you stop?
What the government have
opted for is the introduction of 30temporary
banning orders. These can be brought in as soon as the substance is identified
as potentially harmful, and last for 12 months while the ACMD investigates its
effects and decides whether it should be included in the Misuse of Drugs Act.
Those attempting to import something which has been temporarily banned could
receive up to 14 years in prison, but possessing small amounts for personal use
would not be a criminal act. As the Drugs Commission has pointed out, the fact
that the ACMD’s advice doesn’t have to be sought before something is banned is
a real weakness of this approach, as is the fact that no particular threshold
of harm has to be reached before something can be made illegal. This will
impact on medical research and industries that work with chemicals, who could
see products vital to their work suddenly becoming unavailable without warning.
A different approach, and
one I did suggest to the government when I was in the ACMD (though it was
predictably rejected) is to follow the example of New Zealand and 31create a new
Class for drugs, Class D. This would be a holding category for new substances,
with quality-controlled sales at limited doses restricted to over 18s, and
health-education messages on the packaging. People will know what they’re
taking, and we can monitor use while we work out whether it’s something that
needs stricter controls. We could combine this with drug testing (cf the Dutch
Drug Information and Monitoring System, page 124) and with greater use of
amnesty bins in clubs, where visitors are required to discard illicit drugs
before entering and security staff put anything they find during searches. With
this information we would be in a far stronger position to gather evidence
about harms and behaviours than with a simple blanket ban. We wouldn’t risk
criminalising large numbers of young people for experimenting with new substances,
and we would avoid knee-jerk reactions to legislate as fast and as harshly as
possible. For most young people the effects of being given a criminal record
for drug possession will be much more damaging to their lives than the effects
of the drug.
The very least we ought to know
Above
all, whatever approach a government takes, there is a sensible 32minimum
amount of data we ought to have before a decision is made about a new drug. The
ACMD’s report about mephedrone wasn’t the only one which was notable for its
lack of substantial facts. A few months later, 33a Europol
report recommended a Europe-wide ban, opening its section on mephedrone with: “There are no formal pharmacokinetic and pharmacodynamic studies on
mephedrone. There are no published formal studies assessing the psychological
or behavioural effects of mephedrone in humans. In addition, there are no
animal studies on which to base an extrapolation of potential effects.”
These are the very organisations that ought to be filling in these gaps in our
knowledge so we can make informed decisions about how to reduce harm. Yet
rather than wait to gather this evidence, they produced recommendations on the
basis of almost nothing.
·
Pharmacology. What receptors,
transporters and enzymes are relevant to this drug? (Tests should take less
than 4 weeks.)
Ideally,
we would also know some other things about the drug. We can establish how
addictive it is, and whether it has a withdrawal syndrome, by doing experiments
on rodents. These are standard tests which are performed all the time by
pharmaceutical companies, are not difficult to set up and run, and should take
no more than a month. It would be useful to know the drug’s chemistry, whether
it dissolves in water, or evaporates at a low enough temperature to be smoked,
so we can predict how it’s likely to be taken. Equally, the most likely form
the drug will be sold in on
the street is as a hydrochloride salt, so we should synthesise these and study
new drugs in that form.
Another thing we could do
to learn more about new drugs as they appear is to set up a 34Drugs
Information and Monitoring System (DIMS) like the one they have in the
Netherlands, which is a fascinating example of applying common sense to drug
use. Across the Netherlands there are a number of hospitals where drugs can be
tested. Users take their drugs to the centre knowing that they will not be
arrested. After the tests they are given information on what the drug is,
health and safety advice to help them decide whether to take it or not, and
what to do if they get adverse effects. Not only does this offer an opportunity
for harm prevention, but also the Dutch authorities get to know exactly what
drugs are in circulation and where, and they can catch “bad batches” before
they do too much damage. We should set up a similar system in the UK.
Conclusion
There
are some important 35lessons to
be learnt from the mephedrone debacle. The first is that the police shouldn’t
make public statements or hold press conferences on the basis of hearsay or
presumption, and the media should apply some traditional journalistic
principles to their coverage of issues around drugs, especially legal highs. Gathering
evidence, giving coroners time to undertake proper drug testing, and generally
allowing the scientific process to take place before claiming that the drug is
harmful, serves the public interest far better than generating hysteria. People
understand that much of the reporting on these issues is exaggerated, which is
why the media coverage of the supposed harms of mephedrone led to an increase
in use. If the media, police, or any other public body wants to be trusted by
the public they need to limit themselves to reporting facts, and be seen to do
so.
The government and its
advisers need to focus on making decisions based on evidence rather than
headlines. There needs to be proper research investment into the science of new
drugs. Obtaining basic pharmacological facts about
mephedrone would have taken at most a few weeks, at little cost, and yet the
ACMD’s nine-month review didn’t even contain these. Having some guidelines on
what a report should include, like our minimum dataset, would be a step in the right
direction. This would be compatible with temporary banning orders, although I
think they are an inadequate response to the radical overhaul of the Misuse of
Drugs Act that we need.
Should mephedrone have
been banned? The ban may well increase the harms rather than reduce them, as
users switch back to more harmful substances like cocaine. An editorial in the Lancet shortly after the ban criticised both the
government’s attitude to the ACMD, and the rushed process to recommend making
mephedrone Class B. As they said: 36“It is too
easy and potentially counterproductive to ban each new substance that comes
along rather than seek to understand more about young people’s motivations and
how we can influence them … Making the drug illegal will also deter crucial
research on this drug and other drug-related behaviour, and it will be far more
difficult for people with problems to get help.”
A final lesson from this
episode is the need to educate people about the dangers of poly drug use,
especially mixing other things with alcohol. When new drugs appear, we really
don’t know how they will interact with others, and mixing them could
substantially increase the harms. With alcohol it is particularly important not
to combine it with other drugs that suppress breathing, like opiates and
GHB/GBL. This is what killed Hester Stewart, who took GBL after she had been
drinking, as well as Joslyne Cockburn,
Louis Wainwright and Nicholas Smith. If in doubt, don’t
drink and drug.
The original cathinone: khat
37Khat is a
shrub that grows in East Africa and on the Arab Peninsula. Its leaves have mild
stimulant properties when chewed, similar to the leaves of the coca plant that
grows in South America. Although the drug is rarely used outside a few cultural
and national groups – mostly Somalis, Yemenis and Ethiopians – they’ve taken
the habit with them as they have migrated across the world, creating a small
global trade.
With many
of these health problems, it can be hard to establish if the cathinone itself
is the cause. Khat is usually consumed in poorly ventilated “mafreshi” (chewing
houses) along with a large number of cigarettes, so much of the increased risk
of cancers and heart attacks may actually be due to smoke inhalation. Dangerous
pesticides have been detected on the leaves, which people are reluctant to wash
off because they believe it reduces the leaves’ potency. Users often consume a
lot of fizzy drinks as they chew, which may cause tooth decay and diabetes, and
young people are now trying to increase the stimulant effect by having caffeine
drinks at the same time, which will put more strain on the heart.
These behavioural changes
can cause social problems for chewers and their families. Heavy users – who are
usually men – absenting themselves physically and psychologically for hours at
a time can cause family tensions, especially if a significant proportion of
their income is being spent on the drug. Since the tobacco-smoking ban, some
men have taken to hosting chewing parties in their homes, disrupting time for
homework and leaving the women without a social space as it’s seen as a single
sex activity. Women who do use the drug tend to do so alone, and seem more
likely than men to become dependent, possibly because there aren’t the same
cultural controls around using it socially – just as those who drink at home
are more likely to become dependent than those who drink in the pub. Job
prospects can be hampered by long hours spent chewing, or being late or absent from work because of lack of sleep. This can be a real problem among
marginalised communities who find it difficult to get work anyway.
Notes
1 they hadn’t taken mephedrone at all• Teenagers’
deaths “not caused by mephedrone”, BBC news, URL-48, May 28th
2010
2 Joslyne Cockburn• Teenager’s Death Latest Linked to
Mephedrone, Andy Bloxham, URL-49, March
30th 2010
3 died from bronchopneumonia caused by a streptococcal A infection• Police Rule Out ’Legal High’ Link To Death, Lulu Sinclair, URL-50, December
16th 2009
4 ripped off his own scrotum• Legal drug teen ripped
his scrotum off, Vince Soodin, URL-51, November
26th 2009
5 though this turned out to have been made up• Mephedrone:
the anatomy of a drug media scare, Nic Fleming, URL-52, April 5th
2010
6 the media through publicising the drug were contributing to its
astronomical rise in use• Virtually a drug scare: Mephedrone
and the impact of the Internet on drug news transmission, AJM Forsyth,
International Journal of Drug Policy, 2012. See also URL-166.
7 Israeli scientists working for an insecticide company started
experimenting with cathinones• Mephedrone – scientific
background, ISCD, URL-53, accessed
December 10th 2011
8 survey of Tayside schoolchildren and university students in February
2010• How bubbles blasted its way into Tayside,
Graham Huband, URL-54, May 31st 2010
9 fourth most popular drug amongst clubbers• Mixmag
survey 2009, Winstock, A. (2010) Results of the 2009/10 Mixmag drug
survey. Oral evidence to the ACMD.
10 £10 a gram• Consideration of the Cathinones,
ACMD, March 31st 2010
11 46-year old man with underlying health problems who repeatedly
injected large doses intravenously• npSAD (National Programme on Substance
Abuse Deaths) Drug related deaths in the UK Annual Report,
URL-55, 2009
12 about 40 deaths have been avoided• Banned drug may
have saved lives, not cost them, Sheila Bird, Statistics Bulletin, URL-56, November
22nd 2010
13 drop in soldiers testing positive for cocaine in the army so far fewer
were kicked out• Mephedrone and cocaine: clues from Army
testing, Sheila Bird and Patrick Mercer, URL-57, accessed
December 10th 2011
14 £600,000 in import tax• URL-58, April 8th
2010
15 up to 85% of users have reported experiencing cravings for the drug• Instability of the ecstasy market and the new kid on the block:
mephedrone, Brunt et al, Journal of Psychopharmacology, September 8th
2010
16 more likely to have engaged in risky sexual behaviour• Mephedrone use among regular ecstasy consumers in Australia,
Ecstasy and related drug trends Bulletin, URL-59, December
2010
17 the report was only in draft form and still under discussion when the
chair rushed off to give Alan Johnson their recommendation in time for him to
brief the press• Lancet editorial, URL-60, April 17th
2010
18 we had almost no evidence (Figure 7.1)• Consideration
of the cathinones, URL-167, ACMD,
March 31st, 2010
19 Eric Carlin said the decision to ban
mephedrone was “unduly based on media and political
pressure”• Government adviser Eric Carlin quits over mephedrone, BBC News, URL-61, April 2nd 2010
20 Dr Polly Taylor said that she “did not have trust”• Mephedrone to be made Class B drug within week, BBC News, URL-61, March 29th 2010
21 “the usual cycle
of exaggeration, distortion, inaccuracy and sensationalism”• Tweaking, bombing,
dabbing and stockpiling: the emergence of mephedrone and the perversity of
prohibition, Measham, F.; Moore, K.;
Newcombe, R.; Smith, Z., Drugs and Alcohol Today 10 (1), March 12th 2010
22 media’s obsession with the drug sped up the decision to ban it• Addicted to distortion: the media and UK drugs policy, Jon
Silverman, Safer Communities 9 (4), 2010
23 “The unanimous
recommendation to ban the drug made by the scientists, clinicians and other
experts on the Advisory Council on the Misuse of Drugs to prevent tragedies in
the future was based on painstaking evidence.”• Decision to outlaw mephedrone
drug not connected to teen deaths, This Is Scunthorpe, URL-62, January 11th 2011
24 about £50• Mephedrone: still available and twice
the price, Winstock, Mitcheson and Marsden, URL-63, November
6th 2010
25 as low as 22% in 2009• Miaow Miaow on trial: truth
or trumped up charges?, Nic Fleming, URL-64, March 29th
2010
26 ecstasy pills seized in mid-2010 contained no MDMA at all• Ecstasy “disappearing” from British clubs, Jim Reed, URL-65, June 20th
2010
27 A huge seizure of sassafras oil• World Wired Web,
Mike Power, in How mephedrone shook the drug trade
issue of DrugLink, January/February 2010
28 most mephedrone was at least 95% pure• Consideration
of the Cathinones, ACMD, March 31st 2010
29 linked to the banning of BZP• Mephedrone and the ACMD: lessons from BZP and New Zealand’s “Class D”
experiment?, Transform, URL-66, March 18th 2010
30 temporary banning orders• Misuse of Drugs:
Temporary Class Drugs, Home Office, URL-67, August
2011
31 create a new Class for drugs, Class D• Mephedrone:
the Class D solution, David Nutt, URL-68, March 17th
2010
32 minimum amount of data• ISCD suggested minimum data set for any new drug that raises concerns
about harms, ISCD, URL-69, accessed December 10th 2011
33 a Europol report• Joint Report on a new psychoactive substance: 4-methylmethcathinone
(mephedrone), Europol–EMCDDA, URL-70, March 2010
34 Drugs Information and Monitoring System (DIMS) like the one they have
in the Netherlands• The Drug Information and Monitoring
System (DIMS) in the Netherlands: Implementation, results, and
international comparison, Tibor Brunt, Raymond Niesink, Drug Testing and
Analysis, 2011
35 lessons to be learnt from the mephedrone debacle• Hysteria
and hubris: lessons on drugs control from the Scunthorpe Two, David
Nutt, URL-71, May 28th 2010
36 “It is too easy and potentially counterproductive to ban each new substance
that comes along• A collapse in integrity of scientific
advice in the UK, Lancet editorial, URL-60, April
17th, 2010
37 Khat is• Khat
(Qat): Assessment of the risk to individuals and communities in the UK, ACMD, URL-72, December 2005
1.
Drug-related
factors include how the drug reaches the brain, and
what it does when it gets there. Tolerance and withdrawal also affect its
addictiveness.
2.
Social
factors include the availability and acceptability
of using the drug, the prevalence of advertising, how the drug makes groups
behave, and the economic and social costs.
3.
Personal and
biological factors are factors such as age, gender
and genetics.
Addiction
in history
Our
understanding of addiction has increased as more drugs have become available,
and as their role in society has changed. Until the 19th century, heavy
drinking or use of other drugs wasn’t seen as a special category of behaviour,
but as a sin of excess, similar to overeating – gluttony was a problem because
you were eating too much, not because food itself was
a bad thing. Although excessive use of drugs was seen as problematic, the
majority of people usually didn’t have access to enough potent substances to
have that problem. An exception was the 1Gin Craze,
of the 18th century. Technological advances and several years of good harvests
led to a fall in the price of food, giving the urban poor in London
discretionary income for the first time, which they started to spend on the
powerful liquor that was being made from the grain surplus. Alcohol harms
increased substantially, especially amongst the more vulnerable members of
society. This changed the general perception of alcohol, and eventually led to
the formation of the Temperance Movement, which recognised that there was
something particular about alcoholic beverages that led to patterns of
dangerous and compulsive use. What really ended the Craze, however, was a
series of bad harvests, which pushed up the price of food again and reduced the
availability of gin.
As purer and more
powerful substances became available at the end of the 19th century, drugs
started to be seen as a special sort of social menace, and our understanding of addiction started to be seen in
psychological terms. Someone with an “addictive personality” was considerd
morally weak, unable to resist the temptation posed by drugs, unlike good
law-abiding citizens. Now that there was widespread access to drugs, it became
clear that there was some kind of 2relationship
between being marginalised from society and drug addiction. The fact that
groups like Native Americans, Australian aborigines, gay people and poor people
seemed to be more likely to become addicts was seen as confirming the moral
basis for their place in the social order. Willpower alone was thought to be
enough to give up drugs, possibly accompanied by therapy to uncover the
psychological reasons for becoming addicted. Therapists were trained in
Freudian psychoanalysis, and would search for underlying causes of addiction
such as repressed childhood memories or the fear of taking on the
responsibilities of adulthood.
In the second half of the
twentieth century, developments in our understanding of how the brain works challenged
this approach. The discovery of chemicals in the brain that work in similar
ways to common drugs of abuse, and receptors apparently designed to respond to
them, led to addiction being analysed in biological rather than psychological
terms. We now understand that repeated use of a drug can cause physical changes
to our brains, resulting in a kind of “brain disease”, in the same way that
strain on the heart can lead to heart disease. Neuroimaging techniques in the
last 15 years have allowed us to see these changes for the first time,
confirming that these changes are physical and to an extent irreversible. (See
box How does neuroimaging work? on page 150.)
As with any other sort of
disease, individuals are at risk of addiction to different degrees depending on
their genes, background and environment. If people in marginalised groups are
more likely to become addicts, this is because of the stress caused by their
position in society, not because
being a member of that particular group makes them weak and immoral. An
“addictive personality” is now understood to describe someone who is
particularly vulnerable to this disease, not someone lacking in willpower.
Addiction is largely preventable and treatable, just as diabetes is, but for
some people the make-up of their brain or the circumstances of their life make
addiction almost inevitable, and blaming them for their vulnerability is
unfair. To put it another way: 3when a
highly educated, high-status man like David Cameron, who is protected from drug
abuse by numerous factors in his life (such as being born to a rich family and
going to a top school and university) uses cannabis and doesn’t get addicted,
this isn’t because he’s morally superior to someone else who does become
addicted. The same is true for 4President
Obama, who has admitted to cocaine use before he came to office.
Some recent work has
identified the neurological similarities between drug addictions and other
types of behavioural addiction, such as compulsive eating or gambling, which
seem to involve the same psychological and biological mechanisms in the brain.
Researchers such as Jim Orford have suggested 5we ought to
think of drug addiction as a special form of behavioural addiction, which can
occur with any (initially) pleasurable activity, from shopping to exercise. In
some ways, this takes us full circle, to a pre-19th century model of excessive
behaviour – drugs do have some special qualities, but the mechanisms by which
they can become the most powerful drives in people’s lives are similar to those
involved in other pleasurable and repeated activities. These mechanisms are
both psychological and biological, and are central to how our brains work.
The brain mechanisms of addiction
Addiction
involves both the pleasure chemicals in the brain, and the processes by which
we learn repeated behaviours. This process is very complicated, involving many
mechanisms and different neurotransmitters. Figure 8.2 shows some of the
different elements involved. On the left, we can see the positive elements of a
drug experience – it might create pleasure,
reduce suffering, lay down powerful memories or reveal a new perspective that
seems particularly meaningful.
Figure 8.3 shows how 6different
neurotransmitters are believed to be involved in these “push” and “pull”
factors. Dopamine is involved in drive and desire and perhaps reward;
endorphins give peace and pleasure, reduce suffering, and numb pain; GABA and
glutamate regulate memory; serotonin may be involved in attributing meaning to
experience. Noradrenaline seems to be related to impulsivity and compulsivity,
which is why amphetamines can help people with attention disorders – because
stimulants reduce impulsivity.
Dopamine seems to play a
key part in addiction. It is released in special brain regions when we feel a sense of reward and achievement, helping
us to learn what we did to feel good so we know to repeat the activity in the
future. Neuroimaging has allowed us to see dopamine being released when people
take cocaine and other stimulants and also when we succeed at activities such
as playing video games. Addiction to video gaming is becoming increasingly
common, especially as the internet makes 24-hour play possible. (An extreme
example of this was the 7Korean
couple who let their baby starve to death while they played a computer game
that involved rearing a virtual child.)
This loss of control has
two factors. A drug can enhance the “push” factors, creating an overwhelming
desire to do something, or it can reduce our ability to resist behaviours, even
if we know they will have negative consequences. Most often it’s a combination
of both. Over time, this can lead to an inability to resist cravings which a
non-addict has no difficulty
in overcoming. This explains a common complaint of addicts that they don’t want
to continue with their addictions and don’t enjoy them anymore, but can’t stop
because taking the drug has become a kind of involuntary reflex.
Addiction is particularly
common among people with lower numbers of dopamine receptors, and this is true
even for drugs which don’t directly release dopamine themselves. Alcohol
primarily stimulates the GABA receptors, for example, but studies of alcoholics
and their families have found that 8alcoholics
have fewer dopamine receptors than their non-alcoholic relatives. Increasing
the number of dopamine receptors also reduces alcohol intake. In 9tests on
rats that have been made addicted to alcohol, injecting them with a virus that
makes more dopamine receptors results in the rats drinking less.
The issue of the number
of dopamine receptors an individual has is complicated, however, because
although this is partly genetically determined, the number can vary according
to our environment as well. Tests with rhesus monkeys, who have similar social
patterns to humans, have found that 10high-status
monkeys have more dopamine receptors than low-status monkeys, and lower-status
ones take more cocaine and alcohol when exposed to these drugs. Even more
interestingly, the number of receptors can change over time in response to
social experiences. When the dominance is reversed, the number of receptors in
the monkey that was formerly lower status goes up, and the amount of cocaine it
takes goes down.
If dopamine is involved
in motivation and drive, it’s the brain’s natural opiates (endorphins,
enkephalins and dynorphins) that give us the sensation of reward. When these
chemical messengers are released they make you feel happy and reduce pain; they
also play an important role in mother/child bonding. Heroin and other opiates
primarily interact with this
system, changing the receptors in a way similar to how stimulants change
dopamine receptors. This means that heroin addicts often feel miserable even
when they are “clean”. We are learning that many other drugs that mainly work
on other types of receptors also interact with endorphin receptors. Alcohol
seems to release endorphins, which is why some new treatments for alcohol
dependence involve using drugs that block these receptors, stopping
alcohol-induced pleasure or craving. There’s some evidence that endorphins are
also involved in our development of liking for tobacco and stimulants. Some
recent work from my research group has shown that 11amphetamine
releases endorphins, which may help us to develop new treatments for addiction
to this kind of stimulant.
What is tolerance and why does it occur?
Tolerance
occurs when repeatedly doing something changes the way we react to it. When we
take drugs, the brain usually responds to the overstimulation that the drugs cause,
by desensitising the target receptors – each hit creates less of a high so you
need to take successively larger doses to achieve the same effect. The more
frequently you take a drug, the more quickly tolerance builds up, because your
brain has less time between doses to readjust. For example, 12if you use
ketamine about once a month, an effective dose
could be as little as 20 mg, whereas if you use it daily you might eventually
need to take 200mg to feel any effect at all. The most extreme form of
tolerance happens during binges, when someone keeps themselves in a constant
state of intoxication for a prolonged period, sometimes as long as a couple of
days. Figure 8.5 shows a graph of brain activity during a cocaine binge:
Sometimes people can
develop “reverse tolerance”, where repeated use leads to extreme sensitisation
instead of the normal reduced sensitivity. Some cocaine users, for example, can
suddenly find themselves acutely sensitive to its effects. This is dangerous,
because it can cause effects such as seizures. However, it might possibly have
some therapeutic benefits: some of my earliest research was on the possibility
of creating an anti-depressant effect by
using sensitisation to cocaine to increase dopamine function in the brain. (The
experiments weren’t very successful – we could show it happened but couldn’t
identify a mechanism or understand why!)
13Sensitisation
can be seen in behavioural addictions such as gambling. People respond to “near
wins” (getting three out of four matches on a fruit machine, for example) with
a sense of reward almost as good as if they’d actually won something. This
encourages them to continue playing, as they’re getting some of the high they
want even though they’re actually losing. Fruit machines and scratch-card
lotteries are often designed to ensure a higher-than-chance frequency of near
misses – the sensation of nearly winning can be created when a fruit machine
shows two winning symbols and a third just below or above it, for example.
Withdrawal
and craving
As well as physical
symptoms there are psychological effects. Most withdrawing addicts suffer from
low dopamine levels, creating anhedonia (a form of
depression that makes them unable to feel pleasure). This can last for weeks, months or even years, creating powerful cravings
for the drug, and is usually the strongest force driving addicts to relapse.
Jim Orford has suggested that a lot of 14addiction
starts as pleasure seeking, but when withdrawal kicks in, the main drive
becomes reducing the suffering of withdrawal. This is particularly true for
most smokers: tobacco is usually unpleasant to start with, but once someone is
addicted withdrawal is even more unpleasant so relieving that discomfort is
experienced as pleasurable (Figure 8.6).
There will usually be
both physical and psychological symptoms in any withdrawal, and it can be hard
to distinguish between the two because expectation plays such an important role
in our experiences of drugs. Many regular drug users will feel very attached to
the process of preparing and consuming their substance of choice and will crave
this context almost as much as the drug itself. Feeling anxious or having
trouble sleeping after stopping might be a psychological or psychosomatic
response to this sense of loss, rather than a purely physical response. An
example of how we can distinguish between physical and psychological symptoms
is when cannabis users are given rimonabant, which blocks the effects of the
drug on cannabis receptors. The users continue to smoke cannabis, thus satisfying
their psychological cravings for it, but don’t experience any psychoactive
effects. What these studies have shown is that even under these circumstances
cannabis users will experience
withdrawal symptoms, proving that cannabis has a physical withdrawal syndrome.
Diagnosing
addiction
Addiction is really about
experiencing cravings and losing control over your actions, not just physical
tolerance and withdrawal. Although all these often do go hand-in-hand, if the
psychological cravings are mild or
non-existent we wouldn’t call someone an addict. Most of us go into caffeine
withdrawal overnight, for example, and some people can experience headaches and
lethargy as a result, but very few would find it psychologically traumatic if
wasn’t available for a while. (There is more about this distinction in chapter
12.)
·
Feeling a strong desire or
compulsion to take the substance.
·
Difficulties in controlling how
much you take and how often, and finding yourself unable to stop.
·
Physical withdrawal symptoms.
·
Signs of tolerance and having to
increase your dosage.
·
Continuing to take the substance
even when it is obviously doing you harm.
The exact
form that addiction takes depends on the substance involved and the social
context. What we think of as classic drug-seeking behaviours are largely based
on people addicted to heroin and crack: committing crimes or engaging in
prostitution to buy drugs, stealing from family and friends, lying about drug
use, neglecting their children and spending all their time either intoxicated
or looking for drugs. Of course, this becomes a vicious cycle: as family and
friends stop trusting them, they lose their homes and jobs, go in and out of
prison, their children go into care, their lives become more and more miserable
and the only thing that can relieve their suffering is the drug.
Is there an “addictive personality”?
We know of
a number of traits that make people vulnerable to specific drugs. There is a
genetic component to alcoholism, for example, which has been proved by 15Danish
studies that have shown that the sons of alcoholic fathers have the same
elevated risk of developing alcoholism whether they stay with their natural
father or are adopted by non-drinkers. There are almost certainly hereditary
elements to addictions to other drugs as well. Our genes can determine how
quickly we metabolise drugs; this is a consideration in addiction, because the
faster we process a drug the more severe our withdrawal reaction will be. 16The enzyme
that clears nicotine from the body has two versions, one which results in a
high metabolism and the other in a low metabolism; in studies of withdrawal in
smokers, the faster nicotine leaves the body the more likely the person is to
relapse when they try to stop.
There are variations on
endorphin and GABA receptors which can make people more or less sensitive to
certain drugs. Being more sensitive may make you more vulnerable to addiction,
because the drug will have a more powerful effect. Conversely, 17male
children of male alcoholics have alterations in GABA receptors that make them less sensitive to alcohol so they can consume more than
their friends from the first day they start drinking. This makes them drink
more, and so become dependent more rapidly. The number of receptors someone has
also plays a role. Having low numbers of dopamine receptors, for example, is
associated with alcoholism and cocaine use. 18High opioid
receptor levels in the brain also predict drug use and craving for opiates, and
possibly for alcohol as well.
Other traits that can
affect vulnerability to addiction are environment-and gender-related:
·
The conditions someone has
experienced in the womb: 19if mothers use drugs while
pregnant, their children may be more likely to become addicted to those same
drugs in later life.
·
Although most addicts are male,
drugs usually have more of an effect on women, because women are smaller and
have a higher proportion of body fat (and fat
doesn’t absorb most drugs). The menstrual cycle produces hormones
(neurosteroids) that act in the brain and affect the actions of alcohol and
other drugs.
·
Impulsivity. A tendency to act
without thought for the long-term consequences of your actions can make you
more likely to take drugs and become addicted. On the other hand, stimulants
make people less impulsive, and some people take them partly as self-medication
for their impulsivity.
·
Gender. Men tend to be more
sensation-seeking, and there are also social factors around loss of control
which make men more likely to become addicts than women.
Protective factors – why some people don’t get addicted to drugs
·
Health concerns. Fear of drugs’
negative consequences (which may or may not be in proportion to the actual
risk), can protect against addiction.
It is
important to maintain a distinction between using drugs and being vulnerable to
addiction: many people who don’t use drugs at all would be likely to become
addicted if they did use them!
Conclusion
All of this
is important because minimising the harms done by drugs necessarily involves
avoiding and treating addiction. In the next chapter, we’ll look at whether
addiction can be cured, and the most common and effective treatments in use
today. As with any other public-health problem, identifying risk factors, in
order that people can make informed decisions about what they choose to do, is
an essential part of reducing harm. Unravelling the complex factors that drive
addiction, and helping people to stay in control of their own behaviour,
requires improving our understanding of these risk factors.
How does neuroimaging work?
In the
last fifteen years, we’ve developed new techniques (20“neuroimaging”)
that allow us to take pictures of the brain in action. These have vastly
improved our understanding of how the brain is made up and how it works.
However, interpreting the images produced is often difficult, partly because
there’s a lot of variation between individuals, and partly because drug users
rarely use just a single drug (making it hard to associate a particular brain
activity to a specific drug). At the moment imaging can only show us
correlations and say little about causality.
There are two main types
of imaging techniques. The first is positron emission
tomography (PET). We can use a radioactive
isotope as a “tracer” by attaching it to a substance (such as glucose or a
drug), that we know behaves in a certain way in the brain. When injected into
the bloodstream the molecules of the glucose or drug are carried into the
brain. The isotope has a very short half-life (ie it decays quickly). When an
atom of the isotope decays, it emits a positron, which is the same as an
electron but has the opposite charge. When the emitted positron collides with
an electron, the two annihilate one another and emit energy. Because there are
many free electrons in the body, the collision usually occurs less than 1mm
from the decaying isotope, ie very close to where the injected substance
accumulated in the brain, so if we can pin-point
where the collision occurred, we can see where the substance was within the
brain. The energy emitted from the collision is seen as two gamma rays
radiating at 180 degrees to one another, which can be detected some distance
outside the head by the 21PET camera.
Samples are taken over a period of about an hour; the information about the
energy of the gamma rays and whereabouts in the camera they were detected is
then processed by a computer to produce an image called a
PET scan (eg Figure 8.7 on page 152). Here’s an example of how PET is used: we know that the chemical
flumazenil binds to GABA receptors, so by doing a PET scan on someone who has
been injected with a flumazenil tracer we can identify where GABA receptors lie
and how many there are in a particular area.
Neuroimaging
techniques have played a central role in the development of our understanding
of addiction. They have enabled us to confirm the role of dopamine in many
addictions, although conversely they have also revealed that opiate addiction
may not really involve dopamine at all. We’ve been able to study the parts of
the brain involved in craving, by giving cues (such as personalised auditory
memories of drug taking) and looking at brain activity. For example, Figure 8.7
shows the distribution of GABA-A receptors in the brain, which is where alcohol
takes its effect. However, some drugs are difficult to study with neuroimaging,
because we don’t have reliable tracers – for example we have yet to find good glutamate tracers.
Notes
1 Gin Craze, of the 18th century• Alcohol: First
Report of Session 2009–10, House of Commons Health Committee, December
10th 2009
2 relationship between being marginalised from society and drug
addiction• The Stigma of Substance Abuse: a Review of the
Literature, Centre for Addiction and Mental Health, URL-73, August
18th 1999
3 when a highly educated, high-status man like David Cameron•
Cameron – the rise of the new conservative, Francis Elliott, Fourth
Estate, 2007. See also URL-174, Cameron admits: I used dope at Eton, the Guardian, February 11, 2007
4 President Obama, who has admitted to cocaine use before he came to
office.• For sources see Wikipedia, URL-31.
5 we ought to think of drug addiction as a special form of behavioural
addiction• Problem Gambling and Other Behavioural Addictions,
Jim Orford, in Drugs and the Future: Brain Science,
Addiction and Society, David Nutt et al, Elsevier, 2007
6 different neurotransmitters are believed to be involved in these
“push” and “pull” factors• Which neurotransmitters are involved is still a
subject of research.
7 Korean couple who let their baby starve to
death• Girl starved to death while parents raised
virtual child in online game, URL-168, the Guardian, March 5th, 2010
8 alcoholics have fewer dopamine receptors than their non-alcoholic
relatives• Overexpression of dopamine D2 receptors reduces
alcohol self-administration, Panayotis K Thanos, Nora D Volkow, et al,
Journal of Neurochemistry (78), 2001
9 tests on rats that have been made addicted to alcohol• As above.
10 high-status monkeys have more dopamine receptors than low-status
monkeys• Characterising organism x environment interactions
in non-human primate models of addiction: PET imaging studies of D2 receptors,
Michael Nader et al, in The Neurobiology of Addiction, Oxford University Press,
2010
11 amphetamine releases endorphins• Stimulation of endorphin neurotransmission in the nucleus accumbens by
ethanol, cocaine, and amphetamine, Foster Olive et al,
Journal of Neuroscience 21 (1), 2001
12 if you use ketamine about once a month, an effective dose could be as
little as 20 mg, whereas if you use it daily you might eventually need to take
200mg to feel any effect at all• Ketamine: a scientific
review, Celia Morgan and Valeria Curran, ISCD, September 15th 2010
13 Sensitisation can be seen in behavioural addictions such as gambling• Problem Gambling and Other Behavioural Addictions, Jim
Orford, in Drugs and the Future: Brain Science, Addiction
and Society, Nutt et al, Elsevier, 2007
14 addiction starts as pleasure seeking, but when withdrawal kicks in,
the main drive becomes reducing the suffering of withdrawal• Problem Gambling and Other Behavioural Addictions, Jim
Orford, in Drugs and the Future: Brain Science, Addiction
and Society, David Nutt et al, Elsevier, 2007
15 Danish studies that have shown that the sons of alcoholic fathers• The Danish longitudinal study of alcoholism 1978–2008,
Joachim Knop, Danish Medical Bulletin, (58) 8, 2011
16 The enzyme that clears nicotine from the body has two versions• Genetic variability in CYP2A6 and the pharmacokinetics of
nicotine, JC Mwenifumbo and RF Tyndale, Pharmacogenomics
8(10), October 2007
17 male children of male alcoholics have alterations in GABA receptors
that make them less sensitive to alcohol• Reactions to Alcohol in Sons of Alcoholics and Controls,
Marc Schuckit, Alcoholism: Clinical and Experimental Research 12, 1988
18 High opioid receptor levels in the brain also predict drug use and
craving for opiates• Brain opioid receptor binding in early
abstinence from opioid dependence, Tim Williams et al, British Journal
of Psychiatry (191), 2007
19 if mothers use drugs while pregnant, their children may be more likely
to become addicted to those same drugs in later life• Drugs
and the Future: Brain Science, Addiction and Society, David Nutt et al,
Elsevier, 2007
20 “neuroimaging”• Brain imaging in addiction,
David Nutt, Anne Lingford-Hughes and Liam Nestor in Addiction
Neuroethics, Elsevier, 2012
21 PET camera• which is in fact a “scintillation counter”.
Introduction
Case study 1: Tony Adams and alcohol
In the
early 1990s, 1Tony Adams
was one of the Premier League’s most popular footballers, going from strength
to strength on the pitch. Off it, he was battling a serious addiction to
alcohol, which landed him in prison for drink-driving, and led to the breakdown
of his marriage and his eventual retirement from the game. He hit rock bottom
after he went on a 7-week drinking binge following Euro ’96, and finally sought
help; he credits Alcoholics Anonymous with helping him stay off the booze, and
he has now been abstinent for nearly a decade and a half. In an effort to learn
to feel pleasure from other activities, he started to educate himself, took up
the piano and developed an interest in the arts. He has spoken publicly about
his alcoholism, primarily in his autobiography Addicted,
and has set up a rehabilitation clinic for sportsmen and women with
substance-abuse problems.
Case study 2: Pete Doherty, heroin and crack
Pete
Doherty, the former singer of the Libertines and Babyshambles, has been engaged
in 2a very
public battle with heroin and crack addiction for over a decade. Despite the
seriously-harmful consequences his addiction has had on his life, and the
knowledge that it will probably kill him, he can’t seem to find an effective
treatment. He has spent time in jail for stealing from a former band-mate, for
drink driving, and for possession of various drugs (most commonly heroin), and
at the time of writing is in prison for possession of cocaine. Because of the
intense media interest in his drug use, his repeated trips to rehab have been
widely publicised, as have his frequent relapses. At Doherty’s most recent
court appearance his solicitor said “he takes no pleasure in his addiction.
It’s one thing, he said publicly, he would not wish upon his worst enemy. He is
acutely aware of the agonising nature of addiction”.
Case study 3: Amy Winehouse
Much
like Pete Doherty, singer Amy Winehouse combined a highly successful music
career with chronic relapsing addictions to a number of drugs, until her death
in July 2011. She was 3introduced
to heroin and crack cocaine by her former husband, and is known to have 4overdosed
at least once on a mixture of heroin, crack, ecstasy, ketamine and alcohol.
However, despite the media focus on her illicit drug use, it was her alcoholism
that she struggled with most, and is probably what killed her in the end. It
was the only drug found in her system when she died, alongside traces of
Librium, which is commonly used to help alcoholics through withdrawal; her
father claims that 5she had
seizures while attempting to stop drinking shortly before she died, and it’s
well known that these can be fatal.
Psychological
treatments
A different psychological
treatment is cognitive behavioural therapy (CBT). CBT identifies the internal, mental,
social and environmental triggers that lead to drug taking, and develops coping
strategies to avoid triggers leading to relapse. Some of the skills learned are
practical – for example avoiding certain places and situations; others are
internal – such as managing cravings by trying to remember the negative effects
of the drug; and others are interpersonal – such as learning to say “no”
convincingly to offers of drugs or alcohol. The addict learns to plan how to
handle stressful situations and emergencies, and the possibility of “failure”
is incorporated into the recovery plan. By preparing psychologically for the challenges the addict will inevitably face, it is hoped they
will establish better coping mechanisms than by relying on willpower alone.
In the chaos of many
addicts’ lives, psychological treatment may not be effective until their drug
use has become more regular and stable. It is also extremely difficult to give
someone therapy while they are either on drugs or in withdrawal, because they
are too agitated and distressed. Keeping weekly appointments with a therapist
may be all but impossible for somebody who has very little structure or
schedule to their lives. Pharmacological substitutes, such as methadone or
buprenorphine for heroin, have an important role to play in stabilising people
to the point where psychological treatment
can be effective; we explore these substitutes next.
Pharmacological substitutes
There are two types of
substitutes:
·
Full agonists. A substitute agonist is a
chemical that fits the receptors in the brain as precisely as the drug of abuse
itself, but that is less harmful (either because it produces a lesser but
longer-acting “high” or because it can be taken by a safer method). Nicotine
gum and patches, and methadone, work in this way.
Other pharmacological treatments
There
are other sorts of drugs that can be used to treat addiction:
·
Antagonists. These block the effects of the drug altogether, so that there is much
less temptation to use it. For example, rimonabant blocks the cannabis
receptors, making cannabis ineffective. Naltrexone stops heroin working, and
can be used to prevent opiate addiction if users take it regularly; long-acting
preparations including depot injections can make this easier. (For some people
with opioid addiction, taking naltrexone can be made a condition of their
continuing to work. For example, requiring addicted doctors and pharmacists to
take naltrexone reduces the risk of their misappropriating supplies of drugs in
their workplace.) A new kind of antagonist is the vaccine, which we’ll discuss
in chapter 16.
·
Pseudo-antagonists. Whereas antagonists just block the positive effects of drugs,
pseudo-antagonists actually produce negative effects. For example, Antabuse
mimics the oriental flushing reaction to alcohol, by blocking the person’s
ability to break down the acetaldehyde that alcohol is converted into. When
people drink after taking Antabuse they feel
quite unwell and so get put off drinking any more. As we learn more about the
biological factors which are protective against addiction, we will be able to
develop more of these sorts of treatments.
·
Disease-modifying
agents. These are drugs that can stop aspects of
addiction that lead to relapse. A good example is acamprosate (Campral) which
reduces conditioned craving for alcohol. Some 6opioid antagonists,
including nalmefene and naltrexone, are now being used to reduce the effects of
drinking so that bingeing is lessened. The possibility of developing 7drugs to
reduce stress-induced drug relapse is currently under investigation.
What is
heroin?
The drug itself causes
little physical damage to the body, apart from chronic constipation. However,
it causes severe damage indirectly:
·
There is a high rate of overdosing
among heroin users, because the combination of its low safety ratio and the
fact that the street supply is of varying strengths, makes it hard for people
to judge the correct dose.
·
Many addicts also suffer general
ill health from heavy smoking, alcohol consumption and poor diet.
Why do people take heroin, and why can’t they stop?
The withdrawal syndrome,
while not life-threatening, is extremely unpleasant and distressing, because
the body experiences the opposite effects of the drug. Where heroin creates
profound relaxation, in withdrawal addicts get muscle cramps and tremor,
producing a symptom known as “restless legs”. (This is where the phrase “kicking
the habit” comes from). Constipation is replaced by diarrhoea, low blood
pressure with rapid pulse, drowsiness
with insomnia, and a general sense of comfort and ease with fever and chills,
gooseflesh, and irritability. This lasts for a week to ten days, and if an
addict tries to detox without help when they still have access to heroin they
will find it almost impossible to stop themselves taking it to end the
nightmare of withdrawal.
Physical detox is only
the start of the struggle to stay off heroin. The psychological cravings can be
exacerbated by an inability to feel pleasure from anything else, and this can
last for months or years. If taking heroin was a response to trauma, having to
relive the experience without the safety-net of the drug can be unbearable.
Material deprivation and social isolation will undoubtedly have deteriorated
since the habit began, and addicts may have few economic options outside crime
and prostitution (especially if they have a criminal record for dealing,
possession or stealing). Many heroin addicts say that the drug has long since
ceased to give them any pleasure, and
they are fully aware that it makes the chaos of their lives worse. But however
miserable they may be on it, they are even more miserable without it.
Using heroin to treat heroin addicts
Advantages and disadvantages of methadone treatment
Methadone
usually comes as green liquid that is swallowed under supervision at a clinic
or pharmacy, although it is sometimes prescribed to be injected. The addict no
longer has to commit crimes to fund their habit, can avoid withdrawal safely,
and visiting the clinic every day gives some structure to their lives and
access to other therapies. Having less of an up-and-down several times a day,
and needing to spend less time drug seeking, makes it easier to rebuild
relationships with family and to make practical arrangements for their lives.
And anything that stops people injecting four times a day will reduce harm from
infections; indeed, 8methadone
has been proved to reduce the spread of AIDS.
Methadone is far from
perfect. Though safer than street-grade heroin, it still causes respiratory
depression, and if users take heroin at the same time they are at serious risk
of overdose. Some people manage to hold down jobs, but most long-term methadone
users can’t work as the drug leaves them somewhat “stoned”, so they remain
relatively deprived and socially isolated. The cheaper formulations are very
sweet and can lead to loss of teeth, although there are sugar-free varieties.
If methadone is left around the house, children sometimes drink it by mistake
thinking it’s syrup and can die. On weekdays these problems don’t occur so much
because the drug is taken at the clinic under supervision. However, at the
weekend the addict is given two days’ supply to take away, which is often
injected contrary to what was intended, or sold to buy heroin. The final disadvantage of methadone is that its withdrawal syndrome is very
painful and longer-lasting than heroin’s.
Buprenorphine – a better solution?
Buprenorphine is an
example of how good scientific research and feedback on addicts’ behaviour in
the real world can produce better treatments. Buprenorphine addresses several
specific problems created by methadone: it lasts up to three days so there is
no need to give take-away doses, so it is less likely to get diverted and sold
on the street; it isn’t sweet
so if children do come across it they’re unlikely to take it by accident, and
if they do it won’t kill them; and it doesn’t knock people out the way
methadone does, making it easier to hold down a job and take part in normal
life.
Evaluating
treatments
In the
run-up to the UK 2010 general election, the Conservative party produced some
provocative statements about long-term methadone treatment, arguing that taking
it for just six weeks should be enough to get most heroin addicts stable enough
to abstain. David Burrows, who was their spokesman on criminal justice at the
time, was quoted saying 9“the public expects that addicts have to get off drugs but too many end
up parked on methadone. They become dependent on it and end up not being able
to contribute to their families or society.”
This attitude towards
drug addiction derives from the views expressed in Breakdown
Britain, a 2006 report by Iain Duncan Smith’s think tank, the Centre for
Social Justice. The report claimed that the addicts and counsellors it had
spoken to thought that, for government-run services, abstinence was a better
aim than harm reduction through controlled drinking or methadone treatment.
It’s unclear what their research methods were, as this viewpoint goes against 10a
substantial body of evidence which shows exactly the opposite. Although this
hasn’t been pursued as a policy since the coalition took power, it does mark a
departure from the harm-reduction treatment model that the former Labour
government were working with, which was one of the few areas of drug policy
where they actually took on board evidence and
expert advice.
One of the problems we
face with addictions is that if abstinence is our only measure of success then
none of the treatments we currently use are particularly successful. The very
best long-term residential care – 3 to 4 months in a private addiction
treatment clinic with access to psychological treatments and medical and
pharmacological help – might lead to 1140% of
heroin addicts still being abstinent after year. Alcohol outpatient treatments
have a far lower success rate – at best only 1225% are
still dry after twelve months.
Moreover, judging the
success of a treatment on the outcome after 3 or 12 months isn’t adequate.
Addiction isn’t a single transient event like a fractured bone or a chest
infection, which can be “cured”, in the sense that you will be no more prone to
problems in the future than if it hadn’t happened. Addiction is best thought of
as a chronic recurring illness, like diabetes or asthma, where lifelong
treatment is required. Once you’ve had an addiction you’re always at greater
risk of returning to it than those who have never been addicted, because you
have an underlying vulnerability and your brain has changed as a result of
repeated drug use. Longitudinal studies show lifetime relapse rates similar to
asthma, diabetes or hypertension 13(Figure
9.5). As with these illnesses, relapse shouldn’t be seen as a moral “failure”.
Instead, the most helpful attitude seems to be to re-evaluate the treatment
model and maybe try something new.
Fortunately, when we look
beyond abstinence as the only measure of success, there are a great number of
interventions that can reduce the harms caused by
addiction. Since the costs of medical intervention are carried by the public,
one good metric is economic – does this intervention save money overall? Given
the enormous costs of problematic heroin use
(in treating HIV and hepatitis, taking children into care and policing
acquisitive crime), methadone treatment is very cost-effective: 14every pound
of investment in methadone results in three pounds saved from these other
sources. Buprenorphine is likely to be similarly cost-effective, and is
probably better in the long term, though methadone may be better for
stabilising people as it’s more like heroin.
This view
misses the point that these decisions are very different for addicts and
non-addicts. A non-addict will probably find the threat of prison a pretty
strong incentive not to steal to buy drugs – if they don’t have enough money
they’ll go without. For a heroin or crack addict in withdrawal, prison is much
less of a threat, and jail is actually a place where many peoples start their drug habits, rather than kicking them. In fact,
it’s hard to think of anything that would be an effective threat to someone
with a serious addiction. Even if we brought in the death penalty for drug
possession, as in Singapore, we would be unlikely to see all drug seeking cease
– addicts often see friends and acquaintances injure themselves or die as a
result of their habit, and that still doesn’t stop them from using.
The Portuguese experiment
In the
1980s and 90s, Portugal experienced a dramatic increase in the harms done by
illegal drugs, in particular heroin. Although rates of drug use were lower
overall than in other countries in Europe, almost all of those using heroin
were seriously addicted, with the usual attendant problems of high rates of HIV
and hepatitis, acquisitive crime and social disorder. By the end of the 20th
century, 151% of the
population were problematic drug users – 100,000 in a country of only 10
million – and it was recognised as the number one social problem. Pretty much
everyone was personally affected by drug addiction, and there was a lot of
interest in trying to find a new approach that would reduce harm.
In 1999, the Portuguese
parliament approved a new National Strategy, which came into effect in 2001. Under this new strategy, drugs covered
by the UN International Conventions remain illegal, but the penalties for
personal use are no longer dealt with through the criminal justice system.
Anyone caught with less than 10 days’ average supply of a drug (5 g of
cannabis, 1 g of heroin) has it confiscated by the police and they are given a
ticket, requiring them to appear before a “dissuasion board” within 72 hours.
The board is normally made up of two psychiatrists and a legal specialist, who
ask about their drug use, categorise them as a recreational user or regular
user or addict, warn them of the risks they are taking, and offer treatment if
appropriate.
There are a range of
potential sanctions, from a fine, to having social-security benefits cut or
being forced to go to rehab. In practice though, about 1685% of
those sent to the board get a suspension with no sanctions, and most of the
rest are given treatment. Supplying drugs is still penalised: if you’re caught with
more than 10 days’ personal supply you still have to go to court and could face
prison. A good comparison is with traffic offences: dangerous driving might
land you in jail, but failing to wear a seat belt or cycling through a red
light is more likely to result in a fine or having to go on a road-safety
course.
·
The 17number of heroin addicts in
treatment increased from 23,500 in 1998 to over 40,000 in 2010, partly due to
the fact that they no longer have to fear criminal sanctions if they come
forward.
·
The number of new HIV cases among
injecting drug users has reduced from 181,430 in
2000, to 352 in 2008.
·
Halving the number of people
injecting in the last month.
·
19Up to 400
million a year being taken out of the hands of criminals through decreased use.
Although there has been a slight increase in drug use among adults,
there has been 20a decrease
among 15 to 19-year-olds, indicating lower levels of experimentation. This is
very positive, because this was smaller than in neighbouring countries – Spain,
for example – and drug behaviour in teenage years has a strong relationship
with drug use later in life. Nor has Portugal become a destination for foreign
drug users; 2195% of
those caught since the strategy was introduced have been Portuguese.
Preventing
addiction
Could
addiction be prevented? There are certainly external factors that affect its
prevalence, and there is a very close relationship between addiction and the
price and availability of drugs: the cheaper and more available something is,
the more addiction there will be. This applies to both legal and illegal drugs,
and to behaviours such as gambling – in common with many other countries we’ve
seen a substantial rise in gambling addictions in the UK since gambling laws were
relaxed. Even addicts are price sensitive (though less so than non-addicts).
Increasing the cost of cigarettes has caused many smokers to cut down, and
although they remain addicted, smoking 10 a day is far less harmful than
smoking 20. Before addiction sets in, price is even more influential at
stopping people from taking drugs in the first place or going on to use them
extensively. Obviously government regulation can’t have any direct effect on the street price of illegal drugs, but taxing legal addictive
substances is effective in reducing use and addiction.
Conclusion
The Conservative party’s Breakdown Britain report criticised Labour’s policy on the
treatment of addiction, saying that “it has pushed treatment
in the wrong direction, preferring maintenance (substitute prescription) to
recovery.” This statement in itself betrays a lack of understanding of the
mechanisms of addiction – there’s no such thing as “recovery” from addiction in
the way that you can “recover” from a broken arm. Abstinence itself could be
described as a form of maintenance – someone who has been an addict is always
at risk of relapse, and abstinence will require conscious maintenance. In any
lifelong illness, different treatments may be effective at different times, and
someone who finds themselves able to abstain for many years may find that
stress or bereavement causes a relapse which
is then best treated with a pharmacological substitute, at least for a period.
Notes
1 Tony Adams• Addicted, Tony Adams & Ian
Ridley, HarperCollins Willow, 1998
2 a very public battle with heroin and crack addiction for over a
decade.• Pete Doherty jailed for six months, Caroline
Davies, URL-74, May 20th 2011
3 introduced to heroin and crack cocaine by her former husband• Divorce Drama for Amy Winehouse, Simon Perry, URL-75, December
1st 2008
4 overdosed at least once• Amy Winehouse bailed over
drugs video, Anita Singh, URL-76, May 8th
2008
5 she had seizures while attempting to stop drinking shortly before she
died• Amy Winehouse died after detox seizures, dad says,
Maria Puente, URL-77, September 10th 2011
6 opioid antagonists, including nalmefene and naltrexone, are now being
used to reduce the effects of drinking• Evidence-based
guidelines for the pharmacological management of substance misuse, addiction
and comorbidity: recommendations from the British Association for
Psychopharmacology, A R Lingford-Hughes, S Welch, D J Nutt, Journal of
Psychopharmacology (18) 3, 2004
7 drugs to reduce stress-induced drug relapse• Neurobiological
mechanisms for opponent motivational processes in addiction, George F
Koob and Michel L Moal, in The Neurobiology of Addiction,
Oxford University Press, 2010
8 methadone has been proved to reduce the
spread of AIDS• Substitution maintenance therapy in
the management of opioid dependence and HIV/AIDS prevention, WHO/UNODC/ UNAIDS, URL-78, 2004.
9 “the public
expects that addicts have to get off drugs but too many end up parked on
methadone.• Will Conservative plans to overhaul heroin addiction treatment
work?, Denis Campbell, URL-79, April 20th 2010
10 a substantial body of evidence which shows
exactly the opposite• An overview of systematic
reviews of the effectiveness of opiate maintenance therapies: available evidence
to inform clinical practice and research, Laura Amato et al, Journal of Substance Abuse 28
(4), 2005
11 40% of heroin addicts still being abstinent
after year• Factors associated with abstinence,
lapse or relapse to heroin use after residential treatment: protective effect
of coping responses, Michael Gossop et al,
Addiction (97), September 2002
12 25% are still dry after twelve months.• How
effective is alcoholism treatment in the United States?, William Miller,
Scott Walters and Melanie Bennett, Journal Studies of Alcohol (62), 2001. This
paper noted that although only 1 in 4 remained continuously abstinent in the
year following treatment, most of the remainder did drink less intensively,
deriving some benefit from the treatment even if they weren’t completely
abstinent.
13 (Figure 9.5).• Drugs, Brains, and Behavior: The
Science of Addiction, URL-169, NIDA,
August 2010, which quotes source as JAMA 284:1689–1695, 2000
14 every pound of investment in methadone results in three pounds saved
from these other sources• Crutch or cure? The realities of
methadone treatment, David Nutt, URL-80, June 9th
2010
15 1% of the population were problematic drug users• Dr Joao Goulao, in a
presentation first delivered at ISCD summit, November 2010
16 85% of those sent to the board get a suspension with no sanctions• Drug Decriminalization in Portugal: lessons for creating fair and
successful drug policies, Glenn Greenwald, Cato Institute, URL-81, 2009
17 number of heroin addicts in treatment increased from 23,500 in 1998 to
over 40,000 in 2010• What Britain could learn from
Portugal’s drugs policy, Peter Beaumont, URL-82, September
5th 2010
18 1,430 in 2000, to 352 in 2008• Drug Policy in
Portugal: the benefits of decriminalising drug use, Artur Domaslawski, URL-83, June 2011
19 Up to 400 million a year being taken out of the hands of criminals• What Britain could learn from Portugal’s drugs policy,
Peter Beaumont, URL-82, September 5th 2010
20 a decrease among 15 to 19-year-olds• Drug Decriminalization in Portugal: lessons for creating fair and
successful drug policies, Glenn Greenwald, Cato
Institute, URL-81, 2009
21 95% of those caught since the strategy was introduced have been
Portuguese• As above.
Routes of use and main associated harms
1.
Chewing is the slowest route into the brain, with levels of the drug generally
peaking 1–2 hours after chewing begins. Regular chewers of drugs such as khat,
coca leaves and nicotine gum, can develop tooth, gum and jaw problems.
2.
Drinking and
eating. The drug generally takes effect after about
30 minutes. Sometimes this delay means that users find it hard to judge when they’ve had enough, increasing the risk of overdose. This is
why people taking strong alcoholic drinks can get extremely drunk so easily.
Figure 10.1 shows schematically the relative speeds of the most common
routes of use.
Why are drugs used in different forms?
Kinetics and dynamics of addiction
There
are the two measures that determine how addictive a drug is:
·
Kinetics involves the route of use, which largely determines the speed of onset, ie how quickly a
drug takes effect, and the speed of offset, ie how quickly it wears off. Both faster onset and
faster offset tend to increase the
addictiveness of a drug. Figure 10.2 shows the relative speed of entry into the
brain of various drugs in different forms.
From chewing to crack: the history of cocaine
Coca in
the Andes
Cocaine
is 1the
psychoactive component of the coca plant, in which it acts as a natural
insecticide. Coca is native to the foothills of the Andes of Peru and Bolivia,
where it has been used by indigenous people for thousands of years, although
most of the world’s supply is now grown in Colombia. Coca chewing is an
important part of indigenous culture, with a wide variety of uses as a
medicine, in religious rituals and in social life. Coca leaves are presented in
marriage ceremonies, chewed at feasts, help people work for long periods at
high altitudes, and also contain vitamins and minerals which are an important
part of local diets.
When the Spanish
conquistadors encountered coca in the 1500s, it fascinated and quite alarmed
them. The Catholic Church disapproved of its use in
Shamanic rituals, and 2in 1569
they declared that it had satanic powers and that all plantings should be
destroyed. The colonists soon discovered, however, that the indigenous people
were much less productive when they didn’t have coca’s stimulating effects,
particularly in the silver and gold mines where they often refused to work
without their coca rations. In the end, the Spanish accepted the importance of
the practice, and began profiting from the trade by levying a 10% tax on coca
sales.
Cocaine
comes to Europe
Numerous
attempts were made to transport coca back to Europe, but the leaves had usually
lost their potency by the time they’d crossed the Atlantic. It wasn’t until two
new and far stronger forms appeared in the mid-1800s that it became widely used
by Europeans. The first was pure cocaine hydrochloride, which was extracted and
isolated by Friedriche Gaedecke in 1855. The second appeared in 1863, when
French chemist Angelo Mariani hit upon the idea of fortifying alcohol with coca
leaves to produce 3“Vin
Mariani”. This was about 10% alcohol and 8.5% cocaine; it was marketed as a
tonic capable of preventing illnesses such as stomach and lung troubles,
malaria and influenza, “giving life and vigour … invaluable for all bodily and
mental overexertions”. It became hugely popular, with fans as eminent as Queen
Victoria, and Pope Leo XIII who appeared in an advertisement for the drink
(Figure 10.3) and even awarded it a Vatican gold medal.
Meanwhile, the medical
establishment was trying to work out whether this “wonder drug” had real
therapeutic uses. In 1884, Freud began experimenting with it as a cure for
depression and morphine addiction, realising only belatedly that it was almost
as addictive as morphine. It was his colleague Karl Koller who in the same year
recognised its first genuine medical application as a local anaesthetic for eye
and nose surgery, since it both dulls pain and constricts blood vessels,
minimising blood loss. Although a vast improvement on previous sorts of
anaesthetics, this could also be dangerous, as wads of cocaine which had been
put up the nose were sometimes swallowed by mistake, resulting in heart
attacks.
Cocaine was everywhere.
Injecting cocaine intravenously (famously practised by Sherlock Holmes) was
relatively common, and considered pretty unremarkable. Another widely-available
form of cocaine, which became hugely popular in the USA, was in a fizzy soft
drink. In 1886, perhaps inspired by Mariani, a chemist from Atlanta called John
Pemberton created his own alcohol and coca leaf concoction called Pemberton’s 4French Wine
Coca. When Atlanta brought in prohibition later that year, he removed the
alcohol and began selling his unique combination of cocaine, kola nut (which
provided a dose of caffeine), corn syrup and soda water, which became a huge
temperance hit under the name Coca-Cola. Soda fountains sprang up all over the
city and became very popular.
Pemberton sold the company
to a devout teetotaler who started using “decocainised” leaves to flavour the
drink as soon as it became clear that the drug was addictive. In fact, the
biggest battle the Coca-Cola company faced was
over its caffeine content, involving a very high-profile 5court case
against the American government to prove that caffeine was not deleterious to
health.
Understanding
cocaine
By the
early 1900s, the properties of cocaine, including its harms, were starting to
be better understood. In overdose, it constricts the blood vessels in the
heart, which can cause heart attacks, seizures, pulmonary oedema (fluid in the
lungs) or can rupture the aorta. Sometimes heavy use results in a condition
called myocardial fibrosis, where normal heart muscle is replaced with fibrous
tissue so the heart can’t pump blood properly, and cocaine can also increase
thromboxane production, causing blood clots. Regular use can lead to psychosis,
with paranoia, delusions, and a symptom called formication (the phantom sensation
of ants or insects crawling across the skin). Snorting large amounts can lead
to ulcers in the nose or a perforated septum due to loss of blood supply
because the drug constricts the blood vessels. Regularly injecting into
sensitive areas like genitals can lead to necrosis, where the skin dies, which
in severe cases can only be treated with amputation. 6Using
cocaine while pregnant can cause problems for the foetus, and carries an eight
times higher risk of Sudden Infant Death Syndrome.
Cocaine wine (Vin
Mariani) is also more potent and addictive than coca, as it combines cocaine
and alcohol, which together react to form cocaethylene.
This compound is even more harmful than either alcohol or cocaine on their own,
so people drinking cocaine wine are essentially consuming three powerfully
addictive drugs at once – no wonder it was so popular!
Crack
in the cities
The
backlash against cocaine led to ever stricter controls during the first half of
the 20th century, until its outright prohibition and a concerted international
effort to reduce production as part of the War on Drugs. This was partially
successful at first, but the reduction in supply wasn’t accompanied by a
decrease in demand in the West, causing the price of cocaine to sky-rocket. The
increase in international border controls, and rise in costs as large volumes
of the drug were seized, led to producers trying to develop cheaper forms of
cocaine that would be easier to transport. The result was 7crack,
which appeared in the USA in 1984.
Crack is the freebase form of cocaine, ie the base organic substance
(rather than the salt that is formed when the organic base reacts with
hydrochloric acid), although it usually isn’t entirely “pure”, 8because of
how it is produced. Hydrochlorides are more stable compounds so they tend to be
the form street drugs take, but they usually can’t be smoked because they
vaporise at such high temperatures that they burn instead, and become useless.
Crack vaporises at 90°; cocaine hydrochloride vaporises at 190°, and in air
will burn and lose its efficacy before it can reach this temperature.
Along with the lung
problems that always accompany regular smoking, crack users are more likely to
experience psychosis, aggression and heart failure, and are much more likely to
escalate into habitual use and addiction. On pretty much every measure of harm,
our expert panel rated crack as more harmful than cocaine, but particularly on
crime, and loss of tangibles and relationships. This reflects the fact that
crack has become popular amongst a similar poor, urban demographic as those who
take up heroin, and in fact the term “problem drug user” generally now refers
to heroin and crack addicts. Whereas non-crack cocaine tends to be used by
people in employment who fund their drug use out of wages, crack is often funded through crime, leading to the same spiral of loss
of trust with family and friends, marginalisation, and periods in and out of
prison as we see with heroin. Although not as widespread as opiates, at least
in the UK, crack has torn apart communities and destroyed many people’s lives.
(The TV series The Wire gives a realistic and visual
account of the damage that crack causes.)
|
|
Crack cocaine |
Cocaine |
|
Route of use |
smoking |
injecting/snorting |
|
Speed of onset |
10 seconds |
15–30 seconds (injecting) 1–3 minutes (snorting) |
|
Speed of offset |
15 minutes |
15–20 mins (injecting) 30 minutes (snorting) |
|
Drug efficacy |
high |
high |
Why is crack twice as addictive as cocaine?
Cocaine powder is
expensive compared with other “party drugs” such as ecstasy and amphetamines,
but it has a less obvious form of intoxication, making it more socially acceptable
outside of clubs. It encourages self-interested, aggressive and risk-taking
behaviour, and is popular among people employed in areas such as the media and
high finance, where these personality traits
are often associated with success (or with financial disasters, in more recent
years!). In these highly competitive environments, there’s often a lack of
trust, and groups may become socially dependent on the drug as a social
lubricant, usually alongside heavy drinking. Although the price has dropped in recent
years, its expense still makes it a bit of a status symbol, and large doses are
sometimes taken as an explicit sign of wealth and prestige. Because cocaine
both induces anti-social behaviour and makes users less concerned for the
welfare of others, what begins as an experience sought after for its
pleasurable effects can also become the means of escaping the social
consequences of actions while intoxicated. The cocaine user can get caught in a
cycle of egotistical and self-interested behaviour when “high”, that then
drives them back to the drug in order to minimise feelings of regret or
remorse.
Conclusion
This poses some
interesting questions. Should we encourage certain sorts of drug-taking in order to discourage more harmful behaviour?
Although smoking carries its own dangers, it’s definitely less harmful than
injecting – should intravenous heroin users be persuaded to change to smoking
instead? Or perhaps there are ways to reverse the process where drugs become
available in more potent and more addictive forms over time. It’s unlikely that
coca chewing would become popular in the UK, but maybe a weak sort of cocaine
drink or cocaine tea could be developed, as a less harmful alternative to
cocaine powder or crack?
The international damage done by cocaine
When
our expert panel ranked the 20 drugs for “international damage”, it was quickly
decided 9to give
cocaine and crack the maximum score of 100. Although heroin wasn’t far behind,
cocaine was judged as having caused more harm overall – to the people in
producer countries such as Bolivia and Colombia, and in intermediary countries
involved in the trade like Mexico and Guinea-Bissau.
The problems begin at the
plantations. The majority of coca leaf is produced by small-scale farmers with
few other options for earning a living. Growing coca is preferable to other
crops because it has a higher market value, and because it plays an important
part in social life. It can also
grow on difficult terrain, and when it’s cultivated using traditional and
sustainable farming techniques, it can improve soil quality by binding it
together with its roots. Unfortunately, the policy of destroying coca
plantations in order to reduce the global cocaine supply means that farmers
have to focus on getting the maximum yield in the short term, using techniques
which degrade the soil, and they are forced to clear more rainforest when their
crops are burnt or sprayed with herbicide chemicals. It’s been estimated that 10every gram
of cocaine snorted in the UK will have been responsible for 4 square metres of
rainforest being destroyed in Colombia or the Amazon, creating local
environmental problems and contributing to climate change by reducing one of
the world’s biggest carbon sinks.
Aside from
environmental destruction in producer countries, the trade also causes
political and social problems in the transit countries the drug passes through
before it arrives in the places that consume it. The majority of the world’s
cocaine is consumed in North America and Europe, and is channelled to them via
Mexico and West Africa respectively. Mexico has seen the development of
extremely powerful cartels, and there is evidence that they are now controlling
large-scale production in Colombia as well, not just acting as middlemen. A
government-led crackdown on these cartels, which began in 2006, seems to have
exacerbated the violence, with nearly 1135,000
deaths attributed to the drugs war since then, 15,000 of them in 2010 alone.
Most of these have taken place in cities along the northern border between
Mexico and the USA, and this border has become one of the most dangerous places
in the world. Since the mid-2000s, much of the cocaine being consumed in Europe
has started to be12channelled
through unstable states in West Africa such as Guinea Bissau, undermining the
development of democratic institutions or attempts by civil society
organisations to tackle corruption within governments and the police.
Notes
1 the psychoactive component of the coca plant• 20
(mis)conceptions on coca and cocaine, Roberto Laserna, Plural Publishers,
1997
2 in 1569 they declared that it had satanic powers• 20
(Mis)conceptions on coca and cocaine, Roberto Laserna, Plural
Publishers, 1997
3 “Vin Mariani”• High Society, Mike Jay,
Thames & Hudson, 2010
4 French Wine Coca• QI: quite interesting facts about
wine, John Mitchinson and Molly Oldfield, URL-84, December
17th 2009
5 court case against the American government• United
States v. Forty Barrels and Twenty Kegs of Coca-Cola, 241 US 265, 1916
6 Using cocaine while pregnant can cause problems for the foetus, and
carries an eight times higher risk of Sudden Infant Death Syndrome• Illegal drugs: a complete guide to their history, chemistry, use
and abuse, Paul M Ghalinger, Plume, 2003
7 crack, which appeared in the USA in 1984• DEA
History Book, 1876–1990 (drug usage & enforcement), US Department of
Justice, 1991
8 because of how it is produced.• Freebase can be made from cocaine
powder (which is cocaine hydrochloride) using chemical extraction (eg with
ether) in which case it is pure, or from cocaine extract that is not purified
to powder, and then left in an impure state with some of the processing
chemicals (alkali salts) still present in the mixture. Using ether is more
difficult and dangerous for manufacturers, so they usually opt for the second
process. The Wikipedia article Crack cocaine (URL-85) has more
detail on the chemistry.
9 to give cocaine and crack the maximum score of 100.• 20 (mis)conceptions on coca and cocaine, Roberto Laserna,
Plural Publishers, 1997
10 every gram of cocaine snorted in the UK will have been responsible for
4 square metres of rainforest being destroyed in Colombia or the Amazon• Cocaine users are destroying the rainforest – at 4 square metres a
gram, Sandra Leville, URL-86, November
19th 2008
11 35,000 deaths attributed to the drugs war since then• Mexico updates four years of drug war deaths to 34,612, BBC
News, URL-87, January 13, 2011. The estimate is now 40,000.
12 channelled through unstable states in West Africa such as Guinea
Bissau• War on Drugs: Report of the Global Commission on
Drugs Policy, URL, June 2011
The 2007 ban on smoking in public places in the UK
On
July 1st 2007, England became the last nation in the United Kingdom to ban
smoking in public places. With some minor exceptions, any
substantially-enclosed place would now have to display “no smoking” signs and
take steps to stop people from lighting up. 1Individuals
who broke the ban would face a £50 fine, while owners could be charged £2,500
for failing to prevent smoking on their premises. Despite the media depicting
the ban as “controversial”, 2three
quarters of adults supported the legislation before it was brought in, and
support has remained high ever since.
Keeping places smoke free
is just one of the public-health measures introduced in the last 50 years to
reduce smoking. Others have included restrictions on tobacco advertising,
warnings on cigarette packets, raising the age of sale to 18, and increasing
the price through taxes. In 2011, the British government announced plans to ban
the display of cigarettes in shops, and announced that they were considering a
ban on any kind of branding, requiring plain generic packaging instead. All
these measures have been fiercely resisted by the tobacco industry, but they have
undoubtedly had a positive effect on the health of the nation: the proportion
of British adults who smoke has dropped from about 340% in 1978
to about 20% today, saving thousands of lives. Many of the regulations I’ve
suggested for reducing the harms of alcohol are inspired by the successes of
the tobacco control movement. The story of tobacco is a paradigm case of what
happens when drug companies are allowed to create markets of millions of
addicts, and what governments can do to rein in those markets without making a
drug illegal.
What is
tobacco?
Most
of the tobacco we consume today is made from the dried leaves of the tobacco
plant nicotiana tabacum, although there are many
other species with a 4long
history of use. It is native to the Americas and has been used there for thousands
of years. European explorers were introduced to it in the 16th century, and
colonial settlers soon began cultivating it for export home. Sir Francis Drake
introduced pipe-smoking to Britain in the 1570s, and the habit soon spread
through English society, although tobacco remained relatively rare and
expensive. King Philip II of Spain started producing cigars in Seville in 1614,
and cigarettes were invented by beggars who would collect discarded cigar butts
and roll the leftover tobacco in thin strips of paper. The French court’s
practice of sniffing snus (snuff) was brought back to Britain by Charles II,
and this became the aristocrats’ favourite way of taking tobacco, while the
lower orders smoked it in pipes.
Ready-made cigarettes
were invented in Turkey, and became popular with British soldiers when they
were fighting alongside Turks during the Crimean War. These were
hand-manufactured initially, but they suddenly became much cheaper in the 1880s
with the invention of automatic cigarette-rolling machines. The inclusion of
millions of cigarettes in soldiers’ rations in the First and Second World Wars
led to huge increases in the number of people addicted to tobacco. Since the
1970s, Western governments have been adopting public-health measures to reduce
the social costs of tobacco and have seen a substantial drop in the number
of smokers. However, in much of the rest of the world smoking is still on the
rise, with devastating effects. The WHO has estimated that 5tobacco
will account for 10% of all deaths worldwide by 2015.
What are tobacco’s harms and benefits?
Tobacco
smoke is highly toxic. It contains 6at least 60
chemicals known or suspected to cause cancer in humans, including arsenic,
benzene and lead, as well as carbon monoxide, which damages the heart and blood
vessels. Smoking carries a substantial risk of developing a range of lung
problems, such as chronic bronchitis, emphysema and asthma, as well as a
20-fold increase in the likelihood of developing lung cancer. It constricts
blood vessels, which can cause heart problems, cardiovascular disease, and
stroke. This risk is often compounded by difficulties with heavy breathing,
which make smokers less likely to take exercise and more likely to be
overweight.
Because its intoxication
effects are mild, tobacco isn’t associated with violent or antisocial
behaviour, although 7smoking
during pregnancy can damage the foetus by reducing its oxygen supply. Discarded
matches and cigarette butts can cause fires; it’s suspected that the 8fire in
King’s Cross that killed 31 people in 1987 was started by a smoker’s match.
Because tobacco is legal, it’s not associated with international crime (apart
from some smuggling to evade tax) and the sale of cigarettes does generate
large revenues for governments (although it creates substantial economic costs
at the same time). Policy Exchange have calculated that 9cigarette
taxes raise £10 billion a year, but the cost to the economy of treating tobacco
related health problems is £13.7 billion.
The longer the habit
continues, the more the risks increase, particularly after the age of 30, as
the body becomes less able to repair itself. David Spiegelhalter has calculated
that 10each
cigarette takes 11 minutes off your total lifespan, based on the fact that a 30
year old smoker of 30 cigarettes a day will die on average at 69, ten years
younger than someone who never smoked.
Second-hand
smoke is also dangerous. It’s 11classified
as a carcinogen by the WHO, and given a “class A” rating by the USA
Environmental Protection Agency, in the same carcinogenic class as asbestos and
arsenic. A 12review by
the UK Scientific Committee on Tobacco and Health in 2004 found that exposure
to second-hand smoke contributes to medical conditions such as lung cancer,
heart disease, asthma attacks and reduced lung function. Two years later, 13the US
Surgeon General reiterated these findings, emphasising that children are
particularly at risk, and may suffer ear problems, acute respiratory
infections, more severe asthma, slower lung growth, and an increased risk of
Sudden Infant Death Syndrome (“cot death”). Although the risks are much lower
than for those who smoke themselves, second-hand smoke is still responsible for
14600,000 deaths a year
worldwide, 11,000 of those in the UK.
Although it’s
questionable whether tobacco has any health benefits at all, there is some
evidence that in later life it may reduce the risks of Parkinson’s disease.
While tobacco was used as a medicine for thousands of years by indigenous
cultures in the Americas, their patterns of use were very different to those of
today’s cigarette-smokers. Peace-pipe ceremonies were highly ritualised and
relatively rare, participation was usually limited to certain people (such as
chiefs, medicine men and patients), and the smoke was “tasted” rather than
inhaled. These factors 15protected
the users from becoming addicted to tobacco and from the carcinogenic effects
of the drug. Tobacco’s role in peace-pipe ceremonies was largely symbolic, carrying
the thoughts and prayers of the participants towards heaven in the smoke it
produced. Tobacco in Native American ceremonies is about as close to modern
cigarette smoking as the consumption of wine in the Christian communion is to
binge drinking.
Because of tobacco’s
sacred status in the Americas, when tobacco was first brought to Europe it was 16treated as
a cure-all for everything from tetanus to migraine although in fact smoking is
far more harmful than beneficial. Research is ongoing as to whether isolated
components of tobacco, which can be consumed in safer ways than smoking, might
have some medicinal value. A lot of research has looked at nicotine,
particularly because
a very high proportion of people with schizophrenia smoke, and 17it’s
thought that nicotine has anti-psychotic and cognition-impairing properties and
may be protective in low doses. New types of nicotinergic anti-psychotics are
currently being studied which don’t contain nicotine but act on the same
receptors. However, while some ingredients may have some therapeutic value,
tobacco leaves in their natural form contain so much tar and so many
carcinogenic chemicals that they would have to be extremely
beneficial to be worth the risks, and there is no evidence that they are.
Figure 11.1 shows some of the harms of smoking, compared with those of cocaine
use.
|
|
Cocaine 18(700,000
users) |
Tobacco 19(7 million
users) |
|
Deaths per year |
Medium – 20about 250 in England and Wales in
2010 |
Very high – 21about 100,000 in the UK a year |
|
Physical damage |
Medium – 22about 800 non-fatal poisonings,
some other heart damage |
Very high – 231.5 million hospital admissions
for tobacco-related disease every year |
|
Psychological damage
|
Cocaine psychosis is rare but can occur in heavy users |
None |
|
Dependence |
Medium – 24about 12,000 people in treatment
for cocaine addiction in 2007/8 |
Very high – 25basically all 7 million smokers
addicted |
|
Loss of tangibles and relationships |
Some – 26can cause poverty, risk-taking,
anti-social behaviour |
Very low |
|
Economic cost |
Low – hard to estimate but 27not more than
£50 million a year |
Very high – 28£13 billion a year |
|
International damage
|
Very high – 2940,000 murders in Mexico,
violence in Colombia, rainforest destruction |
Medium – 30deforestation, fertilisers
deplete soil, farmers are exploited |
Tobacco does release
dopamine in the brain, and so creates sensations of pleasure, but this effect
is very mild compared with other stimulants, even for people who are
genetically predisposed to enjoy the drug more than others. Most of the
pleasure of smoking is due to the social context and the relief of addictive cravings. Smoking is a sociable activity,
and it’s acceptable to ask for cigarettes, lighters or rolling papers, even
from strangers; smokers also tend to have a strong sense of group identity and
create social bonds while consuming cigarettes. While these benefits are real,
they could equally be generated through other activities that pose lower health
risks to the individual and those who passively inhale their smoke. Ultimately,
what drives most habitual smokers to use the drug repeatedly are the cravings
produced by their nicotine addiction; they may say that they find smoking
relaxing and enjoyable but a large part of these pleasures is the relief of no
longer being in nicotine withdrawal.
How do we know that smoking causes lung cancer?
As long
ago as 1604, King James I of England described smoking as a 31“custom
loathsome to the eye, hateful to the nose, harmful to the brain [and] dangerous
to the lungs”. In the late 1700s, a London doctor noted 32a link
between using snuff and cancers of the nose, and by the 331850s the
health effects of tobacco were being debated by medical professionals in the Lancet. The first strong evidence of a 34link between
lung cancer and tobacco-smoking was published in 1912, and over the next four
decades the evidence mounted. When the results of 35Richard
Doll’s study of 40,000 doctors over a period of 20 years was published in the
1950s, showing a 20-fold increase in the likelihood of developing lung cancer
among smokers, a causal relationship seemed incontrovertible.
At first, tobacco
companies took a relatively subtle approach towards the growing evidence that
they were marketing a lethal drug. They advertised directly to doctors with
claims that their cigarettes were less harmful than other brands, and to the
public with slogans like 36“More
doctors smoke Camels than any other cigarette”, to associate smoking and good
health. Doll’s initial research was worrying, but the industry hoped that the
public wouldn’t really pay much attention to a statistical study. Then in 1953,
Dr. Ernst Wynder published a paper showing that 37mice that
were painted with tobacco tar developed tumours, proving that tobacco tar was
carcinogenic. This was a much simpler sort of experiment to communicate to the public, and was widely
reported in the press. Within the industry this wave of negative publicity was
termed the “1954 emergency”, and led to them developing one of the most
successful PR campaigns in history.
Within weeks, the PR
company hired by “big tobacco” had designed a strategy that has become a
blueprint for other powerful industries. Rather than try to disprove the
evidence (which would have been impossible), they focused on trying to make the
link seem less certain. As long as people thought that the issue was still scientific
“controversy” rather than “consensus”, and other hypotheses were seen as
probable, action would be delayed, and in that delay they could continue to
sell large numbers of cigarettes. They began with an advert entitled 38A Frank Statement to
Cigarette Smokers, which appeared in 448 daily newspapers on January 4,
1954, reaching an estimated 43 million Americans. Its essential claims were
that:
·
Medical research of recent years
indicates many possible causes of lung cancer.
·
There is no agreement among the
authorities regarding what the cause is.
·
There is no proof that cigarette
smoking is one of the causes.
What the tobacco industry
was exploiting was the fact that it’s difficult to prove a cause and effect relationship conclusively. Just because two
events have a correlation doesn’t necessarily mean that one has caused the
other. 39A might have caused B, or B
might have caused A, or they might both have been caused by C, a third factor
that might not be immediately obvious from just looking at A and B. And even
when you have proved that A and B are correlated, and that A causes B rather
than the other way round, you still have to identify a mechanism. As we saw
with cannabis and schizophrenia, there can be lots of confounding factors that
make a definitive answer hard to come by.
Why is smoking so addictive?
About
a fifth of adults in Britain smoke. Of these, 4075% want to
quit and 79% have tried and failed in the past. What is it about tobacco that
makes it so difficult to give up? It’s partly the substance itself. Nicotine is
an addictive drug that leads to rapid and marked withdrawal reactions when
people try to quit; these withdrawal reactions are felt by many smokers every
morning, leading to the first cigarette of the day. Also, tobacco smoke
contains substances that block the important brain enzyme
monoamine oxidase (MAO) which can itself cause dependence. (The bright areas in
the PET images in Figure 11.1 show the prevalence of MAO in a non-smoker’s
brain, and a smoker’s.). This breaks down dopamine, so if the enzyme is
blocked, levels of dopamine are increased, leading to an improved mood. In
withdrawal, dopamine levels fall, and depression can result. So tobacco smoking
has two components, both of which contribute to its addictiveness.
In my clinical work, I’ve
come across people who’ve had to have both legs amputated after developing
peripheral arterial disease from smoking. This is a terrifying example of the
power of addiction, because, unlike having lung cancer, they would have got
better if they’d stopped. Not being able to quit even after you’ve lost a leg,
and continuing to smoke until
your second leg has to be removed, shows just how powerful the drive to smoke
can be.
Any addict will
experience powerful cravings which can be triggered by the environments and
social groups they associate with taking the drug. For smokers, the temptation
is there every time they walk into a newsagent, see images of people enjoying cigarettes,
or pass someone else smoking. Part of the aim of public-health measures like
smoking bans has been to reduce these triggers: if smoking is made more
inconvenient, and ex-smokers don’t have to sit in smoky places, it makes it
easier to fight the cravings. There’s some evidence that smoking bans can help
prevent people from taking up the habit in the first place. A study in 2001 of
teenagers in Massachusetts found that, although there wasn’t much difference in
the numbers who experimented with cigarettes, they were 4135% less
likely to be habitual smokers in towns that had smoking bans. Public-health
measures have also reduced smoking amongst teenagers in the UK. 42In 1991,
the number of 11–15 year olds who smoked was 16%; by 2005 this had dropped to
5%.
Public-health responses and industry resistance
Warning labels were introduced
on cigarette packets across the EU in 2003, with pictures of cancer-riddled
lungs and other graphic images appearing alongside them in the UK in 2007.
These seem to have been reasonably effective: a survey in 2008 found that 4330% of
current smokers said the warnings helped them smoke less. 2011 saw the
announcement of a new policy that will 44require
shops and newsagents to put cigarette packets “under the counter” rather than
on display behind the cashier. (Australia leads the world here, and soon will
require plain packets for all cigarettes.) It’s hoped that making cigarettes
less visible will reduce the temptation for people to make casual purchases of
cigarettes as a result of nicotine cravings triggered by seeing the packets.
Cigarettes in vending machines were banned from
October 2011; this is particularly important because it removes an easy way for
young people to bypass the age restriction on purchase.
At every step of the way,
the tobacco industry has resisted these measures. Part of the strategy has been
misinformation, deliberately spreading doubt and uncertainty about the validity
of the science that shows their drug causes harm or is addictive. Another tack
has been to discredit the public-health measures themselves, arguing that these
are ineffective or punitive. They’ve suggested alternative measures, such as
ventilation in place of smoking bans, claiming that they’re just as effective,
although 45independent
research has shown otherwise. The tobacco industry has supported institutes and
research centres to conduct scientific studies that disagree with the majority
of the evidence about tobacco harms. As it has become clear that industrialised
countries are going to continue to restrict the sale and use of tobacco, the
industry has aggressively targeted developing nations. 46Within a
few decades, 80% of tobacco related deaths will occur in the developing world.
The tobacco industry’s
most successful ploy, however, was to switch from promoting cigarettes as a
sign of health, adulthood and responsibility, to promoting smoking as a
desirable habit precisely because it is risky and subversive. This allowed them
to tap two new markets: the rebellious youth culture that developed in the
1960s, and women. Freud’s nephew Edward Bernays, who is often called “the
father of PR”, devised a stunt in 1929 in which beautiful women were hired to
appear at New York’s Easter Parade, smoking and holding banners calling their
cigarette a “torch of liberty”. The 47association
between female emancipation and smoking has had a positive result on tobacco
companies profits pretty much everywhere it’s been tried, and though male smokers
still outnumber female smokers, the proportion of women is rising, with a
corresponding rise in health problems. Official statistics show that 48in 2006–8
lung cancer caused more deaths in women than breast cancer, almost all of these
deaths due to smoking. Since the 1950s there has been a 49600%
increase in women’s death rates for lung cancer.
Like the alcohol
industry, for a long time tobacco companies argued that they didn’t need statutory regulation and that voluntary codes
were enough to improve their behaviour and reduce harm. The attitude within
governments has fortunately changed on this score, and although there’s still
more to be done to reduce the influence of the tobacco industry, at least
making laws to control its reach is recognised as the most effective way to
improve public health. This change in attitude has taken a long time, for (as
with alcohol) the industry has had a big ace up its sleeve in terms of
influencing policymakers: many of the people making decisions about how tobacco
should be regulated have themselves been addicted. Smoking wasn’t even
recognised as an addiction in the United States until 1989 – before that it was
referred to as a “habituation”, downplaying how difficult it was for many
people to stop. The fact that many politicians were smokers themselves
undoubtedly played a role in this sort of thinking.
Consequences of the UK smoking ban
Did
the UK 2007 smoking ban work? It’s important to evaluate any policy to
determine whether it’s been effective in achieving its aims, and whether it’s
had any unintended consequences. The main aim of the ban was to protect people
from the effects of second-hand smoke; given that 50compliance
was above 98%, it undoubtedly achieved this. A study of bar workers measured
the amount of cotinine (a byproduct of nicotine that gives the best measure of
exposure to tobacco smoke) present in their saliva, and found it had 51dropped by
76% after the ban was brought in.
There were some immediate
and obvious health benefits to the change. 52Air quality
in bars, which had previously been at “unhealthy” levels, dramatically
improved, encouraging non-smokers into them. It also benefited people with lung
conditions: 53a third
said it helped keep them out of hospital. There was also a 542.4%
reduction in heart attacks in England in the 12 months following the ban,
although we don’t know if this was related to lower levels of passive smoking
or direct smoking, as there was also a marked drop in cigarette sales. A year
after the ban, it was estimated that 552 billion
fewer cigarettes had been smoked in the period June 2007–2008, compared with
the year June 2006–2007. This has partly been attributed to the ban, although
raising the age of sale to 18 and increasing tax also helped to reduce demand.
Whether the ban achieved
one of its secondary aims – to reduce the environmental triggers and help
people give up their addiction – is more uncertain. In the year following the
ban, there was a 5622% increase
in demand for NHS stop-smoking services, although this may have just been a
short-term gain. Another study found that 57prescriptions
for anti-smoking drugs increased by 6.4% in the nine months before the ban, but
fell by 6.4% in the nine months after. It’s possible that the publicity around
the change may have influenced people who already wanted to quit, but once they
had stopped we were left with a hard-core of smokers with little motivation to
quit. These may have found access to outdoor smoking areas and contact with
other people who smoke more influential than the fact they could no longer
smoke inside.
We’ve seen how easy it is
for well-intentioned policies to end up having perverse effects when they don’t
take into account the real-world situation in which they’re going to be
implemented, but so far predictions about negative consequences of the ban have
not been borne out. 58MP John
Reid opposed the bill, saying that it would increase smoking in the home, when
in fact there was a rise in the number of families not
allowing smoking at home, 59from 61% in
2006 to 67% in 2008. Nor was there mass civil disobedience by frustrated
smokers, nor widespread non-compliance by proprietors, and public support has
remained steady at about 76%. Apart from a few isolated cases of people openly
refusing to accept the ban, compliance has been high, although some places do
hold after-hours smoke-ins, which tend to be tolerated by councils and police
in the same way that alcohol lock-ins are. The claims by sites like 60Opposingthe-UK-smokingban.org that smokers have been murdered and violently attacked for their habit
since the ban don’t seem to have any basis in reality; in fact, the most 61well-known
incident of “smoke rage” was aimed at a non-smoker, when a restaurant owner in
Turkey was killed in 2009 after trying to enforce the smoking ban which had
just been implemented there.
Some
businesses have suffered loss of revenue, although this was a predictable
consequence rather than a perverse one. 62175 million
fewer pints were sold in pubs between July 2007 and April 2008 than in the year
before (which would actually mark an improvement to the nation’s health if it
hadn’t in all likelihood been replaced with drinking cut-price supermarket
alcohol at home). The solution to the hospitality trade’s problems, as we said
in chapter 6 on alcohol, is not to reintroduce smoking, but to encourage people
back into the pub by removing the price differential betwen off-licence and
pub. The improved air quality does seem to have encouraged non-smokers to spend
more time at their local: in an opinion survey a year after the ban, 6311% of
people said they were now spending less time in the pub, but 13% said they were
going there more, partly because it was now a more pleasant place to be.
Freedom
and choice
It’s important to make
clear how my position differs from theirs. I think our goal should be to reduce
the harm done by drugs, and because sending people to prison causes more harm
than drugs, it is an ineffective and unjust policy. That’s not the same as
thinking that people should be free to do just what they like. I do believe
that restricting people’s rights to engage in all
risky activities would be disproportionate and unfair – there would be a
general outcry if we tried to ban horse riding, for example. But when
considering the issue of free choice about the drugs we consume we have to bear three things in mind.
Firstly, you are only
free to choose if you have correct information, and this means being free from
false or misleading presentations of the benefits and risks of an activity.
Advertising is always going to emphasise benefits and obscure harms, and so it
confounds our freedom to choose. When tobacco advertising was still permitted,
the tobacco industry used images of youth, health, beauty and desirability to
imply that this is what the outcome of using cigarettes would be, when the
truth is that half of all smokers will end their days dying of a
smoking-related disease. Today, branded packaging uses light colours, pictures
of filters, and words like “mild” to give the impression that these cigarettes
will be healthier, when research shows that 64the harm
they cause is the same as any other brands. The groundwork done by popular
culture to glamorise drug-taking is particularly notable with cigarettes, since
for most people their initial experiences are unpleasant – they have to be
motivated by positive ideas of what smoking means in order to come to enjoy it.
Since documents used during tobacco trials in the 1990s were made public, we
have huge amounts of proof of the ways in which 65the
industry distorted evidence, misled customers, and lied publicly about the
dangers of their product. Protecting people’s freedom to choose requires
providing them with objective facts and ensuring they aren’t given false
information.
And thirdly, while libertarians
emphasise their right to live without being influenced by others, drug-taking
isn’t an isolated, personal matter. Your freedom to have a drink and get in
your car directly affects other people’s freedom to be safe on the road, just
as your freedom to have a cigarette where you like affects other people’s
freedom to choose whether or
not to be exposed to your smoke. An important part of this impact on other
people is the costs that are covered by public services. I believe, as the
majority of people in the UK do, that free public healthcare (ie the NHS)
benefits everybody, and that nobody should remain untreated even if their
illness is partly self-inflicted. Tobacco addicts are also taxpayers, and while
banning smoking in public places restricts them as smokers, it increases their
freedom as taxpayers by releasing money from treating tobacco-related
illnesses.
Conclusion
Smoking
was banned in public places because tobacco is harmful, both to smokers and to
those exposed to second-hand smoke. Around half of those who use tobacco
regularly will die of a tobacco related disease; and around 6611,000
people a year die in the UK from the effects of passive smoking, out of a total
of 80,000 tobacco-related deaths 67(Figure
11.2).
Smoking is extremely
addictive, and many people find it very difficult to give up, even when they
know it’s harming them and others around them. When people in poorer countries
take up the habit, where the risks are compounded by poor diets, by not having
access to healthcare, and by high levels of pollution, the likelihood of
tobacco causing illness is even higher. At current trends, we will have allowed
tobacco to 68kill a
billion people by 2030.
Criminalisation would
create a huge black market, and would probably face so much non-compliance that
it would be unenforceable. It would also deprive governments of tax revenue
(which covers some of the costs of treating tobacco-related diseases), and we
would lose our ability to reclaim some of the industry’s enormous profits.
Instead of seeing this as a moral issue to
be punished through the criminal justice system, governments have recognised
that tobacco addiction is a public-health crisis, to be dealt with through
education, giving support to drug users, restricting availability, raising
prices, and controlling the companies that make money out of getting people
hooked.
Our efforts to minimise
the harms done by tobacco show us both the dangers of allowing a drug to be
openly marketed in society, and some of the most effective steps we can take to
reduce the harms which have resulted.
Notes
1 Individuals who broke the ban would face a £50 fine, while owners
could be charged £2,500 for failing to prevent smoking on their premises• A quick guide to the smokefree law, Smokefree
England/Department of Health, URL-88, 2008
2 three quarters of adults supported the legislation• As above.
3 40% in 1978 to about 20% today• Smoking ban has
saved 40,000 lives, Jeremy Laurence, URL-89, June 30th
2008
4 long history of use• Exotic Substances: in introduction and global spread of tobacco,
coffee, cocoa, tea and distilled liquor, sixteenth to eighteenth centuries, Rudi Matthee, in Drugs and Narcotics in
History, Cambridge University Press, 1995
5 tobacco will account for 10% of all deaths worldwide by 2015•Fact
sheet, WHO, URL-90, accessed December 7th 2011
6 at least 60 chemicals known or suspected to cause cancer in humans• The Tobacco Atlas, WHO, URL-91, accessed
December 10th 2011
7 smoking during pregnancy can damage the foetus• The
Tobacco Atlas, WHO, URL-91, accessed
December 10th 2011
8 fire in King’s Cross that killed 31 people in 1987 was started by a
smoker’s match• On this day, BBC, URL-92, 18th
November 1987
9 cigarette taxes raise £10 billion a year, but the cost to the economy
of treating tobacco related health problems is £13.7 billion• Cough Up, Policy Exchange, URL-42, March
18th 2010
10 each cigarette takes 11 minutes off your total lifespan• Time for a smoke? One cigarette reduces
your life by 11 minutes, Mary Shaw, Richard Mitchell and Danny Dorling,
British Medical Journal 320(7226), January 1st 2000
11 classified as a carcinogen by the WHO• A quick
guide to the smokefree law, Smokefree England/Department of Health, URL-88, 2008
12 review by the UK Scientific Committee on Tobacco and Health in 2004• Second hand smoke: a review of evidence since 1998,
Scientific Committee on Tobacco and Health, URL-93, November
2004
13 the US Surgeon General reiterated these
findings• The health consequences of involuntary
exposure to tobacco smoke: a report of the surgeon general, URL-94, June 27th 2006
14 600,000 deaths a year worldwide, 11,000 of those in the UK•Fact sheet,
WHO URL-90, accessed December 7th 2011
15 protected the users from becoming addicted to tobacco• Tobacco use by Native Americans: sacred smoke and silent killer,
Joseph Winter (ed.), University of Oklahoma Press, 2000
16 treated as a cure-all for everything from tetanus to migraine• Medicinal uses of tobacco in history, Anne Charlton,
Journal of the Royal Society of Medicine 97 (6), June 2004
17 it’s thought that nicotine has anti-psychotic and cognition-impairing
properties• A review of the effects of nicotine on
schizophrenia and antipsychotic medications, Edward Lyon, Psychiatric
Services, October 1st 1999
18 (700,000 users)• Drug Misuse Declared: Findings from the 2010/11 British Crime Survey, Office of National Statistics, URL-108, July 2011
19 (7 million users)• Statistics on Smoking: England
2011, NHS the Information Centre, URL-109, 2011
20 about 250 in England and Wales in 2010• National
Programme on Substance Abuse Deaths, International Centre for Drug
Policy, 2010
21 about 100,000 in the UK a year• extrapolated from the figure of 81,700
in England, from Statistics on Smoking: England 2011,
NHS the Information Centre, URL-109, 2011
22 about 800 non-fatal poisonings, some other heart damage• The Cocaine Trade, House of Commons Home Affairs Committee,
URL-110, February 23rd 2010
23 1.5 million hospital admissions for tobacco-related disease every
year• Statistics on Smoking: England 2011, NHS the Information
Centre, URL-109, 2011
24 about 12,000 people in treatment for cocaine addiction in 2007/8• The Cocaine Trade, House of Commons Home Affairs Committee,
URL-110, February 23rd 2010
25 basically all 7 million smokers addicted• This is because the
definition of being a “smoker” in most surveys means smoking sufficiently
frequently for nicotine addiction to have taken place.
26 can cause poverty, risk-taking, anti-social behaviour• The Cocaine Trade, House of Commons Home Affairs
Committee, URL-110, February 23rd 2010
27 not more than £50 million a year• Nicola Singleton, Rosemary Murray
and Louise Tinsley, Home Office, URL-111, 2006. In
this report, Class A drug use in 2003/4 was estimated to be around £15.4bn, of
which problematic opiate and crack cocaine use accounted for 99% (£15.3bn).
This means that the cost of all other Class A drug use totalled £100m. Assuming
that (at the very most) cocaine powder accounted
for half of these costs, it still won’t exceed £50m a year.
28 £13 billion a year• Cough Up, Policy
Exchange, URL-42, March 18th 2010
29 40,000 murders in Mexico, violence in Colombia, rainforest
destruction• See chapter 10.
30 deforestation, fertilisers deplete soil, farmers are exploited• Growing Tobacco, WHO Tobacco Atlas, URL-112, accessed
December 10th 2011
31 “custom loathsome to the eye, hateful to the nose, harmful to the
brain [and] dangerous to the lungs”• A Counterblast to
Tobacco, King James I, URL-95, 1604
32 a link between using snuff and cancers of the nose• Cautions against the immoderate use of snuff, John Hill,
printed for R. Baldwin and J. Jackson, 1761
33 1850s the health effects of tobacco were being debated by medical
professionals in the Lancet• The Great Tobacco Question: is
Smoking Injurious to Health?, Lancet, 1856
34 link between lung cancer and tobacco-smoking was published in 1912• Primary malignant growth of the lung and bronchii, Isaac
Adler, Longmans, Green, 1912
35 Richard Doll’s study of 40,000 doctors over a period of 20 years was
published in the 1950s• British doctors study,
Richard Doll, British Medical Journal, 1950
36 “More doctors smoke Camels than any other cigarette”• original advert,
Camel cigarettes, URL-96, 1949
37 mice that were painted with tobacco tar developed tumours• Tobacco smoking as a possible aetiological factor in bronchiogenic
carcinoma: a study of 684 proven cases, Wynder, Journal of the American
Medical Association, 1950
38 A Frank Statement to Cigarette Smokers•
Legacy Tobacco Documents Library, URL-97, 1954
39 A might have caused B, or B might have caused A, or they might both
have been caused by C, a third factor that might not be immediately obvious
from just looking at A and B.• A simple example of a flawed association is
between shoe-size (A) and reading ability (B). If you survey shoe-size and
reading ability in a large population, there is a very strong correlation.
However, large shoe-size does not cause a person to
be good at reading; in fact, shoe-size and reading-ability are more accurately
correlated with a third factor, age (C) – adults have bigger feet than
children, and many children are still just learning to read. A less trivial example is the current investigation
between taking cannabis (A) and schizophrenia (B); both may be linked to a
genetic variation (C) that predisposes a person both to take cannabis and to
suffer from schizophrenia.
40 75% want to quit and 79% have tried and failed in the past• A quick guide to the smokefree law, Smokefree
England/Department of Health, URL-88, 2008
41 35% less likely to be habitual smokers in towns that had smoking bans•
Local Restaurant Smoking Regulations and the Adolescent
Smoking Initiation Process, Michael Siegel et al, Archives of Pediatric
and Adolescent Medicine 162 (5), 2008
42 In 1991, the number of 11–15 year olds who smoked was 16%; by 2005
this had dropped to 5%• From underwear to aircraft noise:
logging 70 years of social change, Office for National Statistics, URL-98, September
2nd 2011
43 30% of current smokers said the warnings helped them smoke less• Survey on Tobacco Analytical Report, European Commission,
March 2009
44 require shops and newsagents to put cigarette packets “under the
counter” rather than on display behind the cashier.•BBC, Tobacco
display ban reminder for supermarkets, URL-159, December
28, 2011.
45 independent research has shown otherwise• Dealing
with the health effects of secondhand smoke, Select Committee on Health
First Report, URL-99, 2005
46 Within a few decades, 80% of tobacco related deaths will occur in the
developing world• Fact sheet, WHO, URL-90, accessed
December 7th 2011
47 association between female emancipation and smoking has had a positive
result on tobacco companies profits• Gender empowerment and
female-to-male smoking prevalence ratios, Sara Hitchman and Geoffrey
Fong, Bulletin of the World Health Organization, URL-24, January
5th 2011. The authors quote an internal industry document from 1991: “To
convince fashionable, modern, independent and self-confident women aged 20–34
that by smoking [Virginia Slims], they are making better/more complete
expression of their independence.”
48 in 2006–8 lung cancer caused more deaths in women than breast cancer• Cancer incidence and mortality in the UK 2006–2008, Office
for National Statistics, URL-100, June 2011
49 600% increase in women’s death rates for lung cancer• An epidemic of smoking-related cancer and disease in women,
URL-101, August 2010.
50 compliance was above 98%• A quick guide to the
smokefree law, Smokefree England/Department of Health, URL-88, 2008
51 dropped by 76% after the ban was brought in• A
quick guide to the smokefree law, Smokefree
England/Department of Health, URL-88, 2008
52 Air quality in bars, which had previously been at “unhealthy” levels,
dramatically improved• As above.
53 a third said it helped keep them out of hospital• Smoking
ban has saved 40,000 lives, Jeremy Laurance, URL-89, June 30th
2008
54 2.4% reduction in heart attacks• Heart attacks fall
after smoking ban, NHS Choices, URL-102, June 9th
2010
55 2 billion fewer cigarettes had been smoked• Smoking
ban has saved 40,000 lives, Jeremy Laurance, URL-89, June 30th
2008
56 22% increase in demand for NHS stop-smoking services• A quick guide to the smokefree law, Smokefree
England/Department of Health, URL-88, 2008
57 prescriptions for anti-smoking drugs increased by 6.4% in the nine
months before the ban, but fell by 6.4% in the nine months after• The impact of the introduction of smoke free legislation on
prescribing of stop-smoking medications in England, Szatkowski et al,
Addiction, July 27th 2011
58 MP John Reid opposed the bill• MPs to challenge
ministers veto on total smoking ban, Patrick Wintour, the Guardian, December 17th 2005
59 from 61% in 2006 to 67% in 2008• A quick guide to
the smokefree law, Smokefree England/Department of Health, URL-88, 2008
60 Opposingthe-UK-smokingban.org• describe themselves as promoting the “freedom to choose” and that
their mission is “to fight against the injustice of smokers being treated as
second class citizens (and to dispel the myth about Second Hand Smoke) in the
UK!” URL-103.
61 well-known incident of “smoke rage” was aimed at a non-smoker, when a
restaurant owner in Turkey was killed in 2009 after trying to enforce the
smoking ban which had just been implemented there• Smoking
ban murder, Reuters, URL-104, July 31st
2009
62 175 million fewer pints were sold in pubs between July 2007 and April
2008 than in the year before• Smoking ban has saved 40,000
lives, Jeremy Laurence, URL-89, June 30th
2008
63 11% of people said they were now spending less time in the pub, but
13% said they were going there more• A quick guide to the
smokefree law, Smokefree England/Department of Health, URL-88, 2008
64 the harm they cause is the same as any other brands• Why cigarette packs matter, Ben Goldacre, URL-105, March
12th 2011
65 the industry distorted evidence, misled customers, and lied publicly
about the dangers of their product• The tobacco industry
documents: an introductory handbook and resource for researchers, Ross
Mackenzie, Jeff Collin & Kelley Lee, URL-106, July
2003. This is a good introduction to Tobacco Documents Online, about 40 million
pages of documents from tobacco companies and industry organisations, released
after the tobacco trials of the 1990s in the USA.
66 11,000 people a year die in the UK from the effects of passive
smoking• Cancer Research UK, URL-107, accessed
December 10th 2011
67 (Figure 11.2).• Sources: Smoking and drinking among adults, 2009. Office for National Statistics; Drug Misuse Declared: Findings from the 2010/11 British Crime Survey
England and Wales, Home Office; Estimates of the Prevalence of Opiate Use and/or Crack Cocaine Use,
2009/10: Sweep 6 report, The Centre for Drug
Misuse Research.
68 kill a billion people by 2030• A quick guide to the
smokefree law, Smokefree England/Department of
Health, URL-88, 2008
What are benzodiazepines and how do they work?
What are the benefits and harms of benzodiazepines?
Medicinally,
benzodiazepines are usually prescribed for anxiety disorders and for people who
have trouble sleeping. About 114% of
older people in the UK take them every night,
and many use them for decades. They can help relieve muscle spasm: they are
used to treat convulsive disorders like epilepsy, and are routinely given
before procedures like endoscopies to reduce anxiety and prevent the formation
of stressful memories. When alcoholics are in acute alcohol withdrawal,
benzodiazepines are used to relieve acute agitation, tremor, seizures, and
delirium tremens.
Physical
dependence
Physical
dependence on benzodiazepines is common. Stopping suddenly can cause severe
withdrawal symptoms and even convulsions, especially if you’ve used them for a
long time. Even when the dose is tapered, some people still experience symptoms
such as rapid heartbeat, insomnia, irritability, anxiety, weight loss and
muscle cramps. However, when coming off is supervised by a doctor, these
symptoms are rarely severe even in long-term users. One study found that 280% of the
subjects, who had taken benzodiazepines for an
average of 17 years to help them sleep, stopped without any trouble with a
gradual reduction in dose and information about sleep hygiene.
·
In Phase 1, the patient has
abnormally-low GABA function and feels anxious all the time.
·
In Phase 3, the doctor tapers off
their dose.
·
Coming off the drugs leads to
Phase 4, where withdrawal makes the patient feel even more anxious than they
felt when they first went to the
doctor. However, once this period of withdrawal has passed, they will probably
feel better than they did before treatment.
In general, although
physical dependence on benzodiazepines is common and
withdrawal can sometimes be problematic, the psychological cravings that
characterise addiction are extremely rare when benzodiazepines are taken as
directed by the doctor. Whether it’s worth risking building up tolerance and
possibly suffering withdrawal symptoms, depends on individual factors –
especially how ill you are and how much the benzodiazepines help you. The
decision requires the same sort of weighing up of the harms and benefits as
with any drug.
Antidepressants and SSRIs
Selective serotonin reuptake
inhibitors (SSRIs) were
first developed in the 1970s. They have become the most-commonly prescribed
type of antidepressants worldwide in the last two decades. Common drugs of this
type are citalopram (sold under the trade names Celexa and Cipramil),
paroxetine (Seroxat), sertraline (Zoloft) and fluoxetine (Prozac).
SSRIs work in both
depression and anxiety disorders. Depression was previously treated with
tricyclic antidepressants such as amitriptyline and imipramine; although SSRIs
are no more effective, 3they have
fewer side effects and almost no abuse potential. They are almost impossible to
overdose on, so they are unlikely to be used to commit suicide, unlike the
tricyclic antidepressant drugs which used to kill many hundreds of people per
year. SSRIs work by blocking the reuptake of serotonin into its nerve
terminals, so that serotonin levels in the brain slowly increase. In some
people this increase in serotonin can be somewhat unpleasant, and insomnia,
anxiety and restlessness commonly occur in the first few weeks of use. As a
result, SSRIs are not abused, because getting used to them requires a lot of motivation.
Over time these negative feelings wear off but the antidepressant effect
remains, lifting the depressive mood or reducing the anxiety state. In the
treatment of anxiety, medications that work on the serotonin system are an
improvement on those that work on GABA, because they don’t lead to a
down-regulation of serotonin receptors in the way that barbiturates and
benzodiazepines down-regulate GABA receptors and cause withdrawal symptoms.
Do SSRIs increase the risk of suicide?
Do
SSRIs cause dependence?
Most
of the psychiatric disorders treated with SSRIs are long-lasting and have high
rates of relapse, and recurrence.
Relapse is when the first episode returns; recurrence is when a new episode of
illness begins after full recovery.
Over a 20-year period, almost everyone who has had one episode of depression
will have another one, and the more frequently it has occurred the more likely
it is to happen again – a kind of vicious cycle. There seems to be a similar
pattern in some anxiety problems such as panic disorders, though others, such
as PTSD, tend to be chronic. The most powerful effect of SSRIs is preventing
the recurrence of these disorders so long as patients continue to take their
treatment.
Rebound and discontinuation
Stopping
taking SSRIs can cause a discontinuation syndrome (which is different from
withdrawal, because in discontinuation the symptoms are different from the
underlying illness). The discontinuation syndrome is characterised by nausea,
dizziness, lethargy, headache and an influenza-like feeling; these symptoms are
definitely caused by the lack of drugs because they’re fully reversed with another
dose. If left untreated they tend to peak after 2 to 5 days, and then decay
quickly over a few more days, although occasionally they can last several
weeks. It may be that people with certain personality traits are more prone
than others to experiencing these symptoms. It’s extremely rare, however, for
someone to find themselves unable come off SSRIs at all.
Painkillers
The physical harms of
milder painkillers are well known. Aspirin is toxic to the stomach and can
cause ulcers, while paracetamol is toxic to the liver. Using codeine and other painkillers incorrectly can actually
sensitise people to pain, causing analgesic-induced headaches. “Incorrect use”
might mean taking too much of the painkiller, or taking it too often, which
might also lead to addiction, but the headaches can happen even if the patient
isn’t addicted. These should stop once the patient comes off the medication.
The pharmaceutical industry and science
·
The company chooses a target drug
to investigate.
·
They run toxicology tests on
animals to determine its safety ratio, its
longer-term effects, and whether it’s addictive.
·
They then move on to studies on
healthy volunteer human subjects to establish correct dosage.
·
After two positive trials, the
company can apply for marketing authorisation.
The majority of my own
research is publicly funded, but of course I also do research on drugs produced
by pharmaceutical companies since many of these are the result of cutting-edge
science and so critical to progressing the field on brain research and
addiction. Given the transparent nature of data collection and the hoops pharmaceutical
companies must jump through to get a drug approved, we’re unlikely to end up
with ineffective or harmful medication. In fact the greater danger is that
pharmaceutical companies stop trying to produce drug treatments for certain
conditions altogether, because the approval process is so difficult. This is particularly the case for mental-health disorders, where it is hard
to carry out effective trials because of the types of people that have these
disorders, and the large number of confounding factors. There is already a
strong conservative streak within the pharmaceutical industry, tending to avoid
new avenues of research, preferring instead to investigate slight variations on
existing drugs that are more likely to reach the marketplace and recoup the
development costs. This is understandable given that 4developing a
new medication now costs about $1 billion. However, it leaves lots of promising
areas under-researched. If big Pharma stops producing drugs for mental-health disorders
altogether and we don’t have some alternative way of producing these drugs, it
will be immensely damaging to people with mental illness, especially as we are
currently in the midst of something of a mental-health epidemic.
The mental-health epidemic
5Mental
health is the biggest health burden in Europe today, costing more than heart
disease and cancer combined. The leading problem for men is alcoholism, and the
leading problem for women is depression. There is an urgent need for better
treatments and better drugs.
Part of the problem in
the UK is that GPs have very little background in mental-health issues –
usually about 15 weeks out of their entire training. Yet this is the number-one
health problem that they will be diagnosing and attempting to treat in their
practice. Of course, GPs have a very high patient load, but the longer a
mental-health problem continues without effective treatment, the worse it will
get, making the GP even more overworked. Our health service will be vastly
improved if much more emphasis is put on dealing with mental-health issues when
they first appear, especially because many ill people self-medicate with
“recreational” drugs in the absence of prescription medication. These patients
often reappear in the medical system many years later with addictions and other
health problems from the toxic effects of what they’ve taken. About a quarter
of male alcoholics are thought to have an undiagnosed anxiety disorder, which
could probably have been treated successfully with SSRIs if it had been identified before they started drinking
heavily. Once they are addicted to alcohol, however, it is much harder to find
effective treatments.
This process of
stabilising a patient can be very difficult, and needs a lot of trust,
especially as many of the drugs prescribed for mental health problems will make
patients feel worse initially. It’s often difficult to make the correct
diagnosis at first, and it’s possible that several different courses of drugs
will have to be tried before an effective one is found. The expertise of the
doctor is crucial at this stage, and a trusting therapeutic relationship is
essential. Unfortunately, once a patient has been stabilised many doctors don’t
want to let the patient have more control over their treatment. This can be very distressing for the patient, and also means
the treatment is less likely to work, because treating mental health disorders
always requires active engagement of the patient: they won’t get better if
they’re just passively expecting the drugs to do it all for them. Ultimately,
the patient is the true expert in their own condition, because they’re the one
experiencing it.
Informed
consent
In recent
years, there have been several incidents of effective medications being
withdrawn by the pharmaceutical companies themselves (rather than by regulatory
bodies) when a small number of patients developed severe side-effects. Of
course such side-effects are extremely unfortunate when they do occur; however,
for people suffering from very serious illnesses where currently approved
medications are considerably less effective than a new drug, or where their
medications already carry substantial side-effects, they may think that even
very serious complications are worth the possible benefits. Pharmaceutical
companies are understandably fearful of litigation, but since it is the patient
who will suffer the consequences if something goes wrong it is nonsensical that
they can’t be allowed to decide to take this risk, especially as we routinely
allow much greater levels of risk-taking when people undergo surgery. With
invasive procedures, a patient is allowed to face even a very substantial risk
of death through informed consent. 6Up to 1 in
7 elderly patients die after surgery – a level of risk that would never be
allowed with a drug.
Rather than allowing
regulatory bodies or pharmaceutical companies to decide which drugs are made
available to patients, perhaps we could develop a new model for approving drugs
based on 7informed
consent. This is a well-established process: the possible dangers of a surgical
procedure are explained in layman’s terms, and the patient’s formal consent
protects those who perform the procedure from litigation should there be an
adverse outcome. Applying this principle to new drugs would facilitate the
current trajectory of medical research, which is increasingly towards “personalised medicine”. These are
medications tailored to particular genotypes or other specific biological
qualities, that will be very beneficial to some people but might be harmful to
others. However, because drugs regulation is largely based on risks and
benefits averaged across a whole population, positive outcomes for identifiable
minorities are often overlooked, and further research on these drugs grinds to
a halt, fuelling a risk-averse approach to drug development, which in turn
prevents people with serious conditions getting the therapies that could help
them. Informed consent could overcome some of this risk-aversion, and would be
far more in tune with modern concepts of patient empowerment and shared
decision-making than paternalistically removing drugs from the market
altogether.
Conclusion
There are
many promising avenues for drugs research, and it’s possible that we’ll be able
to turn the tide on the mental-health epidemic as new sorts of treatment are
developed. On the scientific side, the field is moving extremely quickly and
our knowledge of the brain and of brain disorders expands significantly each
year. However, this research cannot solve the problem on its own. It needs
funding, from pharmaceutical companies or from the public purse; it needs a
political context which allows researchers to explore the potential benefits of
drugs even if they’re illegal; it needs well-trained medical professionals able
to prescribe therapeutic drugs and other forms of treatment appropriately; and
it needs a well-informed public who are permitted to make decisions about the
best course of treatment for their own mental health.
Notes
1 14% of older people in the UK take them every night• Drugs and the Future: Brain Science, Addiction and Society,
David Nutt et al, Elsevier, 2007
2 80% of the subjects, who had taken benzodiazepines for an average of
17 years to help them sleep, stopped without any trouble• Drugs
and the Future: Brain Science, Addiction and Society, David Nutt et al,
Elsevier, 2007
3 they have fewer side effects and almost no abuse potential.• Death and dependence: current controversies over the selective
serotonin reuptake inhibitors, David Nutt, Journal of Psychopharmacology
17(4), December 2003
4 developing a new medication now costs about $1 billion• Drugs and the Future: Brain Science, Addiction and Society,
David Nutt et al, Elsevier, 2007
5 Mental health is the biggest health burden in Europe today, costing
more than heart disease and cancer combined• Cost of
disorders of the brain in Europe 2010, Gustavsson, A., et al., European
Neuropsychopharmacology, 2011
6 Up to 1 in 7 elderly patients die after
surgery• Tens of thousands of surgical patients
dying needlessly because of poor NHS care, says Royal College of Surgeons, Sophie Borland, URL-113, September 29th 2011
7 informed consent.• Informed consent – a new
approach to drug regulation?, David Nutt, Journal of Psychopharmacology,
January 2006
Muscle
and power
Using
highly potent drugs to improve performance in sport dates back to the early
1800s, when a 1participant
in an “endurance walk” used laudanum to keep himself awake for 24 hours. By the
end of the 19th century, 2nitroglycerin
(which is used to stop angina) was commonly used to keep cyclists awake in
six-day marathon races. 3Strychnine
was openly used by some long-distance runners, and drugs including cocaine were
used both recreationally and for performance by cyclists in the Tour de France.
Most of these drugs had the potential for severe side-effects and some athletes
came close to death while competing, or suffered from hallucinations and other
psychological disturbances.
While
amphetamines also were commonly used in the past to increase strength, it’s
unclear whether these sorts of stimulants really make you any stronger – they
might just make you think you’re doing better, giving
you a mental edge. However, they also reduce your control: a famous case was 4the death
of British cyclist Tommy Simpson. He died on a hill-climb in the Tour de France
on a blisteringly hot day, after drinking far too little water, and mixing
brandy with two vials of amphetamines. He started cycling erratically, swerving
across the road, and eventually collapsed and died. What makes this case
particularly tragic is that it’s unlikely the drugs helped him cycle any
faster. What they did do was allow him to ignore the
warning signs of overexertion and overheating which would have forced him to
stop much earlier, and would probably have saved his life.
However, it is drugs
called anabolic steroids that are most commonly used
to build muscle and increase strength. They are taken by thousands of members
of the general public, not just professional sports-people. Because anabolic
steroids are 5the
most-widely used performance enhancer, they almost certainly cause the most
harm, which is why we focus on them here.
What
are anabolic steroids?
6Anabolic
steroids are synthetic drugs that mimic male sex hormones, particularly
testosterone. Their technical name is anabolic-androgenic
steroids: the anabolic part means they
stimulate growth, and the androgenic part means they
“produce maleness”. They are used medicinally to stimulate the growth of muscle
and bone, for example to treat patients with AIDS wasting syndrome, or to help
boys with delayed puberty who aren’t producing enough testosterone themselves.
They are also used to treat anaemia, and to help male transsexuals in the
transition from their original female body (which has more of the sex hormone
oestrogen) to their desired male body (which has more testosterone). Finally,
there is ongoing research into using them as a
male contraceptive.
Who
uses anabolic steroids?
The British Crime Survey
(BCS) estimates that around 50,000 adults use anabolic steroids every year, but
this is likely to be a considerable underestimate. The BCS is a door-to-door
survey, so it under-represents people who live in group accommodation (such as
students and prisoners), those who work in the evenings, and those who spend a
lot of their time out of the house, for example at the gym. These are all
groups who are more likely to use anabolic steroids. In addition, a secretive
sub-culture surrounds the use of anabolic steroids, and many people are
unlikely to be honest about whether or not they take them. The proportion of
young people who have tried them rose from 0.2% in 2001 to 0.5% in 2006, and if
this trend has continued the proportion will be even higher now of course. Most
users are primarily interested in increased strength and power, but some take them for aesthetic reasons,
attempting to achieve an ideal body type. This group of users is very
under-studied, and may have more in common with people with body dysmorphobia
(eg anorexia) than with other drug users or athletes.
What are the harms of anabolic steroids?
Because anabolic steroids
are sex hormones, they have quite different effects depending on the age and
gender of the person taking them. Their androgenic (male-producing) qualities
mean that men are far more likely to use them than women: the ratio of male to
female users is about 10 to 1. Women may find their bodies becoming more
masculine, growing extra body hair, their voice becoming deeper, their breasts
disappearing, and their periods stopping – changes which can be very
distressing and may be permanent. On the other hand, men may find their own
testosterone production gets suppressed. This is analogous to cocaine causing
lower levels of dopamine to be produced naturally by the brain (page 138) – the body recognises that it
has enough androgenic hormones coming in from the anabolic steroids and stops
producing its own supply. This can lead to sexual dysfunction, the growth of
breast tissue, and infertility. These effects can be particularly disruptive if
the user has not yet reached full physical maturity, so it’s very important
that young men are informed of the risks before
they consider starting on these drugs.
How can we reduce the harms of anabolic steroids?
Another harm reduction
measure recommended by the ACMD in their 2010 report would be to make them
illegal to import unless they’re in someone’s possession, and prohibit their
sale and purchase online. Buying from the internet can be unsafe as there is
very little quality control – products are often contaminated with other
substances (which is especially problematic if the drug is going to be
injected) and their strength is very variable, making it hard for people to
judge dosage.
Other
drugs in sport
Drugs
are often banned from sports out of fear that they might improve performance
and pace, even if there’s little evidence that they do. In 2003, American
sprinter 7Kelli White
was stripped of her 100mand 200mgold medals at the World Championship after a
sample tested positive for modafinil, a mild stimulant similar to Ritalin. She
claimed that she used it to treat a medical condition, and avoided a two-year
ban from the sport after arguing that she didn’t think she had to declare it
because it wasn’t on the list of banned substances at the time. Modafinil was
added to this list in January 2004, although it’s doubtful that it actually
makes people run any faster.
Another question is
whether stimulants like amphetamines should be permitted in aerobatics and
other activities involving flying. A few years ago, I was contacted by the
British Aerobatic Association, who wanted to know if there was any evidence on
the effects of stimulants on flying as they were considering a ban on their
use. Although this hasn’t been formally researched, we do have case studies
from the Second World War: 8the German
air force used methamphetamine heavily, which if anything seemed to hinder
pilots’ abilities in the air. Although stimulants can help people stay awake,
they can also get people locked into stereotyped routines, making them less
able to respond to the world around them. For that reason I recommended that
testing for stimulants was not likely to be worthwhile for aerobatics.
Drugs for calmness in sports
Alcohol is a good example
of how the advantage conferred by a drug can be very
dose-dependent. At low doses, alcohol can help us keep calm and so improve our
accuracy because trembling hands put us at a disadvantage, but at higher doses
our coordination deteriorates and our performance declines. If we drink so much
that we become dependent on alcohol, however, we can end up with the shakes if
we don’t drink. Any sports person who becomes
physically dependent on a drug will find that, although it improves their
performance by taking them out of withdrawal, it undermines their ability to
perform overall, and they would have been better off if they’d never taken the
drug in the first place.
Improving mental performance – cognition enhancers
A debate has begun
recently about whether drugs such as modafinil should be banned during exams,
or in the study periods leading up to them, as they may confer an unfair
advantage. This is quite problematic, not only because this would be very
difficult to police, but also because it would raise questions about other
common stimulants like nicotine and caffeine.
Should they be banned before exams as well? In any case, it has not been proved
that modafinil is particularly beneficial to learning. It certainly can allow
people to stay awake and work for longer before they need to sleep, so
increasing the total time available for study. But whether this translates into
improved exam performance is not known. Different sorts of cognitive tasks
require different sorts of brain processing, and sometimes taking drugs to
improve one type of thinking makes it more difficult to engage in another. In
clinical practice, some patients on Ritalin and other stimulants say that the
drug reduces their mental flexibility, so they feel over-focused, less
creative, and engage in fewer tasks.
Is my child addicted to Ritalin?
In
recent years, prescribing stimulants to people with ADHD (attention deficit
hyperactivity disorder), has been controversial. The drug most commonly used
for this is methylphenidate, a mild form of amphetamine (sold under the names
Ritalin or Concerta). There are several aspects to the controversy. Some people
deny that ADHD really exists, or think it is a real disorder but that
stimulants are an inappropriate way to treat it. Others think that, even if some people really do have ADHD and benefit from Ritalin,
the drug is being prescribed inappropriately in a very large proportion of
cases, particularly for children whose parents may just be finding their normal
childish energy challenging.
ADHD is a disorder
characterised by a range of symptoms including a very short attention span, an
inability to concentrate or sit still even if the surroundings are peaceful and
calm, impulsive behaviour such as acting without thinking, and having little or
no sense of danger. Children with the disorder may also have other problems such
as dyslexia, but even if they don’t, they are likely to under-perform in school
because they can’t focus on the tasks that they’ve been set. The result for
many children is that they lose confidence in their abilities and stop trying,
which can cause huge problems throughout the rest of their lives. We can often
recognise a child with ADHD because they seem to be under-performing compared
with what their IQ would suggest they are capable of. ADHDis often treated with
Ritalin. Ritalin is a dopamine reuptake inhibitor, which blocks dopamine
transporters in the brain in a similar way to cocaine. However, when taken
orally it takes about an hour for concentrations in the brain to peak (compared
with about five minutes for cocaine).
So although when it arrives it works very efficiently –9blocking
around 50% of dopamine transporters – it doesn’t produce a “high” and is
unlikely to cause addiction. It’s only when Ritalin is taken in non-prescribed
ways – for example when it’s injected or when crushed up pills are snorted –
that it reaches the brain much faster, and this is when addiction can occur.
Although the rapid rise
in the number of people being diagnosed with ADHD and prescribed stimulants has
led to fears of “over-medication”, 10we still
estimate that only about a quarter of those who would benefit from them are
currently taking them. Indeed, the opposite – not prescribing them because of
doubts about the disorder – seems to be as much of a problem as excessive
keenness to medicate. (However, there may indeed be cases where Ritalin is
misused; we doctors don’t always try non-medical treatments when they would be
appropriate.)
Young
people with ADHD are often very good at some specfic activities such as playing
video games, and it may well be that experimenting with different teaching
techniques, and computer games to train the brain, would be just as beneficial
as drugs. But for now, prescribing stimulants for ADHD sufferers at least gives
them a chance to succeed in our current school system.
The most common cognition enhancer: coffee
11Coffee
originates from East Africa (where it grows in the same sort of terrain as
khat). There are different stories about how and when humans first started to
consume coffee, some of which suggest we copied birds and goats who seemed to
enjoy the stimulating properties of the berries. The raw berries are bitter and
unpleasant to humans, however, and it takes quite a lot of technical expertise
to turn them into a palatable drink. It’s difficult to know if these techniques
were actually learnt around the 8th or 9th centuries, as the myths suggest, or
if they only developed shortly before the first written accounts of coffee
drinking, in Yemen in the mid-15th century.
As coffee spread
throughout the Muslim world and on to Europe, it was met with concern at first.
Attempts were made to ban it as unIslamic or unChristian, but its popularity
made these bans ineffective, and soon huge numbers of coffee houses had sprung
up – over 123000 in
England alone by 1675. Having been criticised for causing illness, coffee now
began to be credited with the ability to cure all sorts of ailments, from
stomach problems to headaches. It is now the most-commonly used drug in the
world, and it’s taste is so popular we now even have a non-active version –
decaffeinated coffee.
The active
ingredient in coffee is caffeine, which is also present in tea and chocolate
(though in smaller quantities). When the brain engages in metabolic activity,
it produces a small molecule called adenosine as a byproduct, which builds up
in the brain and makes you feel tired – a bit like mental lactic acid. Caffeine
blocks the effects of adenosine, which is why it makes
you feel more awake (and why 13your
sensitivity to caffeine depends partly on what sort of adenosine receptors you
have.)
Does
coffee improve performance?
It’s
difficult to be sure whether coffee actually improves performance. Most of us
are physically dependent on it, going into withdrawal overnight, and withdrawal
impairs performance. If a coffee drinker does better on a task after having
some caffeine it’s difficult to know whether this is a genuine improvement or
just compensating for the impairment they experienced before they had their
caffeine fix (ie not a positive factor, just the removal of a negative factor).
This theory is supported by research which has found that 14caffeine
improves performance more in people who are coffee drinkers than those who
normally don’t consume caffeine at all. On the other hand, caffeine certainly
does have effects in itself – researchers use it to model insomnia when they’re
testing sleeping pills, for example – so it’s possible it does provide a mild
cognitive advantage.
Conclusion
15“exhilaration and lasting
euphoria, which in no way differs from the normal euphoria of the healthy
person … You perceive an increase of self-control and possess more vitality and
capacity for work … Long intensive mental or physical work is performed without
any fatigue … Absolutely no craving for the further use of cocaine appears
after the first, or even after repeated taking of the drug.”
The quest for improved
mental and physical performance poses ethical issues about the sorts of drugs
that we want to develop and the sorts of purposes we want them for. In chapter
16 we’ll be looking at the future of drugs – where drug research is taking us,
and the sorts of decisions that might face us in the years to come.
Notes
1 participant in an “endurance walk” used laudanum to keep himself awake
for 24 hours• Dopage: l’imposture des performances,
Jean Pierre de Mondernard, Willmett II Chiron, 2000
2 nitroglycerin (which is used to stop angina) was commonly used to keep
cyclists awake in six-day marathon races• Use of
performance-enhancing drugs in sport, Wikipedia, URL-32.
3 Strychnine was openly used by some long-distance runners• La Fabuleuse Histoire des Jeux Olympiques, Robert Pariente
and Guy Lagorce, Minerva, 2004
4 the death of British cyclist Tommy Simpson• British riders remember Tommy Simpson – a hero to some, to others the
villain of the Ventoux, URL-114, Richard Moore, July 26th 2009
5 the most-widely used performance enhancer• Conveniently, they are also
the most-widely studied.
6 Anabolic steroids are synthetic drugs• Consideration
of the Anabolic Steroids, ACMD, URL-115, September
2010
7 Kelli White was stripped of her 100mand 200mgold medals• Sprinter likely to lose medals, New York Times, URL-116, September
10th 2003
8 the German air force used methamphetamine heavily• Concepts
of Chemical Dependency, Harold E. Doweiko, Cengage Learning, 2009
9 blocking around 50% of dopamine
transporters• Methylphenidate and cocaine have a
similar in vivo potency to block dopamine transporters in the human brain, Nora Volkow et al, Life Sciences 65 (1), May
28th 1999
10 we still estimate that only about a quarter of those who would benefit
from them are currently taking them• Service contacts among
the children participating in the British Child and Adolescent Mental Health
Surveys, T Ford, H Hamilton and R Goodman, Child and Adolescent Mental
Health 10, 2005. The authors examine the most severe form of ADHD: hyperkinetic
disorder.
11 Coffee originates from East Africa (where it grows in the same sort of
terrain as khat)• Exotic Substances: the introduction and
global spread of tobacco, coffee, cocoa, tea and distilled liquor, sixteenth to
eighteenth centuries, Rudi Matthee, in Drugs and Narcotics in History,
Cambridge University Press, 1995
12 3000 in England alone by 1675• Wake up and smell
the coffee in Turkey’s beautiful Izmir, author, URL-119, August
25th 2011
13 your sensitivity to caffeine depends partly on what sort of adenosine
receptors you have.• Association of the anxiogenic and
alerting effects of caffeine with ADORA2A and ADORA1 polymorphisms and habitual
level of caffeine consumption. PJ Rogers, C Hohoff, SV Heatherley, EL
Mullings, PJ Maxfield, RP Evershed, J Deckert and DJ Nutt,
Neuropsychopharmacology 35: 1973–83, 2010
14 caffeine improves performance more in people who are coffee drinkers
than those who normally don’t consume caffeine at all• Association
of the anxiogenic and alerting effects of caffeine with ADORA2A polymorphisms
and habitual level of caffeine consumption, Peter Rogers et al,
Neuropsychopharmacology, 35, 2010
15 “exhilaration and lasting euphoria, which in no way differs from the
normal euphoria of the healthy person …• Uber Coca,
Sigmund Freud, Centralblatt für die gestalt Therapie,
1884
How
do psychedelics work?
All
psychedelics directly stimulate a particular subtype of our serotonin
receptors; these are the 5HT2A receptors and play an important role in higher,
cortical, brain functions. The best-known effect is the production of unusual visuals
– not true hallucinations (which are images that have no basis in reality), but
strange distortions and imaginative additions to images of the things that are
physically present. These can happen both with eyes open and eyes closed.
Psychedelic drugs are also empathogenic – they create
sensations of care, love, and connection to other people and to the natural
world. It’s still a mystery why these natural products and their derivatives
produce visual effects, whereas synthetic SSRIs (which also increase levels of serotonin) just produce changes in mood and
energy. It’s unlikely we’ll be able to unravel this mystery fully as long as
psychedelics remain illegal and research on them is so restricted.
Modern brain-imaging
techniques have shown us that the brain works in many different modes: acting,
seeing, listening, planning and attention, moving, feeling, etc. One is called
the “default mode”, which includes normal “housekeeping” functions, such as
memory, self-reflective thought, and the sense of our body in space.
Psilocybin, a prototypical psychedelic, switches off this mode 1(Figure
14.1), so disrupting the sense of “self”. It seems likely that all psychedelics
do the same. People often describe a psychedelic experience as like “seeing the
world anew”, probably because they break out of the normal routine of brain
processing. It’s because of this effect that our expert panel rated LSD highest
in terms of the drug-specific impairment of mental functioning.
The
discovery of LSD
For
centuries, it was known that a fungus called ergot had peculiar properties.
Some of these were purely medicinal. Ergot constricts blood vessels, so
extracts were used by midwives to prevent women dying from excessive bleeding
after childbirth. This property also helps with migraine headaches, so by the
early 1900s purified ergotamine was being used to treat migraine. Other
properties were more mysterious. Periodic outbreaks of madness and strange
visions amongst whole populations often
coincided with particular climatic conditions that caused the fungus to grow on
crops of rye. There is 2a theory
that the stories of magic and devils reported by the girls of Salem during
their witchcraft trials in 1692 were the result of ergot poisoning.
3“was seized by a peculiar
sensation of vertigo and restlessness … In a dreamlike state, I left for home …
With my eyes closed, fantastic pictures of extraordinary plasticity and
intensive colour seemed to surge towards me.”
4“I lost all control of time:
space and time became more and more disorganised and I was overcome with fears
that I was going crazy … Occasionally I felt as being outside my body. I
thought I had died. My ‘ego’ was suspended
somewhere in space and I saw my body lying dead on the sofa.”
LSD
and psychiatry
Hofmann immediately
recognised that his new compound could be beneficial to psychiatry. The first
thing he did was inform several of his pharmacologist colleagues, who repeated
his experiment with similar results. The drug was then taken by a group of
psychiatrists in Canada, including Humphrey Osmond, Abram Hoffer and Duncan
Blewett, all working at the Saskatchewan hospital in North Battleford. An
immediate result was they changed how they personally approached their patients
– 5they
recorded that they found themselves taking their schizophrenic patients’ accounts of their illness more seriously
after being put in their shoes for a while. They then began doing experiments
on patients, paying great attention to the “set” and “setting” of the
experience.
Set and
setting
6The LSD
trials at Saskatchewan were held in a loving and calm environment. A guide was
present to reassure the drug taker if they felt afraid, but who was otherwise
“self-effacing” – not imposing themselves on the experience. People were
screened psychologically before they were accepted onto the trials, and given a
lot of preparation about what was likely to happen. Afterwards, they could join
support groups to discuss what had happened, with others who’d been through the
same thing. The circumstances were conducive to a positive and insightful
experience that helped people understand in a new way their own actions and
motivations.
Other experiments,
however, were less successful. At another mental hospital in Canada staff
administered the drug and then tied the patients down to the bed while they
were intoxicated. Understandably, their experiences were far less positive. At
the same time, the USA military began experimenting with using LSD as a weapon
to see if they could immobilise whole populations. Recently-uncovered CIA files
suggest that an 7outbreak of
insanity in the French town of Pont-Saint-Esprit in 1951 may have been the
result of American agents deliberately contaminating a batch of bread with the
psychedelic, rather than accidental ergot poisoning as was thought at the time.
Whatever the cause, since those affected had no expectations about what was
going to happen, they were very disturbed by what they experienced.
LSD leaves the laboratory
In 1959 8Leary first
tried psilocybin, the active ingredient in magic mushrooms, and he soon began
experimenting with LSD as well. As someone deeply frustrated by the nature of
American society, he thought LSD was the silver bullet that would transform the
culture he lived in, from a materialist, self-centred, warlike society to one
based on principles of freedom, peace and love. Leary began conducting
experiments with both psilocybin and LSD on students and fellow lecturers. At
first the university authorities approved of the work, until they realised that
Leary had vastly overstepped the remit of the study design he’d agreed to. He
and his colleague Richard Alpert were expelled from the university. They then
continued their experiments in a mansion they bought in New York State.
Leary was extremely
outspoken about his intentions for LSD, which became known colloquially as
“acid”. He thought that everybody in America should be given it to open their
minds to new ways of thinking – they should “turn on, tune
in and drop out”. Many people tried it and did have positive experiences, but others who weren’t warned of the dangers
of the wrong set or setting had frightening “bad trips” which made them
extremely anxious and distressed. As the downsides of both “good” and “bad”
psychedelic experiences became known, LSD began to be seen as highly dangerous,
especially as some of those who had had their perspectives changed by the drug
started to become politically active.
There was a huge
backlash, and in 1966 LSD was made a Class A drug in the USA. The UK soon followed
suit. Even worse, it was placed in Schedule 1, as having no recognised
therapeutic uses, despite warnings from the scientific community that this
would seriously harm research into a set of drugs with unique properties for
treating mental illness. Leary popularised the drug so that everyone could
obtain it on the street, but also led to its prohibition so that it could no
longer be used in legitimate research.
What are the harms of LSD and psychedelics?
Psychedelics are
unpredictable, and taking them requires the right circumstances and proper
psychological preparation – if you took them unknowingly you’d think you were
going mad. People with existing mental-health problems such as schizophrenia
can find that psychedelics worsen their symptoms, and should probably avoid
them unless under medical supervision. In the early days, it was thought that
the effects of LSD were a model for schizophrenia, and it’s certainly true that
taking LSD gives healthy people an insight into that kind of mental
disturbance. However, although there is a similar sort of sense of ego
fragmentation, psychedelic drugs produce mostly visual changes, while with
schizophrenia the hallucinations are mostly auditory (eg 9“hearing
voices”). Psychedelics should probably also be avoided by those who have high
levels of anxiety as they’ll find the lack of control unsettling. Such people
are unlikely to be tempted to take them anyway – some of my patients are so
anxious they are frightened to take even an alcoholic drink (let alone take
LSD) in case it undermines their sense of self-control.
Obviously there is a
greater chance of having an accident if a lot of the normal “housekeeping”
functions in the brain aren’t operating, although the risk of this is often
overstated. For example, there is a common misconception that people who take
LSD will start believing they can fly and jump out of windows. There is no
evidence that this has ever happened, and it’s possible that this apocryphal
tale stems from 10an edition
of Spiderman in 1971 where a young man takes LSD and hurls himself off a building, only to be saved by the superhero. (It’s
worth pointing out that each year dozens of people in the UK severely injure or
kill themselves falling out of windows or off balconies and roofs while drunk.)
What are the benefits of psychedelics?
Not
only are psychedelics anti-addictive in themselves, but they may be useful in
treating addiction to other drugs. Some of the early trials in Saskatchewan
gave LSD to alcoholics, initially with the idea that if it gave them a bad
experience it might shock them out of their behaviour. What happened instead
was that the psychedelic gave some of them a new perspective on their lives,
helping them face up to the damage they were doing to their families and
friends, and this new empathy motivated them to change their behaviour. Similar
changes in thinking are often reported by alcoholics successfully completing
the 12-step AA programme. Since then there have been at least 11five other
studies that have found LSD helps people overcome alcoholism.
Many people describe
psychedelic experiences as profoundly meaningful, which may help them develop a
sense of purpose in life or envisage an alternative to being stuck in a rut
with alcohol. This may also extend to treating low moods more generally, as
many depressed people are stuck in a vicious cycle where their depression
prevents them doing anything to
alleviate their depression. LSD, psilocybin and similar drugs might open up a
different way of thinking, allowing people to improve their situation. (I am
now conducting a study funded by the Medical Research Council, to see if we can
use a single treatment with psilocybin to help people recover from depression.
We expect to have the results around 2015.)
On the more physiological
side, many people who suffer from 12cluster
headaches self-medicate with psychedelics, which seem to be the only effective
therapy for this disorder. These headaches are so severe that they can drive
people to the point of suicide. The vasoconstrictive properties (constricting
blood vessels in the head) of LSD and magic mushrooms somehow interrupt this
pain like no other drugs. As with MS sufferers denied cannabis, and terminal
cancer patients denied morphine, it’s utterly inhumane that the legal
restrictions on these drugs mean that the only way people suffering from these
disorders can get the medicine they need is by becoming criminals.
Should scientists take LSD?
One
line of enquiry which was being studied before LSD was made illegal was its 13use in
problem solving. This may seem surprising because most people find it hard to
focus when tripping, and it’s certainly true that people taking LSD don’t
perform particularly well on standard psychological tests.
As psychologist Arthur Kleps explained in 1966, “if I were
to give you an IQ test and during the administration one of the walls of the
room opened up giving you a vision of the blazing glories of the central
galactic suns, and at the same time your childhood began to unreel before your
inner eye like a three-dimensional colour movie, you would not do well on the
test.” However, psychedelics can induce creativity, by lowering the
psychological defences around “getting something wrong” and helping to see
problems from new angles. With the right set and setting, this can be directed
towards familiar problems, sometimes with spectacular results.
Taking LSD in this way has
been known to deliver moments of inspiration to designers, architects and
engineers. There are many stories about near-perfect technical designs which
have suddenly become obvious while contemplating the problem on the drug. In LSD – the Problem Solving Psychedelic, written in 1967, the
authors recount several examples of this. One was a furniture designer who
completed a chair design while on LSD which was successfully modelled into a
functional dining chair with no substantial changes from the original concept.
(These pieces of furniture are extremely difficult to create and the designer
was used to new chairs taking two months and ten trial models to complete.)
Another example was an engineer who worked in Naval Research and had been
trying to design an special detection device for five years without success.
Within minutes of contemplating the problem on LSD he had found the solution and the device was then patented and used by the US
Navy. A third example was an architect who took the drug to help him design a
shopping centre and was able to visualise it in its entirety: “Suddenly I saw the finished project. I did some quick
calculations … it would fit on the property and not
only that … it would meet the cost and income requirements … I began to draw
…my senses could not keep up with my images.” The image stayed with him
just as sharply after the drug experience had ended, and his design was
accepted and constructed.
Even in the
less-obviously creative fields of hard science, LSD can be profoundly
beneficial. In fact, it played a role in the two biggest discoveries in biology
of the 20th century. 14Francis
Crick, who discovered the double helix structure of DNA with James Watson, and 15Kary
Mullis, who invented the 16polymerase
chain reaction (PCR), had both taken the drug, and attributed some of their
understanding and insights to it. Mullis has gone so far as to say: “would I have invented PCR if I hadn’t taken LSD? I seriously doubt
it … [having taken LSD] I could sit on a DNA molecule and watch the polymers go
by. I learnt that partly on psychedelic drugs.”
Mushrooms and other psychedelics
17There are
many other kinds of psychedelic drugs that have different effects to LSD but
broadly share the same risks and benefits. The most common ones you’re likely
to encounter are covered here.
Psilocybin is found in psychedelic “magic” mushrooms. It’s inert itself, but
breaks down in the body to psilocin, which is a potent pyschoactive substance.
Psilocybin is found in mushrooms all over the world: we know most about their
history in religious ceremonies in South and Central America, but the Sami in
Siberia have a long history of using fly agaric mushrooms in shamanic rituals,
and it seems likely that magic mushrooms
were used by the ancient Greeks in the Elysian fields. Psilocybin’s effects are
very similar to LSD, but psilocybin is much shorteracting, lasting 20 to 30
minutes, so it’s much more practical than LSD for use in brain imaging when we
study the effects of psychedelics.
Ibogaine is the active ingredient in plants of the iboga family, native to West
Africa. It’s used within medical and ritual ceremonies in the Bwiti cult,
primarily in Gabon and Cameroon. It’s one of the most long-lasting
psychedelics, with trips sometimes going on for days. Ibogaine seems to be able
to prevent or minimise withdrawal symptoms from opiates and alcohol, which,
combined with the new perspective it gives people on their behaviour, may make it a highly effective treatment for
addiction. Several centres around the world are now using this approach,
although adequate clinical trials have yet to be conducted so we don’t know how
safe or effective it is, and it can’t be recommended. Ibogaine is legal in the
UK.
Why were magic mushrooms banned in the UK?
Psilocybin
occurs naturally in over 200 species of fungi which grow in the wild in many
parts of the world, including the UK. The species which is native to Britain is
psilocybe semilanceata, known as “liberty caps”,
which grow in shady and woodland areas in the autumn. It’s unclear how long
they’ve been deliberately used for their psychoactive effects: in the 18few
recorded incidents of people taking them accidentally, the unexpected sensory
distortions were experienced as poisoning. Although there are some theories
that they were used in pagan rituals in Britain in the past, there’s very
little evidence of this, and it’s possible that their effects were unknown or
unappreciated until the 1960s.
Magic mushrooms first
came to widespread attention in the west in 1957 after an amateur mycologist
and his wife took part in a 19Valeda
mushroom ceremony in Mexico. They recorded their experience in a magazine
article, which prompted scientists to start cultivating and investigating
different species, and of course Timothy Leary also helped popularise magic
mushrooms among hippies. British people picking and eating liberty caps in the
autumn, and having largely enjoyable and safe psychedelic experiences in the
countryside, was a common, popular and legal pastime until 2005.
In the early 2000s, the
British government started to become concerned about magic mushrooms. Some
companies had started importing them freeze-dried from the Netherlands and
selling them in shops in the Camden area of London, and this was generating bad
press in the tabloids. Rather than simply banning their sale, the government
decided to act “tough on drugs” and ban their possession altogether. They made
a rushed decision to place them in Class A, even though they were clearly much less harmful than other Class A drugs like crack and heroin. (The
government argument for categorising them this way was that pure psilocybin was
Class A, so the source of the chemical should be as well – although there was
little justification for psilocybin being in this Class in the first place.) If
they had consulted with us on the ACMD we could have told them that this
classification was inappropriate, but in their hurry to be seen to take action
they produced a badly-thought-out piece of legislation without seeking our
advice at all. (Arguably this was illegal, since consulting with the ACMD is
required by law). This was the beginning of the Labour government starting to
ignore the ACMD when passing drugs legislation – and the beginning of the end
for me.
Conclusion
One
organisation that has been campaigning for many years for this is the
Multidisciplinary Association for Psychedelic Studies (MAPS). Although MAPS
focuses mainly on research into treating conditions like post-traumatic stress
disorder and cluster headaches, it recognises the value of psychedelics outside
the medical setting. One of its founders, Rick Doblin, has suggested that
perhaps the way to make these sorts of drugs available in the future would be
to issue 20a licence
once someone has participated in a workshop, or perhaps passed a test, to
ensure that they know how to use them safely. Licensed users would understand
the importance of being in the right frame of mind and environment, and the
dangers and risks of a bad trip. Ideas like this are certainly something to
consider, given the enormous potential of psychedelics to improve people’s
lives.
Notes
1 (Figure 14.1),• Neural correlates of the
psychedelic state as determined by fMRI studies with psilocybin,
URL-171, Robin L. Carhart-Harris et al, PNAS, vol. 109 no. 6 2138–2143,
February 7th, 2012
2 a theory that the stories of magic and devils reported by the girls of
Salem• Egotism: The Satan loosed in Salem?, Linnda
Caporeal, Science (192), April 2nd 1976
3 “was seized by a
peculiar sensation of vertigo and restlessness … In a dreamlike state, I left
for home … With my eyes closed, fantastic pictures of extraordinary plasticity
and intensive colour seemed to surge towards me.”• LSD: my problem child, Albert Hofmann, McGraw-Hill Book Company,
1980
4 “I lost all
control of time• As above.
5 they recorded that they found themselves taking their schizophrenic
patients’ accounts of their illness more seriously• Hofmann’s
Potion: The Early Years of LSD, Connie Littlefield, URL-120, 2002
6 The LSD trials at Saskatchewan• As above.
7 outbreak of insanity in the French town of Pont-Saint-Esprit in 1951• A terrible mistake, Hank Albarelli, Trine Day, 2009
8 Leary first tried psilocybin, the active ingredient in magic
mushrooms, and he soon began experimenting with LSD as well• Hofmann’s Potion: The Early Years of LSD, Connie
Littlefield, URL-120, 2002
9 “hearing voices”• Schizophrenia, National
Institute of Mental Health, URL-118.
10 an edition of Spiderman in 1971• The Amazing
Spiderman issues #96–98, Stan Lee, Marvel Comics, May–July 1971
11 five other studies that have found LSD helps people overcome
alcoholism• Lysergic acid diethylamide (LSD) for alcoholism:
a meta-analysis of randomized controlled trials, Teri S. Krebs and
Pal-Orjan Johansen, Journal of Psychopharmacology, 2011
12 cluster headaches self-medicate with psychedelics• Will
Harvard drop acid again?, Peter Bebergal, URL-121, June 9th 2008
13 use in problem solving• LSD – The Problem Solving
Psychedelic, PG Stafford and BH Golightly, Award Books, 1967
14 Francis Crick• Nobel
Prize Genius Crick was High on LSD when he discovered the secret of life, Alun Rees, the Mail
on Sunday, August 8th 2004
15 Kary Mullis• BBC Horizon – Psychedelic Science –
DMT, LSD, Ibogaine – Part 5, BBC, 1997
16 polymerase chain reaction (PCR)• The polymerase chain reaction is used
to “amplify” a small amount of DNA, to produce a larger quantity that makes
testing possible or easier. It is used every day in every aspect of life
sciences, including forensic investigation and medical diagnosis.
17 There are many other kinds of psychedelic drugs• High
Society, Mike Jay, Thames & Hudson, 2010
18 few recorded incidents of people taking them accidentally• As above.
19 Valeda mushroom ceremony in Mexico• Seeking the
magic mushroom, Robert Gordon Wasson, Life Magazine, June 10th 1957
20 a licence once someone has participated in a workshop, or perhaps
passed a test, to ensure that they know how to use them safely• Will Harvard drop acid again?, Peter Bebergal, URL-121,
June 9th 2008
1“Public enemy number one in the
United States is drug abuse. In order to fight and defeat this enemy, it is
necessary to wage a new, all-out offensive.” Richard Nixon, 1971.
The
other “war on drugs”
High-strength
drugs have been a common feature of battle zones, starting with the use of gin
by William of Orange’s soldiers (and hence the phrase “Dutch courage”). Large
quantities of morphine were made available to soldiers in the Franco-Prussian
and American Civil wars and were especially popular after the invention of the
hypodermic syringe. Cigarettes were popularised by Turkish troops in the
Crimean War and the expansion of the cigarette market was helped by the
inclusion of cigarettes in ration packs in the two World Wars. A common effect
of fighting in a war is post-traumatic stress disorder (PTSD) – which was known
as “shell shock” in the World War I and “battle fatigue” in World War II. In
the past, PTSD was treated with bromides and barbiturates, and trials are currently being conducted on the use of psychedelics and
ecstasy to treat the disorder in soldiers. For many veterans past and present,
however, the most reliable and accessible drug for dealing with the trauma of
war has been alcohol. The twentieth century also saw the widespread use of
stimulants to enhance performance on the battlefield, though it’s arguable they
may have been more of a hindrance than a help. (See box Amphetamines
and war below.)
What’s surprising to us
today is not so much that these drugs were used in the context of war, but how
widely known and accepted the practice was. During World War I, 2Harrods
sold gift packs containing cocaine and heroin with the tag-line “a welcome present for our friends at the front”, and during
World War II there were advertisements encouraging people to “send your boys Benzedrine”. (Benzedrine is an amphetamine.)
But whereas these drugs were dispensed or approved by military doctors, for
performance enhancement and pain relief, the use of drugs by USA troops in
Vietnam was unsanctioned, and mostly involved cannabis and opiates. 3Around 50%
of the troops tried opium and heroin, half of whom started showing signs of
addiction; two thirds of the troops used cannabis regularly. What frightened
the Nixon administration was the prospect of large numbers of addicts flooding
back into civilian life as the war settlement was negotiated and the military
demobilised. This, coupled with the highly-public use of cannabis and
psychedelics by the flower power counter-culture, created the cultural
background to the War on Drugs. In fact, most of the USA soldiers using opioids
in Vietnam stopped easily once back in the safety of the USA.
Amphetamines and war
The
use of drugs has historically been common in the military, with soldiers trying
to survive physical danger and lack of sleep and cope with the psychological
trauma of experiencing and inflicting violence. Today, Western armies have
strict drug-testing regimes because of concerns that drugs will impact on
soldiers’ health and performance in the theatre of
war. But there was a time when the widespread use of certain substances,
particularly stimulants like amphetamine, were thought to hold the key to
military superiority. This theory was tested to its limit during World War II.
Amphetamine was the drug
of choice for the Allies – 4the British
alone used 70 million amphetamine tablets over the course of World War II –
which helped soldiers to stay awake and alert for long hours. The Germans,
meanwhile, were dosed up on Pervitin, a pill form of methamphetamine. Today,
the most widely-used form of methamphetamine is the freebase that can be
smoked, commonly known as “crystal meth” because it looks like a crystalline
rock. (Crystal meth has a similar relationship to amphetamine as crack cocaine
to cocaine powder.) When methamphetamine is smoked, it is more powerful and
addictive than amphetamine partly because it reaches the brain faster. However,
even when both drugs were being taken orally as pills in World War II, the
methamphetamine in Pervitin worked faster than the amphetamine in Benzedrine,
giving bigger highs, more energy, and helping soldiers stay awake for longer –
at least at first.
As the war progressed, it
became clear that these drugs were addictive, and that any performance
improvement they created was at best short lived; the advantage of increased
energy was soon outweighed by side-effects, including irritability,
restlessness, inability to focus, and psychosis. Another classic side-effect
was the development of stereotypy – involuntary,
repetitive movements or behavioural patterns that impair the person’s cognitive
flexibility and judgement. This could be
extremely dangerous when flying planes or handling guns and weapons.
Methamphetamine takes longer to be processed by the body so its side-effects
last longer, as well as being more severe, and it produces more withdrawal
exhaustion when it is stopped. 5After 1941,
Pervitin was dispensed with much more discretion. (It’s possible that the
choice of drug affected outcomes of battles such as the North African campaign,
because the amphetamine-taking Allies were more likely to able to sleep during
the day, while the methamphetamineu-sing Germans couldn’t rest and couldn’t
think as flexibly.)
Amphetamines are also
given to soldiers in non-government armies under conditions where unpredictable
behaviour rather than strict discipline are seen as advantages, such as in
unconventional war zones. 6Child
soldiers in Sierra Leone, for example, are often dosed up on amphetamines
before they fight, to make them more violent and less fearful – and the
militias who recruit them probably think children who develop amphetamine
psychosis make better soldiers. Disarming and rehabilitating these children is
especially difficult as many are also dealing with drug addiction when they try
and re-enter civilian life.
The aims of the War on Drugs
Nixon’s
speech came ten years after the 71961 UN Single Convention on drugs.
This had already set the tone of the debate as a moral battle in which the use
of certain sorts of drugs for pleasure was an evil to be eradicated, rather than a public-health issue to be
managed. To quote the Convention Document, those who made the legislation were:
·
Concerned with the health and
welfare of mankind.
·
Conscious of their duty to prevent
and combat this evil.
The War on Drugs has been
very costly, and it would seem logical to try and work out whether it has
achieved its stated aims. When we try and evaluate the success of these
policies, we need to ask three questions. (A) Has the War on Drugs reduced
supply? (B) Has it reduced demand? And (C) has it minimised harm?
A. Has the War on Drugs reduced supply?
In
2003, 8The No. 10
Downing Street Strategy Unit produced an analysis of the harm caused by heroin
and crack use in the UK, and gave a comprehensive overview of the supply-side
strategies employed in the War on Drugs. These interventions have ranged from
trying to reduce the production of the raw materials in source countries, to
targeting street dealers in the UK. The aim has been to restrict the supply of
drugs to consumers, so price rises and users consume less. The report evaluated
the effectiveness of each of these strategies in turn.
Whatever the approach,
the report pointed out that higher-up members of the drugs trade rarely suffer
when supply-side interventions focus on farmers. Instead, the high-ups move to
remote regions or different countries when attempts to control production start
to take effect. Given the unequal terms of trade for most export commodities that
small-scale farmers grow (such as coffee and sugar), it is never difficult for
organisations with money to persuade or coerce them into switching to illicit
crops. The report concluded that as long as there is a lucrative market for drugs in rich countries, and large numbers of easily exploited farmers
in poor countries, it will be almost impossible for us to reduce substantially
the quantity of drugs produced.
Once drugs arrive in the
UK they are bought by wholesalers and distributors, and though police and
customs do try to disrupt this part of the supply chain, it’s very
resource-intensive and difficult to make an impact as we know relatively little
about this part of the supply chain. A far easier target is the thousands of
street dealers. High-visibility policing can reduce their presence, and appease
the public and media demands for action on drugs. But dealers are easily
replaced and in any case removing a dealer removes only small quantities of
drugs from the system. Disrupting retailer
activity in the UK occupies a lot of police and court time, but doesn’t stop
people who want drugs getting their hands on them.
B. Has the War on Drugs reduced demand?
|
|
Opiates |
Cocaine |
Cannabis |
|
1998 |
12.9 million |
13.4 million |
147.4 million |
|
2008 |
17.35 million |
17 million |
160 million |
|
% increase |
34% |
27% |
8% |
Whether we’re talking
about problem drug users addicted to heroin and crack, or recreational users
who occasionally smoke cannabis, a quick glance at official statistics (9Table 15.1)
shows that the War on Drugs has failed to reduce demand. Although precise
figures are hard to come by, the UN estimates of annual drug consumption across
the world from 1998 to 2008 show a substantial increase for opiates, cocaine
and cannabis, and there’s no reason to believe that there have not been similar
increases for amphetamines, ecstasy, and new designer drugs. The proud
exhortation of the UN in 2001 that we’d have a drug-free world in 2010 has been
exposed as a ridiculous rhetoric rather than a thought-out plan.
Although the War on Drugs
is presented as a war on producers and dealers, in
practice the focus has always been on the much easier target – the users. (Many
of these are small-scale dealers themselves, selling to a handful of people in
order to fund their own habits.) Addicts have a disease and are not in control
of their actions, so putting them in prison is not only inhumane and extremely
expensive, but it’s completely useless in helping them manage their addiction.
(10Only a fifth of the 50,000
problem drug users who end up in jail in the UK every year are given
treatment.) Getting a criminal record or going to jail reduces the addicts’
chance of being able to rebuild their lives even if they do stop using the
drugs. Moreover the stress, boredom, and culture of prison creates more
addicts, rather than incentivising them to give up. 11About 20%
of prisoners are addicted to opiates, and 7% try heroin for the first time in
jail. Overall, targeting and imprisoning drug users does not reduce demand.
In general, criminal
sanctions have very little influence on the prevalence of drug use in a
population, which seems to be affected more by cultural trends, fashion and
norms than the legal framework. 12A
comparative study of Australian states found that there was no relationship
between how punitively the criminal justice system treated cannabis and levels
of cannabis use, and this lack of correlation is replicated world-wide.
Government-led education programmes, such as the 13USA’s Drug
Abuse Resistance Education (DARE) programme (which also operates in the UK) has
been found in some instances to increase drug use
among participants in the short-term, probably because the children involved
have developed an interest in the substances they’ve been told to “Just Say No”
to. Over the long-term, research has found no difference between participants
and non-participants, and 14in 2001 the
US Surgeon General placed the DARE programme in the category “Does Not Work”.
Does criminalisation reduce the drug supply?
Locking
up large numbers of people might be considered worthwhile if it reduced the
supply of drugs to others. Is there any evidence that this is the case? The
problem is, the people that go to prison are the wrong ones. Across the world, 15two million
drug offenders are currently in jail – about a quarter of the total prison
population. Most are imprisoned for non-violent
crimes, and most are at the very bottom of the drugs trade – small-scale
dealers, user-dealers, drug mules who take small quantities over borders, and
those convicted for possession.
On the rare occasions
that people higher up within criminal organisations are arrested, bribes and
expensive lawyers can usually secure their release. And even when drug cartels
are successfully smashed by law enforcement agents, this doesn’t reduce harm,
and may even increase it as competing groups battle over the new markets. As
long as the demand remains, somebody will produce the drugs to meet it. 16Small-scale
seizures and imprisoning those at the very bottom of the supply chain has no
dampening effect on the business.
C. Has the War on Drugs minimised harm?
The
short answer is, no. In fact it has done the opposite: it has increased harm
for pretty much everyone. This is a well known amongst policy-makers, though
rarely openly acknowledged. The most controversial aspect of the No. 10
Strategy Unit Report was its attempt to evaluate whether supply-side
interventions might have been successful at harm reduction, pointing out that “current policies are underpinned by an assumption that reducing
drug availability and increasing price reduces harm.” The report heavily
implied that this assumption was false, since there is little evidence that (a)
supply-side seizures are able to reduce availability and increase price or (b)
that overall levels of harm respond in any straightforward way to changes in
price or availability where they do occur. 17The report,
unsurprisingly, was suppressed by the government, but released under the
Freedom of Information Act and leaked to the media and is now available online.
This is a common pattern: anything that tries to measure or evaluate the
success of the War on Drugs inevitably finds that it has failed, so evaluation
and measurement are either suppressed, or not carried out in the first place.
In terms of demand-side
interventions, some of this increase in harm has been intentional – primarily,
the harm caused by criminalising millions of people around the world. But a
great many other sorts of harm have been
more or less accidental, perverse effects which although predictable were not
intended by those who instigated the War. These “perverse effects” include:
1.
Increasing the spread of infectious
disease.
2.
Causing terminally ill people to
die in agony.
3.
Increasing instability and
unaccountability in financial systems.
4.
Holding back research on new
medicines.
5.
Increasing levels of drug-related
violence and crime.
6.
Increasing the number of users by
forcing them to become dealers.
7.
Bringing the law into disrepute;
allowing discriminatory policing.
8.
Diverting attention away from the
dangers of alcohol and tobacco.
1. Increasing the spread of infectious disease
Injecting
drug users are a group who are particularly vulnerable to health problems from
blood-borne viruses such as hepatitis and HIV. Across the world, 183 million
injecting drug users are living with HIV, and another 13 million are at risk of
contracting it. This poses a public-health risk not only to the users
themselves, but to their families, sexual partners, and others in society.
Harm-reduction measures such as needle exchanges have been shown to reduce
dramatically the prevalence of blood-borne viruses among drug users. However,
some countries have taken the attitude that, since this group is using
substances controlled under the international conventions of the War on Drugs,
they shouldn’t have access to clean needles to reduce their chances of becoming
infected, or treatment if they do become unwell.
The situation is
particularly bad in Russia, where the failure to implement needle exchange
programmes or other harm reduction approaches when HIV appeared has resulted in
one of the highest new infection rates in the world today – 19about
60,000 new cases in 2009, according to theUN AIDS program. 20Two thirds
of these cases are linked to intravenous drug use, and many of the remainder
are the result of sex with drug users. In some cities, antiretroviral medicines
to treat AIDS are denied to drug users, speeding up their progression from HIV
to AIDS.
There are other indirect
health problems that result from this denial of healthcare to injecting drug users. Living in poverty for many years
with low immunity and irregular or inadequate access to medication means that
many of these people develop 21“TurBo-HIV”,
contracting TB on top of the immunodeficiency virus. Many treatment programmes
will only treat them for one health problem at a time, forcing them to choose
between being treated for their addiction or for their TB. Since drug users’
lives are often chaotic anyway, being unable to receive holistic care means
that they often move between different treatment programmes, stopping and
starting courses of different sorts of medication – exactly the circumstances
that cause viruses to mutate. The result is one of the highest rates of
multidrug-resistant TB in the world, a hazard to health that extends beyond the
users themselves, affecting Russian society at large. This situation could
largely have been prevented if injecting drug users had been viewed as sick
patients requiring medical help; instead, the attitude fostered by the War on Drugs
was that they were immoral people deserving punishment.
2. Causing terminally ill people to die in agony
While heroin is a harmful
drug, it’s perverse if trying to reduce its use forces many people with
terminal cancers 22to live the
last months or years of their lives in agony, when an adequate supply of cheap
morphine tablets would make them bearable. The palliative-care movement within
the Indian state of Kerala has managed to relax the rules around the prescription of opiates, but in 27 other Indian
states it remains almost impossible to provide morphine for those who need it
most. (This is particularly galling as India is one of the world’s biggest
suppliers of opium, and morphine tablets cost only pennies to produce.)
Campaigning groups such as Human Rights Watch have argued that freedom from
pain should be considered a human right, and have compared the testimonies from
terminal cancer patients without access to painkillers to the testimonies of
those who have suffered torture. They continue to campaign to remove medical
morphine from the War on Drugs.
3. Increasing instability and unaccountability in financial systems
The
illicit drugs trade is the second largest in the world, second only to oil. The
money involved – perhaps 23£300
billion a year – is about 1% of the global economy, and operates almost
entirely under the radar, untaxed and unregulated.
Drugs money is laundered
through front companies and tax havens, and then integrated back into the
mainstream banking system so that criminal organisations can have access to
“legitimate funds”. A number of different techniques are used, such as
small-scale electronic transfers and false invoicing: it’s been estimated that 24in Panama
there is a £1 billion gap every year between money entering and goods exported,
with the difference plugged with the proceeds of various sorts of crime,
primarily drug trafficking.
25Banks, in
turn, are complicit in this process, failing to report or record suspicious
activity, because some are controlled by criminal organisations, and perhaps
also because offshore banking services depend on secrecy for tax evasion and
avoidance. Exposing the activities of drug traffickers would expose the
activities of other clients. Making it easier for large volumes of money to
travel the world without any kind of accountability undermines governments and
is dangerous for the financial system as a whole. There were many causes of the
financial crisis which began in 2008, but a chief reason that the asset bubble
in subprime housing was able to grow so large was that the people in charge of
the banks had no idea where their money was coming from or where it was being invested. In 2010, a single bank, 26Wachovia,
paid $160m to settle a US federal investigation into laundering of illegal drug
money through Mexican currency exchanges. This included a $50m fine for failing
to monitor money used for shipping 22 tons of cocaine. 27Wachovia was
unable to check about $400bn’s worth of transactions to see if money was being
laundered. For such huge sums to pass through a bank’s system without raising
comment shows a very worrying lack of concern for the law and transparency in
financial transactions.
4. Holding back research on new medicines
5. Increasing levels of drug-related violence and crime
As we
discussed in chapter 10, the drugs trade is responsible for very high levels of
violence and crime, both internationally and at home. Attempts to meet this
head-on tend to make the problem worse: often it’s 28when a
government says it’s going to “crack down” on the illicit trade that violence worsens,
as we’ve certainly seen in Mexico.
The criminal organisations
that supply drugs are often involved in people-trafficking and modern slavery,
and they actively work to corrupt and destabilise governments. 29Al Qaeda is
principally funded by opium and cannabis production, and 30Mexican drug
cartels are involved in kidnapping, counterfeiting and business extortion, as
well as being responsible for tens of thousands of murders.
The
corrupting effects of drug money have been seen most recently in the West
African countries which have become the transit routes for cocaine travelling
from South America to Europe. In an address in December 2007, UN Office on
Drugs and Crime (UNODC) Executive Director Antonio Maria Costa described
Guinea-Bissau as 31“under siege. The threat posed by drug traffickers is so great that the
state is on the verge of collapse … So much drug money flowing in so easily, is
a true curse: it is perverting the economy and rotting society.” In 2010, the leaders of both the army and the navy were sanctioned for
trafficking cocaine, showing that this corruption has reached to the highest
levels.
In the UK, drug users
commit a very high proportion of acquisitive crime. 3285% of
shoplifting and 80% of domestic burglary is committed by problem drug users,
which is unsurprising considering that a heavy heroin habit costs £300 a week,
and a bad crack addiction can cost over £500 a week. 33There are
over 300,000 problem drug users in the UK, but surprisingly, it is a hard-core
of 3430,000 who commit over half of
all drug-related crime, costing the country £11 billion a year, or £360,000
each. Providing a methadone or heroin prescription for these people would cost
a fraction of £360,000, but many users are afraid to begin treatment programmes
because of the possibility that once the authorities know they use drugs, they
will be targeted and imprisoned.
6. Increasing the no. of users by forcing them to become dealers
35In 1955,
there were 57 registered heroin addicts in the UK. Most of these were under the
medical supervision of their GP who helped to treat or manage their addiction.
This option was then outlawed, as “public” opinion saw it as the state
condoning a drug-using lifestyle. (The new UK coalition government is
resurrecting this old rhetoric as it tries to save money and appease voters by
stopping substitute prescribing – see page 167.) Today, there are estimated
to be at least 300,000 registered addicts, with fewer than half going into
treatment over the course of each year. While there were many social, demographic
and technological changes fuelling this huge rise in the number of addicts, one
was undoubtedly the fact that creating a black market for drugs simultaneously created drug “pushers” – people with an incentive
to get others hooked on addictive drugs in order to make money. Many of the
pushers were addicts themselves who had to buy heroin illegally, now that they
no longer received heroin on prescription. They found small-scale dealing was
the easiest source of funds, creating a kind of pyramid scheme where every
addict created ten or more new ones. In fact, in 1955 the government was warned
that this would be an effect of banning the drug, in an article published in The Times in 1955 entitled 36The Case for Heroin. Over five decades
later, they’ve certainly been proved right, and at last we have some 37new trials
of heroin-prescribing under way with promising results.
7. Bringing the law into disrepute; allowing discriminatory policing
In
2000, an enquiry led by 38Viscountess
Runciman produced a report into the policing of drugs in the UK, with a
particular focus on cannabis. The report concluded that:
“There can be no doubt that, in implementing the law, the present concentration
on cannabis weakens respect for the law … It gives large numbers of otherwise
law abiding people a criminal record. It inordinately penalises and
marginalises young people for what might be little more than youthful
experimentation. It bears most heavily on young people in the streets in cities
who are also more likely to be poor and members of minority ethnic communities.
The evidence strongly indicates that the current law and its operation creates
more harm than the drug itself.”
The Runciman report also
found evidence of political or discriminatory policing. Individual police
officers were given a large degree of personal discretion about how strictly
they enforced laws on cannabis. This let some police officers pursue other
agendas, such as the control of young men from ethnic minorities by
disproportionately prosecuting them for possession, as illustrated clearly by
the official statistics on stop-and-search and court procedures. The Runciman
report was pivotal in cannabis being downgraded from Class B to Class C, but
the drug was re-graded shortly afterwards,
and ten years on discriminatory policing continues. 39People from
black communities are 6 or 7 times more likely to be arrested if they’re found
with drugs than people from other ethnic groups, and 11 times more likely to be
imprisoned. This sours the relationship between these communities and the
police, normalises criminality, and was a significant factor in provoking the
2011 riots in London.
8. Diverting attention from the dangers of alcohol and tobacco
40Each year,
tobacco kills 5 million people across the world, while 41alcohol
kills 1.5 million. By comparison, 42illicit
drugs kill around 200,000 people between them. Even taking into account the
much smaller populations who use these drugs, in many cases they are
considerably less deadly. Yet the levels of money and political will expended
on trying to eradicate their use far exceeds the levels spent on public-health
measures to reduce the harms of alcohol and tobacco. In addition, the small
expenditure on reducing alcohol and tobacco consumption is counteracted by
advertising from the drinks and tobacco industries which associate these drugs
with health and beauty. Politicians often say that criminalisation is designed
to “send a message” that the use of certain drugs is unacceptable because of
the harm they cause to individuals and society. Unfortunately, the resultant
message perceived by many millions of people around the world is that alcohol
and tobacco are acceptable – and we all pay the price for that.
Why
are we still at war?
After
forty years, thousands killed, millions imprisoned, and 43$1 trillion
spent (44or $2.5 trillion depending on
who you ask), we are still no closer to controlling either the supply- or
demand-side of the illicit drug trade. Government interventions on the supply
side are seen as a cost of business, like a tax rather than a serious threat;
and the billions spent on DARE programmes and locking up users haven’t stopped
the inexorable rise of drug use in most parts of the world. In its own terms,
the War on Drugs has failed, and the evidence shows it was also the wrong
strategy for
harm reduction. The intentional and perverse effects of the war have spread
disease, held back medical research, brought the law into disrepute, and ruined
the lives of millions.
But still our politicians
keep fighting, at least while they hold power. 45Mo Mowlam,
who had been responsible for Tony Blair’s anti-drugs policies, called for full
legalisation after she’d left politics in 2002. Former Home Secretary 46Bob Ainsworth
spoke out about decriminalisation when safely out of the Cabinet and in
opposition. Former presidents 47Bill
Clinton and Jimmy Carter criticised the War on Drugs in a recent documentary. 48Jimmy
Carter wrote an article entitled Call Off the Global Drug
War in The New York Times, and in November
2011, along with many Nobel prizewinners, international statesmen, and other
public figures, wrote a public letter entitled 49The Global War On Drugs Has Failed: It Is Time For A New Approach. And in 2002, an ambitious UK backbencher called David Cameron said in
a debate in the House of Commons 50“drugs policy has been failing for decades”. Yet now that
he’s Prime Minister, Cameron talks just as “tough on drugs” as every other
politician, and Obama, while supporting having a more open debate on drugs
policy, always takes pains to make it clear he himself is absolutely committed
to prohibition.
Our politicians have
backed themselves into a corner. In making the “tough on drugs” stance the only
electorally-viable policy, and attacking anyone who proposes an alternative,
they are forced to ignore the evidence all around them and the solutions that
follow from seeing the world as it is, not as we pretend it is to fit in with a
given political view point. This
may be an easy vote winner at election time, but in the longer term it’s bad
for democracy, bad for science, and bad for the millions of casualties around
the world affected directly and indirectly by this unwinnable War.
What are the alternatives?
If you
criticise the War on Drugs, the stock media response is to accuse you of
wanting to see heroin “on the supermarket shelves”. This is a
ridiculously-reductive response to the wide range of options available for
dealing with drugs once prohibition stops being the only policy that can be
considered. For a start, there is a big difference between legalisation and
decriminalising possession. In Portugal, heroin, cocaine and cannabis remain
illegal, but possession of small amounts doesn’t carry any criminal sanctions,
like minor traffic offences in the UK. Decriminalisation allows countries to
focus on harm-reduction strategies while staying within the terms of the UN
Single Conventions, but leaves all the supply-side problems intact. If we
wanted to go further and make certain drugs legally available, 51there are
lots of alternatives to unregulated sales:
·
Making drugs available on
prescription, so your doctor can monitor your use and help you through
withdrawal if you wish to stop.
·
Licensed premises for consumption
on site, like pubs or the Dutch cannabis cafes. These licences could be
exclusive, so that a place which is allowed to sell ecstasy can’t sell alcohol,
for example, and licensees could be partially responsible for the behaviour of
their customers. The Dutch coffee shops that sell cannabis are not only banned from selling alcohol, but also don’t allow tobacco smoking on
the premises.
Comparing the harms of smoking cannabis with going to prison
Even
though UK police officers often choose not to arrest or prosecute people when
they’re caught with cannabis, it remains the most common illicit drug to come
before the courts because it’s by far the most commonly used. Smoking cannabis
and taking other drugs is a unique type of crime because it’s a crime against
yourself – the state has decided that the harms are so great you should be
penalised, even to the point of imprisonment, to protect you from it. This only
makes sense as a harm-reduction measure if taking cannabis is considerably more
harmful than going to jail. The main concerns people have about
cannabis are that: it causes mental-health problems; it’s a gateway to other
sorts of more harmful drugs; it might impair your career; it can lead to
addiction; and it imposes economic costs on society. Let’s compare for a moment
these harms done by smoking cannabis and the harm done by going to prison.
Cannabis can certainly
cause mental-health problems. As discussed in chapter 5, when I was on the ACMD
we calculated that around 52one in 5000
cannabis users will develop schizophrenia as a result of using the drug, and
more will suffer short-term psychotic symptoms and depression. There is a risk,
but it’s relatively low. Going to prison on the other hand, is associated with
very high levels of stress and depression. 53Prisoners
are about 10 times more likely to commit suicide than the general population,
and 54about 40% of men and 60% of
women have some form of neurotic disorder. (Although these conditions may have
preceded going to jail, making it difficult to establish cause-and-effect,
these confounding factors are also true for cannabis.) Imprisoning people for
using cannabis is clearly not going to protect their mental health.
If
anything, prison is the biggest gateway of all, being awash with drugs and
having very little in the way of other sorts of stimulation or sources of
pleasure. Opiate use is particularly high, and 7% of prisoners say they first
tried heroin in jail. The fact that Justice Secretary 55Ken Clarke
has been talking about “drug-free wings” in prisons is an open acknowledgement
of the fact that even in the state’s most tightly controlled spaces of all we still
can’t control the supply of drugs. In fact, attempts to deter substance abuse
through drug testing in prisons is actually making this gateway effect more
severe. Cannabis and its breakdown products can be detected in urine for weeks,
whereas heroin clears from the body much faster. Testing positive for drugs can
result in an increase in sentence, so prisoners have found a way to reduce the
likelihood of being caught: use heroin instead of cannabis. Far from protecting
them, imprisoning cannabis users will make them more likely to start using hard
drugs.
It’s unlikely that
anyone’s career is seriously impaired these days by admitting that they’ve
tried drugs. Many of our MPs feel they can acknowledge cannabis use now, and
Obama has even admitted to having taken cocaine, though British politicians
have yet to be so honest. Although heavy use and addiction disrupts working
life, low levels of cannabis consumption seem quite compatible with it, and may
even be beneficial for some creative people. Prison, in contrast, is definitely
bad for your career. 56Research by
the Department of Work and Pensions has found that the unemployment rate of
ex-offenders is over 50%, and having a criminal record of any sort makes
rejection probable for around 50% of job vacancies.
We say that someone is
addicted when they keep repeating behaviour despite adverse consequences. About
5710% of
cannabis users become dependent, exposing themselves to health risks from heavy
use, and falling behind at school or under-performing at work because they
spend so much time intoxicated. Although it’s hard to make a direct link
between addiction to a drug and criminal behaviour, reoffending could be seen
as comparable to addiction because even though someone’s life has been harmed
by committing crime they still end up repeating
criminal behaviour. Ministry of Justice figures in 2010 showed that 5850% of
prisoners re-offend, in large part because when they leave prison they find it
so hard to get a job or housing, which are the two most important factors in
helping people stay away from crime. Imprisoning people for cannabis use is
likely to get them caught up in a cycle of crime far more damaging that being
addicted to the drug.
Finally, there’s the
issue of economic cost. While the economic burden of cannabis use is hard to
calculate, it must be far lower than the 59£38,000 it
costs to keep somebody in prison for a year, and support them afterwards when
they’re unemployed or suffering mental-health problems. Imprisoning cannabis
users places a huge burden on the police and courts, far greater than the drug
itself.
So, prison is worse for
people’s mental health, more likely to lead to hard drug use, more likely to
ruin someone’s career, more likely to lead to a cycle of destructive behaviour,
and is far more expensive for society than cannabis: imprisoning people for
using cannabis increases harm, rather than reducing it. An alternative model
for punishing those caught in possession of cannabis is the “Cameron approach”.
When 60David
Cameronwas caught with the drug at Eton, he was made to write out hundreds of
lines of Latin; there are certainly thousands of young people across the UK
whose lives would be immeasurably improved if this became public policy.
Notes
1 “Public enemy number one in the United States is drug abuse• The Nation: The New Public Enemy No.1, URL-122, June 28,
1971
2 Harrods sold gift packs containing cocaine and heroin• Can we imagine a Britain where all drugs are legal?, Mark
Easton, URL-123, December 16th 2010
3 Around 50% of the troops tried opium and heroin• Narcotic
use in Southeast Asia and afterward: An interview study of 898 Vietnam
returnees, LN Robins, JE Helzer, DH Davis, Archives of General Psychiatry,
32(8), 955–961, 1975
4 the British alone used 70 million amphetamine tablets over the course
of World War II• Concepts of Chemical Dependency,
Harold E Doweiko, Cengage Learning, 2009
5 After 1941, Pervitin was dispensed with much more discretion• Psychotherapy in the Third Reich: the Göring Institute,
Geoffrey Cocks, New Brunswick, NJ, 1997. Orders were given that Pervitin was to
be kept “under lock and key” once side effects were recognised by military
doctors.
6 Child soldiers in Sierra Leone, for example, are often dosed up on
amphetamines before they fight• URL-156.
7 1961 UN Single Convention on drugs• Office
of Drugs Control, URL-22, 1961
8 The No. 10 Downing Street Strategy Unit produced an analysis of the
harm caused by heroin and crack use• Strategy Unit Drugs
Report Phase One – Understanding the Issues, URL-124, May 12th
2003
9 Table 15.1• Reproduced from p4 of War on Drugs: Report of the Global Commission on Drugs Policy, URL-125, June 2011
10 Only a fifth of the 50,000 problem drug users who end up in jail in
the UK every year are given treatment• Strategy Unit Drugs
Report Phase One – Understanding the Issues, URL-124, May 12th
2003
11 About 20% of prisoners are addicted to opiates, and 7% try heroin for
the first time in jail• Compendium of Reoffending
Statistics, URL-127, May 10th 2011
12 A comparative study of Australian states found that there was no
relationship between how punitively the criminal justice system treated
cannabis and levels of cannabis use• The impact of cannabis
decriminalisation in Australia and the United States, Eric Single, Paul
Christie and Robert Ali, Drug and Alcohol Services Council South Australia, URL-128, 1999
13 USA’s Drug Abuse Resistance Education (DARE) programme• Youth illicit drug use prevention: DARE long-term evaluations and
Federal efforts to identify effective programs, United States General
Accounting Office, URL-129, January 15th 2003
14 in 2001 the US Surgeon General placed the DARE programme in the
category “Does Not Work”• Youth violence: A report of the US
Surgeon General (chapter 5), David Satcher, URL-130, 2001
15 two million drug offenders are currently in jail – about a quarter of
the total prison population• After the War on Drugs –
Options for Control, Transform Drugs Policy Foundation, URL-131, February
2006
16 Small-scale seizures and imprisoning those at the very bottom of the
supply chain has no dampening effect on the business• Strategy
Unit Drugs Report Phase One – Understanding the Issues, URL-124, May 12th
2003
17 The report, unsurprisingly, was suppressed by the government, but
released under the Freedom of Information Act and leaked to the media and is
now available online• No 10 Strategy Unit Drugs Project:
Phase 1 Report: “Understanding the Issues”, Transform, URL-132, accessed
December 10th 2011
18 3 million injecting drug users are living with HIV, and another 13
million are at risk• Injecting Drug Use and HIV, UNAIDS,
URL-133, accessed December 12th 2011
19 about 60,000 new cases in 2009• Inadequate Fight
Against Drugs Hampers Russia’s Ability to Curb HIV, Michael Schwirtz, URL-134, 16th
January 2011
20 Two thirds of these cases are linked to intravenous drug use, and many
of the remainder are the result of sex with drug users• Russia’s
HIV care must centre on drug users, Maria Golovanevskaya, URL-135, January
26th 2011
21 “TurBo-HIV”, contracting TB on top of the immunodeficiency virus• Tur-BoHIV, Timur Islamov Charitable Foundation, URL-136, 2010
22 to live the last months or years of their lives in agony,• The Pain Project, Al Jazeera, URL-137.
23 £300 billion a year – is about 1% of the global economy• After the War on Drugs – Options for Control, Transform
Drugs Policy Foundation, URL-131, February
2006
24 in Panama there is a £1 billion gap every year between money entering
and goods exported• Strategy Unit Drugs Report Phase One –
Understanding the Issues, URL-124, May 12th
2003
25 Banks, in turn, are complicit in this process, failing to report or
record suspicious activity•As above.
26 Wachovia, paid $160m to settle a US federal investigation into
laundering of illegal drug money through Mexican currency exchanges. This
included a $50m fine for failing to monitor money used for shipping 22 tons of
cocaine• How a big US bank laundered billions from Mexico’s
murderous drug gangs, the Guardian, URL-138, April 3rd
2011
27 Wachovia was unable to check about $400bn’s worth of transactions• Wachovia to settle drug-money laundering case, (Associated
Press), URL-180, March 17th, 2010
28 when a government says it’s going to “crack down” on the illicit trade
that violence worsens, as we’ve certainly seen in Mexico• Q&A:
Mexico’s drug related violence, BBC, URL-139, August 26
2011
29 Al Qaeda is principally funded by opium and cannabis production• Al Qaeda’s drugs trade keeps them afloat during the economic
crisis, Sebastian Abbot, URL-140, October
16th 2008
30 Mexican drug cartels are involved in kidnapping, counterfeiting and
business extortion• The cartels behind Mexico’s drug war, Kazi
Stastna, URL-141, August 28th 2011
31 “under siege.
The threat posed by drug traffickers is so great that the state is on the verge
of collapse … So much drug money flowing in so easily, is a true curse: it is
perverting the economy and rotting society.”• International conference on drug
trafficking in Guinea-Bissau, Antonio Maria Costa, URL-142, December 19th 2007
32 85% of shoplifting and 80% of domestic burglary is committed by
problem drug users• Strategy Unit Drugs Report Phase One –
Understanding the Issues, URL-124, May 12th
2003
33 There are over 300,000 problem drug users in the UK• Tackling Problem Drug Use, House of Commons Committee of
Public Accounts, URL-143, March 24th 2010
34 30,000 who commit over half of all drug-related crime, costing the
country £11 billion a year• Strategy Unit Drugs Report Phase
One – Understanding the Issues, URL-124, May 12th
2003
35 In 1955, there were 57 registered heroin addicts in the UK• Heroin addiction in the United Kingdom (1954–1964), Thomas
Bewley, British Medical Journal, URL-144, November
27th 1965
36 The Case for
Heroin• The Times, June 14th, 1955
37 new trials of heroin-prescribing under way
with promising results.• Supervised injectable
heroin or injectable methadone versus optimised oral methadone as treatment for
chronic heroin addicts in England after persistent failure in orthodox
treatment (RIOTT): a randomised trial, J Strang, N Metrebian, N Lintzeris et al, Lancet
375: 1885–95, 2010
38 Viscountess Runciman produced a report• Drugs and
the law, Report of the Independent Inquiry into the Misuse of Drugs Act,
Chairman Viscountess Runciman, URL-3, 2000
39 People from black communities are 6 or 7 times more likely to be
arrested if they’re found with drugs than people from other ethnic groups, and
11 times more likely to be imprisoned.• Black people six
times more likely to face drug arrest, 172, Mark Townsend, the Observer, October 31, 2010; this Observer
article discusses the analysis by Professor Alex Stevens of recent Ministry of
Justice data, in his book Drugs, Crime and Public Health:
The Political Economy of Drug Policy, Routledge, 2011
40 Each year, tobacco kills 5 million people across the world• Why tobacco is a public health priority, WHO, URL-145, accessed
December 10th 2011
41 alcohol kills 1.5 million• Global Status Report on Alcohol and Health, WHO, URL-146, 2011
42 illicit drugs kill around 200,000 people between them• Overview of global and regional drug trends and patterns,
UNODC World Drugs Report, URL-147, 2011
43 $1 trillion spent• After 40 years, $1trillion dollars, US War on Drugs has failed to meet
any of its goals, Associated Press, URL-148, May 13th 2010
44 or $2.5 trillion• The War on Drugs, URL-178, Time
Magazine, March 25th, 2009
45 Mo Mowlam• ‘Legalise all drugs’ – Mowlam, BBC
News, URL-149, April 28th 2002
46 Bob Ainsworth spoke out about decriminalisation when safely out of the
Cabinet• Can we imagine a Britain where all drugs are
legal?, Mark Easton, URL-123, December
16th 2010
47 Bill Clinton and Jimmy Carter criticised the War on Drugs in a recent
documentary• Breaking the Taboo, (film), Fernando
Grostein Andrade (director), 2011
48 Jimmy Carter wrote an article entitled Call Off the
Global Drug War in The New York Times• URL-173, The
Opinion Pages, June 16, 2011
49 The Global War
On Drugs Has Failed: It Is Time For A New Approach• URL-176.
50 “drugs policy
has been failing for decades”• Tory Contender calls for more liberal drug laws, Marie Woolf, URL-150, September 7th 2005
51 there are lots of alternatives to unregulated sales• After the War on Drugs: Options for Control, Transform, URL-151, February
2006
52 one in 5000 cannabis users will develop schizophrenia• Cannabis: classification and public health, ACMD, April
2008
53 Prisoners are about 10 times more likely to commit suicide• Statistics 8: The Criminal Justice System, Mind, URL-152, accessed
December 10th 2011
54 about 40% of men and 60% of women have some form of neurotic disorder•
As above.
55 Ken Clarke has been talking about “drug-free wings” in prisons• Clark’s vision: a return to Victorian-style prisons with hard
work, discipline… and NO hard drugs, Daily Mail Reporter, URL-153, October
14th 2010
56 Research by the Department of Work and Pensions• Barriers
to employment for offenders and ex-offenders, Hilary Metcalf, Tracy
Anderson and Heather Rolfe, URL-154, 2001
57 10% of cannabis users become dependent• Cannabis:
classification and public health, ACMD, April 2008
58 50% of prisoners re-offend• Compendium of
Reoffending Statistics, URL-127, May 10th
2011
59 £38,000 it costs to keep somebody in prison for a year• Ken Clarke plans radical reform of the prison system,
Andrew Woodcock and Lucy Bogustawski, URL-155, June 30th
2010
60 David Cameron was caught with the drug at Eton, he was made to write
out hundreds of lines of Latin• Cameron – the rise of the
new conservative, Francis Elliott, Fourth Estate, 2007. Exclusive: Cameron DID smoke cannabis, Simon Walters, the Daily Mail, 181, February 12th, 2007
Genetic
sequencing
Within
20 years, it’s likely that every child born in the UK will have their DNA
sequenced at birth, perhaps with the data stored on a microchip under their
skin. The primary purpose of this, from a therapeutic point of view, is to
avoid many of the 1thousands
of deaths a year that occur when people have allergic reactions to the
medication they’re given in hospital. When
someone is brought into an accident and emergency (A&E) department in 2030,
they will have their microchip scanned and cross-referenced with a database of
genetic variants that are known to predict problems with common medicines. This
will save many lives.
(While this scanning
sounds futuristic, in fact it’s already done on a very small scale for one rare
condition called 2phenylketonuria. Every child is tested
shortly after they’re born. Blood is taken from a pinprick on their heel and
tested for a genetic mutation that makes them unable to breakdown
phenylalanine, the amino acid that dopamine and noradrenaline are made from. If
untreated, people with this condition suffer a poisonous build-up of
phenylalanine in the brain, leading to serious damage. Fortunately, testing for
the genetic mutation means that we can put sufferers on a special diet avoiding
high protein foods such as meat, eggs and milk – which contain phenylalanine –
and they can lead relatively normal lives.)
When people are given a
complex intellectual task such as a game where the rules keep changing,
val-vals perform significantly worse than the other types (they make more
errors); however, they 3improve hugely when they’re
given stimulants, as shown in Figure 16.1. Val-mets, on the other hand, show very little change on
stimulants, while met-mets perform worse. This is the principle behind
prescribing stimulants for people with attention disorders, and although your
COMT type doesn’t seem to have a relationship to your likelihood of having
ADHD, it does demonstrate that different people have different reactions to the
same drugs.
We know a few other
things about COMT type and drugs. 4Val-vals
are less pain sensitive, because they produce more endorphins when they are
hurt. They may be more vulnerable to cannabis-induced psychosis. They also
relapse faster when they try to give up smoking, probably because of low
dopamine levels. All these traits together seem to make val-vals more
exploratory, a kind of 5“warrior”
type who is more willing to take risks, while met-mets are the “worriers”, who
are naturally more cautious. One evolutionary theory behind the difference is
that it was beneficial to human groups as we evolved to have both personality
types in roughly equal measure.
While these
findings are interesting, our present knowledge is only the tip of the iceberg,
partly because full genetic sequencing is currently so rare. There could be
enormous potential benefits if millions of people share their genetic data and
their experiences of illness, medication and drug taking via platforms like the
internet. We’ll be able to identify relationships between genes, illness, and
drug effects; this will enable us to inform people about their vulnerabilities
in ways that will make both therapeutic and recreational drug taking much
safer. (That said, when it comes to complex behaviours like drug taking, genes
are never deterministic. Having every known genetic vulnerability to smoking
might increase your chances of addiction about three-fold – but not having
those vulnerabilities will not protect you if you smoke persistently enough.)
What are the risks of genetic sequencing?
Widespread
genetic sequencing will inevitably raise difficult questions. We’ll need to
establish how our genetic data should be used and shared, and how civil
liberties and patient confidentiality can be protected without inhibiting
research. And human genetics is a very sticky area in patent law. (Indeed,
there was a race to sequence the human genome 6between the
publicly-funded Human Genome Project and the private company Celera Genomics.
Had Celera won the race it’s possible that they would have patented the entire
thing, rather than allowing free redistribution and scientific use.)
Understanding individual genetic variations might help us develop new
medicines, but patent law will need to evolve to establish who has rights when
someone’s genetic material is being commercially exploited.
A famous case heard in
1990, 7Moore v Regents of the University of California, revolved around whether a man called John Moore had the right to
benefit financially from a cell line developed from his T lymphocytes, a type
of white blood cell. The court ruled that he couldn’t claim ownership of his
own “discarded material”, such as blood and tissue samples, and that the
University were allowed to exploit the cell line commercially, as it was their
invention. This sets quite a problematic precedent. On the one hand, it’s better if people can’t own their
body parts, as that would mean that they could sell them for organ transplants
or scientific research rather than donating them – but on the other hand, it
seems unfair that an organisation or company should be allowed to make money
out of other people’s DNA in this way.
Treating
addiction
A controversial topic that
will almost certainly be part of the drugs debate in
the next 20 years is the use of 8vaccines to
make drugs ineffective. We already use an immune-based approach to treat
psychoactive drug use in a limited sense now – if people come to hospital with
a cocaine overdose they’re given antibodies that mop up the drug in the blood.
This is a short-term treatment however, as it requires an intravenous infusion
of the antibody, and the effect lasts just a few hours. In theory it should be
possible to actively vaccinate someone against a drug, for example cocaine, so
that when a person takes it the immune system is turned on to mop up the
cocaine in the blood, stopping the drug from getting to the brain. This
approach is theoretically possible for almost all substances, but currently the
techniques to make the body raise its own immune response to a drug do not work
as well as they do for vaccination against viruses such as polio. However, this
is likely to change as more effort is put into vaccine development.
Learning
and unlearning
Much
of today’s drugs research considers how pharmaceuticals can be used to make
psychological treatments more effective. One area where this has had some
success is in “unlearning”, to help people overcome phobias. A phobia occurs
when someone has a very powerful bad memory that overwhelms their rational
reaction to a particular stimulus (such as a spider, or heights). To overcome
the phobia they need to experience being in the presence of the feared object
without feeling fear, and then make that memory more powerful than the phobic
memory. For example, a treatment
devised for people with vertigo is to put them in a virtual-reality environment
that gives them the sensation of being at a great height; at first, they’re
extremely afraid and panicky, but over several sessions their fear diminishes.
What pharmacologists have developed is a drug that helps with forming the good,
anxiety-free, memories.
Memories are made by
changing the level in the brain of neurotransmitters, especially glutamate. The
drug now in use for treatment of phobias is D-cycloserine which makes glutamate
work better; when someone is given it during the virtual-reality sessions, they
overcome their fearfulness more quickly. 9Figure 16.2
compares treatment with D-cycloserine against treatment with a placebo.
We’re now trying to work
out how to apply these kinds of principles in treating addiction, which is also
a learnt behaviour involving memory. The difficulty is that with illnesses such
as phobias or post-traumatic stress
disorder, the memories to be overcome are experienced as negative, so the
patient has a big incentive to try to get better; in contrast, with addiction
the memories laid down are profoundly positive, often the most positive
experiences the patient has ever had. A big challenge in managing addiction is
to help people overcome cravings by remembering the negative impacts of drug
use instead of the positives. In the future, perhaps we’ll use drugs like
D-cycloserine to make somebody “phobic” to a drug they have abused, helping
them to battle addiction.
New
drugs research
Almost all mental-health
problems are prone to relapse; developing drugs that can reduce the factors
that trigger relapse, particularly stress, is an important area of research.
CRF and substance P are both stress hormones, which put you off your food and
stop you sleeping when life is stressful. There is already some research
showing that 10alcohol
craving can be reduced by using substance P antagonists, and in the future we
may have similar or more effective drugs to reduce CRF as well. These would
perform very similar functions to benzodiazepines or SSRIs prescribed for
anxiety disorders, but because they would be targeting the stress hormone
itself rather than GABA or serotonin, they might have fewer side-effects.
We may be
able to make better recreational drugs as well. As discussed in chapter 6, I’ve
done some research on replacing ethanol in “alcoholic” drinks with a safer
alternative such as a reversible GABA-enhancer, and it may be that by 2030
that’s what we’ll all be drinking in the pub. An alternative approach is to
modify alcohol itself to make it safer and more pleasant. We now know that
alcohol works on a set of GABA receptors with different functions, and we have
started to identify the different mechanisms involved. Receptors called Alpha-1
seem to control the sedative effect of alcohol, making you unsteady; 11Alpha-5
receptors make you lose your memory; and we think Alpha-2 or Alpha-3 receptors
make you feel relaxed and happy. In some very interesting studies, participants
were given alcohol with an 12inverse
agonist that counters alcohol’s effects on the Alpha-5 receptor. These
participants performed much better on memory tests than those who had had
alcohol on its own, showing it is possible to reverse at least one of the
effects of alcohol with a drug. In principle, we could make alcohol safer by
combining it with a range of inverse agonists that counter its negative effects
on the other sorts of GABA receptors, too. It’s likely, for example, that if we
could find an inverse agonist for Alpha-1 you would be able to drink without
becoming unsteady on your feet. Ideally, we would develop a version of alcohol
which targets just Alpha-2 or 3, giving us all the sensation of relaxation and
enjoyment without the negative effects.
The Brain Science, Addiction and Drugs Foresight programme
In the
early 2000s, I became involved in the Brain Science, Addiction and Drugs
project. This had been set up as part of the Foresight programme, which was
introduced in the UK in 1992. The Foresight programme gathers expert opinions
about the role science and technology might play in the issues we’re going to
face in the future. The program has looked at strategic issues such as changes
in flooding risks, as well as the social implications of developments in fields
such as fibre optics. As part of the Brain Science, Addiction and Drugs project
I co-edited a book called 13Drugs and the Future, which gathered
together some of our most up-to-date research, and explored the policy issues
governments will need to face in the coming decades.
1. The “high performance” scenario
In the
“high performance” scenario, decisions are evidence-based, and the main focus
for the use of drugs is the enhancement of performance. On this basis, it’s
expected that Britain has strong economic growth, in part because of its
attractiveness to “knowledge nomads” (an elite class of highly mobile workers
who migrate around the world moving between jobs in the knowledge economy). One
of the things they like about
Britain (in this hypothetical scenario) is our highly regulated, non-punitive
approach to psychoactive substances, particularly cognition enhancers. Many
recreational drugs are legal and available in high-quality forms to be consumed
in special on-licence premises, although these are costly and there’s a large
black market in cheap generics from abroad. Problem drug-use with all its
associated harms is on the decline.
2. The “neighbourhood watch” scenario
This policy
framework came about in response to a dramatic increase in drug use,
particularly among the young and in poor communities, between 2010 and 2015,
which prompted a moral backlash. Science was blamed for failing to contain the
problem, but those leading the moral tide put most blame on the middle classes
for casually consuming recreational drugs without regard for the misery their
trade caused in the UK and abroad. A highly-punitive system involving drug
testing at work and in schools, and heavy criminal sanctions, have led to a
drop in drug use among the professional classes, and have slowed its spread
elsewhere. However, the erosion of trust in science has meant that much
research into the causes and treatment of drug abuse has been sidelined, and
there’s a growing recognition that to make the policy framework more
sustainable science is required again. The UK has also failed to make any real
headway in shutting down the international supply chain.
3. The “dispense with care” scenario
Grey campaigners are a
highly-mobilised political force and have lobbied very effectively for
expensive life-preserving treatments (drugs to treat Alzheimer’s, etc) to
receive research investment and to be available to the public at large.
However, because successive governments with low-taxation policies are
repeatedly elected, this has led to unsustainable costs, and a degrading of
public services, including the NHS. Although
steps have been taken to provide more funding for the NHS, decreasing its bill
by refusing to treat self-inflicted illness may be indicative of future plans
to reduce its remit.
4. The “treated positively” scenario
What sort of future do we want?
From the industry’s point
of view, getting drugs approved for mental-health disorders is now so difficult
that many companies feel that the costs of
developing them are simply not worth it. Investing $1 billion in a drug that
may never come onto the market at all is a substantial risk, and means that
companies often focus on making slight improvements to currently-approved drugs
rather than exploring more radical options. While of course we need to protect
the public from ineffective or harmful medicines, we also need to be able to
experiment with new treatments. Perhaps the answer lies in smaller companies
that can develop precision drugs, as suggested in the “treated positively”
scenario; perhaps we need much better public funding; or perhaps we could move
to the informed-consent model for drugs approval discussed in chapter 12.
Whatever happens, we will have to think of alternatives if the big
pharmaceutical companies stop developing the drugs that so many ill people rely
on.
Ultimately, a lot depends
on what sort of future we decide that we want. What
actually happens by 2025 will almost certainly involve elements from all four
projected scenarios. Many of the factors that will shape our future are largely
out of our control – including demographic shifts or needing to deal with
climate change – but other factors will depend on the decisions our politicians
make, and the role that we expect science to play in those decisions. It is
unlikely that the pharmaceutical industry will ever have much of an interest in
addiction treatment, for example, so if we want to find new ways of tackling
the disease we’ll need to ensure that public funding continues. Whatever
happens, it’s important that we begin the conversation about the society we
want to create, and the role that drugs will play in that.
Notes
1 thousands of deaths a year that occur when people have allergic
reactions to the medication they’re given in hospital• Genotyping
of Drug Targets: A Method to Predict Adverse Drug Reactions?, C Guzey, O
Spigset, Drug Safety (25) 8, 2002
2 phenylketonuria• NHS Choices, NHS, URL-157, accessed
December 7th 2011
3 improve hugely when they’re given stimulants• Catechol
O-methyltransferase val158-met genotype and individual variation in the brain
response to amphetamine, Mattay et al, Proceedings of the National
Academy of Sciences USA, 2003
4 Val-vals are less pain sensitive• COMT val158met Genotype Affects u-Opioid Neurotransmitter Responses to
a Pain Stressor, Jon-Kar Zubieta et al,
Science, February 2003
5 “warrior” type who is more willing to take risks, while met-mets are
the “worriers”, who are naturally more cautious• Warriors
versus worriers: the role of COMT gene variants, DJ Stein, TK Newman, J
Savitz, R Ramesar, CNS Spectrums, October 2006
6 between the publicly-funded Human Genome Project and the private
company Celera Genomics• The Human Genome Project, The Wellcome Trust Sanger
Institute, URL-158, accessed December 10th 2011
7 Moore v Regents
of the University of California,• (271 Cal. Rptr.146),
1990
8 vaccines to make drugs ineffective• Drugs and the
Future: Brain Science, Addiction and Society, David Nutt et al,
Elsevier, 2007
9 Figure 16.2 compares treatment with D-cycloserine against treatment
with a placebo• Use of D-Cycloserine in Phobic Individuals
to Facilitate Extinction of Fear, Kerry J Ressler et al, Archives of
General Psychiatry, 2004
10 alcohol craving can be reduced by using substance P antagonists• Neurokinen 1 receptor antagonism as a possible therapy for
alcoholism, David George et al, Science, March 14th 2008
11 Alpha-5 receptors make you lose your memory•
Blockade of alcohol’s amnestic activity in humans
by an a5 subtype benzodiazepine receptor inverse agonist, David Nutt et al, Neuropharmacology, 2007
12 inverse agonist•an inverse agonist is an agent that binds to the same
receptor as a drug but induces a pharmacological response opposite to the drug.
(Wikipedia.)
13 Drugs and the
Future,• Drugs and the Future: Brain Science, Addiction and Society, David Nutt et al, Elsevier, 2007
Young
people and drugs
One of
the most promising outcomes of the experiment with decriminalisation in
Portugal has been a reduction in use of drugs by 15 to 19-year-olds. It is particularly risky for people to take drugs when
they’re young, as we’ll explain in a moment. One important harm reduction
measure is to delay experimentation, if it can’t be
prevented altogether. There are several reasons to try and discourage teenagers
in particular from using drugs.
1. Alcohol and tobacco are drugs
Most
parents’ number one fear is that their children will end up addicted to heroin
or crack, and they start the conversation by explaining the dangers of “hard”
drugs. In the process, children can often get the impression that alcohol and
tobacco aren’t really drugs, and aren’t dangerous, when in many ways they’re even more harmful than a lot of illegal
substances, and smoking is highly addictive. Remember that 1half of all
regular smokers and a very large number of regular drinkers will die from
illness caused by their alcohol or tobacco use, and with alcohol you don’t have
to be an addict to face considerable risks.
There’s 2no “safe
level” of drinking and smoking, although some people drink and smoke in safer
ways than others. Most of us have tried these drugs, and many of us use them
regularly, weighing up the harms against the benefits we think we gain from
them. Part of making adult decisions about drugs is learning how to weigh
things up like this, and this is what we need to teach our children to do.
2. All drugs can potentially cause harm as well as pleasure
3. Start telling your kids about drugs from an early age, and be
prepared to discuss your drinking and smoking with them
Ideally,
conversations about drugs should start when your children are six or seven – as
they first become aware of drugs being used and discussed on TV and in films.
Be prepared for them to already have a lot of ideas, both true and false, about
how drugs work and what they do. Make
yourself a reliable source of information, so they’ll come to you when they
have questions. Part of making yourself reliable is being willing to discuss
your own drug use – if you pretend that drinking and smoking are entirely
different to the illegal substances they might be considering, they’ll work out
soon enough that this isn’t true and you’ll lose your credibility. Explain how
you weigh up the risks and benefits when you’re thinking about how much to
drink or smoke, and under what circumstances you think certain kinds of use are
appropriate.
4. Never
inject
5.
Don’t use solvents
3Inhaling
solvents, glue, butane or other aerosols kills about one person a week. They
usually kill instantly, by stopping the heart, and this can happen the very first
time the drug is tried. Solvents are popular amongst young teenagers because
it’s the easiest sort of substance to get hold of, but they’re very dangerous
to experiment with, even just once or twice. Make sure your kids know the harm
they can do. (See box Butane and other solvents on
page 315.)
6. Don’t take drink and drugs at the same time
Mixing
alcohol with other drugs makes the effects of both of them more unpredictable.
There are two reasons for this, one chemical and the other social:
·
Chemically, alcohol sometimes
creates new compounds when combined with other drugs, such as cocaethylene
which is produced when alcohol is mixed with cocaine. 4Cocaethylene is more harmful
than either drug on its own.
Taking other kinds of depressants or
opioids at the same time as alcohol is also dangerous as they can depress
breathing to the point of death. You should be especially careful to avoid
taking ketamine, GHB/GBL, heroin, methadone or any other opiate when you’re
drunk.
7. A criminal record could ruin your career
If you deal drugs, you’re
more likely to be targeted by the police and pursued through the courts, and
the penalties are much more severe. Even passing on small amounts to your
friends is considered dealing in the eyes of the law, so be extremely careful
about doing that. Watch what you say and admit to online, as this could be used
as evidence against you. Never post pictures of yourself or your friends doing
illegal drugs.
8. Find good sources of advice
We’re trying to counteract
this on the ISCD website, drugscience.org.uk, which has a lot of useful information written in an accessible style
that teenagers should be able to understand without difficulty. We will keep
this up-to-date as new substances appear. If you’ve found this book
informative, do encourage them to read it too.
9. If you do take drugs (including alcohol and tobacco) be clear why
you’re doing it
There
are lots of personal reasons people might want to take drugs – sometimes it’s
purely for pleasure, but often it’s to deal with stress and anxiety. A great
many people use alcohol in this way, when it would be far better to go to their
GP and see if they can suggest a therapeutic drug or psychological approach which
is less harmful and less addictive. Having a particularly strong liking for
certain drugs can be an early indicator of mental-health problems – liking
alcohol may be a sign of an anxiety problem, or liking cannabis may be an early
indicator of schizophrenia. About 5a quarter
of male alcoholics have an undiagnosed anxiety disorder, and could have avoided
damaging their bodies if they had been placed on a benzodiazepine or SSRI
rather than self-medicating with what was available in the shops. If you do
have a mental-health problem that you are dealing with by taking alcohol or
illicit substances, you will do yourself much less harm if you move on to less
addictive, medically-approved drugs under the guidance of a doctor or psychiatrist.
If you think your child might be doing this, do try to get them a referral as
soon as possible.
10. If you do get into trouble with drugs, get help quickly
If you think your child
is developing a drug problem it can be extremely distressing, and very hard to
know what to do. It might be tempting to
try to force them into treatment, but the nature of addiction means that
forcible interventions usually won’t work: unless they’re really motivated to
come off the drugs themselves they’re likely to relapse very quickly. There are
no straightforward answers to this, but here are some suggestions:
·
In the first instance discuss with
your child your evidence and fears; educate them (perhaps with the material in
this book) about the risks and harms of drugs.
·
Parental sanctions such as
“grounding” or withdrawal of pocket money may be effective.
11. If you do use drugs, make sure they don’t interfere with your
schoolwork
Experimenting
with drugs can be really exciting, and may be more fun than going to school! If
you’re going to use drugs, it’s really important to keep these parts of your
life separate. Make sure the amount of time you spend doing drugs doesn’t
prevent you doing your homework, and that you’re
in a fit state to listen and pay attention in class – don’t go in regularly
with a hangover or keep missing sleep on school nights. Don’t take drugs into
school, or use them there, or deal on the school grounds: remember that just
passing small amounts onto your friends will be seen as dealing. Even possessing
legal drugs like alcohol will be against your school code of conduct, and could
get you suspended or expelled.
Butane and other solvents
6Solvents
are quite commonly abused by adolescents, because they’re the easiest sort of
drug to get hold of by young teenagers who can’t yet buy alcohol legally. The
solvents are either liquids or gases, which can be taken in a number of ways.
Sometimes they are “huffed”, which means placing some of the substance on a
towel or cloth and breathing in; sometimes they are inhaled directly from the
container; a third method is “bagging” – squirting the substance into a paper
or plastic bag and inhaling. Aerosols are sometimes sprayed directly into the
nose or mouth which is especially dangerous. How long the effect lasts depends
on the substance – with some it lasts only a few minutes, and with others over
an hour. The effects are quite like sudden drunkenness, with impaired
coordination, lethargy and slurred speech, combined with light-headedness and
euphoria.
Although butane, the
solvent the ISCD expert panel looked at across the 16 criteria of harm, didn’t
score very highly overall, it’s very unsafe to experiment with this type of
drug. Solvent users can asphyxiate if they pass out while sedated and choke on
their own vomit, or if they don’t remove
the cloth or bag from their face and continue to inhale the drug while they’re
unconscious. Long-term use can also cause brain damage, harm the liver and
kidneys, and lead to hearing loss and convulsions or limb spasms. But the main
danger is sudden sniffing death syndrome
(SSDS), when a single session results in irregular heartbeat, heart failure and
death. Over half of all deaths from solvents are from SSDS, and a fifth of
those who died had no history of abusing inhalants. This makes it an extremely
dangerous sort of drug to experiment with, even once or twice.
Notes
1 half of all regular smokers• Mortality in relation
to smoking: 50 years’ observations on male British doctors, Richard Doll
et al, British Medical Journal (Clinical research ed.) 328, 2004
2 no “safe level” of drinking• There is no such thing
as a safe level of alcohol consumption, David Nutt, URL-36, March 7th
2011
3 Inhaling solvents, glue, butane or other aerosols kills about one
person a week.• Trends in UK deaths associated with abuse of
volatile substances, Hamid Ghodse et al, International Centre for Drug
Policy, 2010
4 Cocaethylene is more harmful than either drug on its own• The Cocaine Trade, House of Commons Home Affairs Committee,
URL-110, February 23rd 2010
5 a quarter of male alcoholics have an undiagnosed anxiety disorder• Comorbidity of Mental Disorders With Alcohol and Other Drug Abuse,
Darrel Regier et al, Journal of the American Medical Association (264), 1990
6 Solvents are quite commonly abused by adolescents,• Legally Stoned, Todd A Thies, Kensington Publishing Corp, 2009
Useful
websites
·
The Independent
Scientific Committee on Drugs UK (ISCD):
www.drugscience.org.uk
·
The Advisory Council on
the Misuse of Drugs UK:
www.homeoffice.gov.uk/drugs/acmd
·
The National Institute on
Drug Abuse USA (NIDA):
www.drugabuse.gov
·
The National Institute on
Alcohol Abuse and Alcoholism USA (NIAAA):
www.niaaa.nih.gov
·
The National Drugs
Campaign Australia:
www.drugs.health.gov.au
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