Ölümcül Psikiyatri ve Organize İnkar (İngizlice kopya)
Table of
Contents
FDA’s meta-analysis
of suicides in trials with 100,000 patients is deeply flawed............... 47
United Nations
forbids forced treatment and involuntary detention............................... 238
Peter C. Gøtzsche
Deadly Psychiatry and Organised Denial
Abbreviations
Acknowledgements
About the author
1. INTRODUCTION
Silverbacks in the UK exhibit psychiatry’s
organised denial
2. WHAT DOES IT MEAN TO BE MENTALLY ILL?
On being sane in insane places
The demons attack you
Let there be disorder
Psychiatric drugs lead to many wrong diagnoses
The Goodness Industry
Patients are not consumers
More funny and fake diagnoses
3. DEPRESSION
Screening for depression
Antidepressant drugs don’t work for depression
Other important flaws in placebo controlled
trials
Fluoxetine, a terrible drug, and bribery in
Sweden
Harms of antidepressant drugs are denied or
downplayed
The FDA protects Eli Lilly
Massive underreporting of suicides in the
randomised trials
FDA’s meta-analysis of suicides in trials with
100,000 patients is deeply flawed
Another dirty trick: using patient-years instead
of patients
Case stories of suicide on SSRIs
Akathisia is the main culprit
Lundbeck: Our drugs protect children against
suicide
Totally misleading observational studies of
suicide
Antidepressant-induced homicides
The pills that ruin your sex life
Damage to the foetus
The fraud and lies of GlaxoSmithKline
Trial 329 of paroxetine in children and
adolescents
The STAR*D study, a case of consumer fraud?
4. ANXIETY
Sleeping pills
5. ADHD
Childhood ADHD
Adult ADHD
ADHD drugs
ADHD drugs for children
ADHD drugs for adults
Harms from ADHD drugs
6. SCHIZOPHRENIA
Human guinea pigs in America
The chemical lobotomy
Drug trials in schizophrenia
Antipsychotics kill many people
A patient history
Pushing antipsychotic drugs
Eli Lilly’s crimes related to olanzapine
Stigmatisation
Hearing voices
7. BIPOLAR DISORDER
“Mood stabilisers”
A young man’s experience
8. DEMENTIA
We make people demented with psychotropic drugs
9. ELECTROSHOCK
10. PSYCHOTHERAPY AND EXERCISE
Psychotherapy for anxiety and depression
Psychotherapy for obsessive compulsive disorder
Psychotherapy for schizophrenia
Exercise
11. WHAT HAPPENS IN THE BRAIN?
Calling psychiatric drugs “anti”-something is a
misnomer
Genetic studies and transmitter research
Chronic brain damage
Addiction to psychiatric drugs
Drug regulators, the extended arm of industry
Drug dependence is often misinterpreted as
relapse of the disease
The chemical imbalance nonsense
12. WITHDRAWING PSYCHIATRIC DRUGS
The worst drug epidemic ever
How can it be done?
13. ORGANISED CRIME, CORRUPTION OF PEOPLE AND
SCIENCE, AND OTHER EVILS
Lundbeck’s evergreening of citalopram
Psychiatry’s fantasy world
A Danish witch hunt
Lecture tour in Australia
Psychiatry is not evidence-based medicine
Can we reform psychiatry or is a revolution
needed?
14. DEADLY PSYCHIATRY AND DEAD ENDS
The connection between psychotropic drugs and
homicide
How few drugs do we need?
How many people are killed by psychotropic
drugs?
15. FORCED TREATMENT AND INVOLUNTARY DETENTION
SHOULD BE BANNED
Human rights in Europe
Forced treatment
Patients’ rights
My comments
Forced treatment must be banned
United Nations forbids forced treatment and
involuntary detention
Dear Luise
16. WHAT CAN PATIENTS DO?
17. WHAT CAN DOCTORS DO?
18. HELPFUL WEBSITES
Copyright
Abbreviations
ADHD: Attention Deficit Hyperactivity Disorder
4
APA: American Psychiatric Association CI:
Confidence Interval
DSM: Diagnostic and Statistical Manual of Mental
Disorders
EMA: European Medicines Agency
FDA: Food and Drug Agency (USA)
ICD: International Classification of Diseases
GP: General Practitioner
NICE: National Institute for Health and Care
Excellence (UK)
NIMH: National Institute of Mental Health (USA)
OCD: Obsessive Compulsive Disorder
SSRI: selective serotonin reuptake inhibitor, an
antidepressant
UN: United Nations
I am very grateful for the inspiration and
advice I have received from numerous patients and their relatives, colleagues,
friends, lawyers and others, which have improved substantially on what I would
have been able to write on my own. I mention here a few people who have been
particularly inspiring through their books or in other ways, or who have
commented on sections in my book: Peter Breggin, Paula Caplan, Dorrit Cato
Christensen, Jens Frydenlund, Linda Furlini, Jim Gottstein, David Healy, Allan
Holmgren, Lisbeth Kortegaard, Joanna Moncrieff, Luke Montagu, Peer Nielsen,
Peter Parry, Melissa Raven, John Read, Bertel Rüdinger, Olga Runciman, and
Robert Whitaker. At least four of these people have personal experiences from
being a psychiatric patient.
Professor Peter C. Gøtzsche graduated as a
Master of Science in biology and chemistry in 1974 and as a physician in 1984.
He is a specialist in internal medicine; worked in the drug industry 1975-83,
and at hospitals in Copenhagen 1984-95. With about 80 others, he helped start
The Cochrane Collaboration in 1993 with the founder, Sir Iain Chalmers, and
established The Nordic Cochrane Centre the same year. He became professor of Clinical
Research Design and Analysis in 2010 at the University of Copenhagen.
Gøtzsche has published more than 70 papers in
“the big five” (BMJ, Lancet, JAMA, Annals of Internal
Medicine and New England Journal of Medicine) and his scientific works
have been cited over 15,000 times.
Gøtzsche has an interest in statistics and
research methodology. He is a member of several groups publishing guidelines
for good reporting of research and has co-authored CONSORT for randomised
trials (www.consort-statement.org)
STROBE for observational studies (www.strobe-statement.org), PRISMA for systematic reviews
and meta-analyses (www.prisma-statement.org), and SPIRIT for trial
protocols (www.spirit-statement.org).
He was an editor in the Cochrane Methodology Review Group 1997-2014.
Books by Peter C Gøtzsche
Gøtzsche PC. Deadly medicines and organised
crime: How big pharma has corrupted healthcare. London: Radcliffe Publishing;
2013. Translated into several languages, see www.deadlymedicines.dk.
Gøtzsche PC. Dødelig medicin og organiseret
kriminalitet: Hvordan medicinalindustrien har korrumperet sundhedsvæsenet.
København: People’s Press; 2013.
Gøtzsche PC. Mammography screening: truth, lies
and controversy. London: Radcliffe Publishing; 2012.
Gøtzsche PC. Rational diagnosis and treatment:
evidence-based clinical decision-making. 4th ed. Chichester: Wiley; 2007.
Wulff HR, Gøtzsche PC. Rationel klinik.
Evidensbaserede diagnostiske og terapeutiske beslutninger. 5. udgave.
København: Munksgaard Danmark; 2006.
Gøtzsche PC. På safari i Kenya. København:
Samlerens Forlag; 1985.
1
Introduction
Psychiatry is not an easy specialty. It requires
a lot of patience and understanding, and there are many frustrations. I am sure
psychiatrists sometimes get frustrated at patients who continue to destroy
their lives, refusing to take on board the good advice they have been offered
about how they could improve on their attitude to life’s many troubles.
This book is not about the psychiatrists’
problems, however. It is about why psychiatry has failed to deliver what
patients want, and what the consequences are of focusing on using harmful drugs
of questionable benefit. Most patients don’t respond to the drugs they receive
and, unfortunately, the psychiatrists’ frustrations at the lack of progress
often lead to the prescribing of more drugs or higher doses, further harming
the patients.
Psychiatric drugs are so harmful that they
kill more than half a million people every year among those aged 65 and over in
the United States and Europe (see Chapter 14). This makes psychiatric drugs the
third leading cause of death, after heart disease and cancer.
I don’t think there is anything psychiatric
patients fear more than forced treatment, and this is an important reason why
having close contact with the psychiatric treatment system markedly increases
suicides (see Chapter 15). I shall explain why forced treatment is unethical
and should be banned and also demonstrate that psychiatry is possible without
it.
Many psychiatric drugs not only increase total
mortality but also increase the risk of suicide and homicide, while no drug
agency anywhere has approved any drug as being effective in preventing
suicides. Lithium is an exception, as it might possibly reduce suicides (see
Chapter 7).
Widespread overdiagnosis and overtreatment is
another issue I take up. There is huge overdiagnosis of mental disorders, and
once you receive a psychiatric diagnosis everything you do or say becomes
suspect, as you are now under observation, which means that the initial,
perhaps tentative diagnosis, all too easily becomes a self-fulfilling prophecy
(see Chapter 2).
I believe we could reduce our current usage of
psychotropic drugs by 98% and at the same time improve people’s mental health
and survival (see Chapter 14). The most important reason for the current drug
disaster it is that leading psychiatrists have allowed the drug industry to
corrupt their academic discipline and themselves.
I have written this book primarily for the
patients, particularly those who have desperately wanted to come off their
drugs but were met with hostile and arrogant reactions from their doctors, and
I shall explain how it is possible to safely taper drugs (Chapter 12).
I have also written the book for young
psychiatrists in training in the hope that it could inspire them to
revolutionise their specialty, which is badly needed. One sign that psychiatry
is in deep crisis is that more than half the patients believe their mental
disorder is caused by a chemical imbalance in the brain. They have this
misperception from their doctors, which means that more than half the
psychiatrists lie to their patients. I know of no other specialty whose
practitioners lie to their patients. Psychiatrists also lie to themselves and
to the public, and I shall give many examples of official statements that
exaggerate the benefits of psychiatric interventions by five to ten times and
underestimate the harmful effects by a similar factor.
Those at the top of the hierarchy I call
“silverbacks,” since they are almost always males and behave like primate
silverbacks in the jungle, keeping others away from absolute power, which in
nature carries rewards such as easy access to females – in psychiatry this
translates into money and fame. These silverbacks suffer from collective,
organised denial. They refuse to see the damage they cause even when the
evidence is overwhelming. Further, they have united around a number of myths
and misconceptions, which they defend stubbornly but which are very harmful for
patients. Some of the worst, which I shall debunk in this book, are:
·
psychiatric diagnoses are
reliable;
·
it reduces stigmatisation to give
people a biological or a genetic explanation for their mental disorder;
·
the usage of psychiatric drugs
reflects the number of people with mental disorders;
·
people with mental disorders have
a chemical imbalance in their brain and psychiatrists can fix this imbalance
with drugs, just like endocrinologists use insulin for diabetes;
·
long-term treatment with
psychiatric drugs is good, as it prevents recurrence of the disease;
·
treatment with antidepressants
does not lead to dependence;
·
treatment of children and
adolescents with antidepressants protects against suicide;
·
depression, ADHD and schizophrenia
lead to brain damage; and
·
drugs can prevent brain damage.
I shall also explain how I have come to the
conclusion that psychiatric research is predominantly pseudoscience, and why
reliable research constantly tells us a very different story to the fairy tale
that leading psychiatrists want us to believe in.
I am a specialist in internal medicine and took
an interest in psychiatry in 2007 when Margrethe Nielsen from the Danish
Consumer Council approached me with an idea for her PhD thesis: “Why is history
repeating itself? A study on benzodiazepines and antidepressants (SSRIs).”
Her studies showed that, indeed, history has
repeated itself. We have repeated the same mistakes with the SSRIs that we made
with benzodiazepines, and before them with barbiturates. We have created a huge
epidemic of drug overuse with just as many drug addicts on SSRIs as on
benzodiazepines (see Chapter 12).
Margrethe’s findings were not welcomed by two of
her examiners, who had turfs to defend. One, Steffen Thirstrup, worked for the
Danish drug agency, the other, John Sahl Andersen, was a general practitioner.
Our drug agencies have contributed substantially to the current misery, and
most of the drug harms are caused by general practitioners, who prescribe about
90% of the psychiatric drugs.
They rejected her thesis for no good reason, but
having appealed to the University, she defended it successfully.1 If psychiatrist David Healy had not been the third
examiner, she might not have obtained her PhD, which would have been a gross
injustice, as her research is sound and her PhD thesis is considerably better
than many I have seen.
Unwelcome facts are being suppressed all the
time, and I shall give numerous examples of the works of the “doubt industry”
where people incessantly publish seriously flawed research to provide support
for their unsustainable ideas.
After having studied the science carefully, I
note that some people I have met and several organisations have come to the
conclusion that the way we currently use psychiatric drugs and the way we
practice psychiatry cause more harm than good. The general public agrees and
feels that antidepressants, antipsychotics, electroshock and admission to a
psychiatric ward are more often harmful than beneficial (see Chapter 13). I
have no doubt they are right, and the double-blind placebo controlled
randomised trials – which are not so blind as intended – have rather
consistently shown that it is the psychiatrists that think their drugs are
effective, not the patients (see Chapter 3).
Investigators who have not been blinded
effectively can see the exact opposite of what is actually true when they
medicate patients. They see what they want to see, which is what is convenient
for them and for their specialty, not what really happens (see Chapters 3 and
6).
Cochrane reviews have shown that it is doubtful
whether antidepressants are effective for depression (see Chapter 3) and
whether antipsychotics are effective for schizophrenia (see Chapter 6). Some
drugs can be helpful sometimes for some patients, particularly in the acute
phase where a patient can be so tormented by panic or delusions that it can be
helpful to dampen the emotions with a tranquilliser. However, unless doctors
become much more expert in the way they use psychiatric drugs which would mean
using them very little, in low doses, and always with a plan for tapering them
off, our citizens would be far better off if we removed all psychotropic drugs
from the market.
Some people will see this as a provocative
statement, but it isn’t. It is based on solid science, which I shall document.
I am used to being called provocative or controversial, which I take to mean
that I am telling the truth. In healthcare, the truth is rarely welcomed, as so
many people have so many wrong ideas to defend. The silverbacks of psychiatry
have created a fantasy world of their own, which is not evidence-based medicine
and which is riddled by harmful polypharmacy (see Chapter 13).
Silverbacks in the UK exhibit
psychiatry’s organised denial
People critical of psychiatry are often met with
ad hominem attacks from the psychiatric establishment
or with scientific arguments of little merit. This happened to me after I gave
a keynote lecture in 2014 at the opening meeting of the Council for
Evidence-based Psychiatry in the House of Lords, chaired by the Earl of Sandwich,
called “Why the use of psychiatric drugs may be doing more harm than good.” The
other speakers, psychiatrist Joanna Moncrieff and anthropologist James Davies,
gave similar talks and have written critical books of mainstream psychiatry.2-5
Three months later, psychiatrist David Nutt and
four male colleagues (I shall refer to them by a collective “DN”) attacked me
in the first issue of a new journal, Lancet Psychiatry.6 Their paper is only two pages long, but it is so typical
of the silverbacks’ knee-jerk reactions when criticised that I shall describe
it in some detail.
Anti-everything
DN started out by saying that, “Psychiatry is
used to being attacked by external parties with antidiagnosis and antitreatment
agendas.” Silverbacks often say that those coming from another tribe (“external
parties”) are not allowed to criticise them. This arrogant attitude has
unfortunate consequences because many psychiatrists adopt the same position
towards their patients, thinking they need not listen to them or take seriously
their criticism of the drugs they ingest. It is also common for silverbacks to
stigmatise those who dare criticise psychiatry as being anti-something, and DN
use the terms “anti-psychiatry” and “anti-capitalist” associated with “extreme
or alternative political views.”
“New nadir in irrational polemic”
DN were unhappy with newspaper headlines such as
“Antidepressants do more harm than good, research says,” which appeared in The Times and The Guardian after
our council meeting, and they called this a “new nadir in irrational polemic.”
They found it especially worrying that I being a co-founder of the Cochrane
Collaboration, an initiative set up to provide the best evidence for clinical
practitioners, had apparently suspended my “training in evidence analysis for
popular polemic.” Silverbacks usually speak with the same voice as the drug
industry because it so generously supports them financially (see Chapter 13),
and DN are not an exception. We are told: “Depression is a serious and
recurrent disorder that is currently the largest cause of disability in Europe
and is projected to be the leading cause of morbidity in high-income countries
by 2030.” No British understatement here, though there is no way we can
reliably count the number of people with depression. The criteria for the
diagnosis are arbitrary and consensus-based, and they are now so broad that a
large part of the healthy population can get the diagnosis (see Chapter 3). It
is therefore misleading to say that depression is a serious disorder. Most
people have mild symptoms of everyday distress that hit most of us from time to
time; very few are seriously depressed. Worse still, the dramatic increase in
depression-related morbidity that DN speak about has been caused by the
psychiatrists themselves. The drugs they use do not cure depression but turn
many self-limiting episodes into chronic ones (see Chapter 12). This is not
helping patients; it is serving the interests of psychiatry and the
pharmaceutical industry.
“Impressive ability to prevent
recurrence of depression”
The DN group argues that antidepressants are
among the most effective drugs we have in the whole of medicine and mentions
their “impressive ability to prevent recurrence of depression, with a number
needed to treat of around three [to prevent one recurrence].” It certainly
looks impressive but it isn’t true. The trials that have shown these effects,
where half of the patients continue with their antidepressant drug after they
have recovered while the other half is switched to placebo, are totally
unreliable (see Chapter 11). This is because those switched to placebo have to
go cold turkey, i.e. abstinence symptoms occur because their brain has adapted to
the antidepressant, just like alcoholics get into trouble if they suddenly stop
drinking, and these symptoms can mimic depression.
In their praise of antidepressants, DN also say
they have an impressive effect on acute depression. They haven’t. It is likely
that they have no effect at all (see Chapter 3).
DN note that fewer participants on an
antidepressant than on placebo withdrew from the trials because of treatment
inefficacy, which they interpret as evidence that antidepressants are
effective. This interpretation is not appropriate. It is often the combination
of the perceived benefits and harms that determines whether a patient stays in
a trial. A patient who is on an active drug has often guessed this, because of
the drug’s side effects, and might therefore be more inclined to continue in
the trial even if the drug has no effect, particularly since psychiatrists
often tell their patients that it may take a while before the effect appears.
Conversely, patients on placebo have no incentive to carry on and therefore,
more than in the drug group, drop out due to lack of effect.
It is therefore advised in textbooks on research
methods not to focus on the number of patients who drop out because of lack of
effect. It only makes sense to look at the total number of drop-outs, which is
also the most relevant outcome for treatments that are
not curative but only have an effect on the patients’ symptoms.
Patients are the best judges for deciding
whether a perceived benefit of taking a drug outweighs its side effects, and
they find the drugs pretty useless, as just as many patients stop treatment on
antidepressants as on placebo in the trials for any reason.7
Does academic debate increase
suicides?
The DN group mentions that many people who are
not taking antidepressants commit suicide, claiming that a “blanket
condemnation of antidepressants by lobby groups and colleagues risks increasing
that proportion.” In my book about mammography screening,8 I called this the you are killing my
patients argument. Those who raise uncomfortable questions about popular
interventions are accused of being responsible for the death of many people.
But let’s think. If we generalised this argument to become a common ethical
standard, researchers could never question any intervention if it was believed
to save lives. Thus, we would probably still be performing bloodletting in our
hospitals for all kinds of diseases, even for cholera, where such treatment is
deadly.
More importantly, the crux of the argument is
wrong. Antidepressants don’t protect people against suicide (see Chapter 3).
DN claim that most of those who commit suicide
are depressed, but the underlying data do not allow such a conclusion.9 A widely cited study found that most suicides were
related to a diagnosis of depression, but only 26% of the people were known to
have been diagnosed with depression before they killed themselves. All the
others got a post-mortem diagnosis based on a so-called psychological autopsy,
and it is self-evident that establishing a diagnosis of a psychiatric disorder
in a dead person is a highly bias-prone process. Social acceptability bias
threatens the validity of such retrospective diagnosis-making. Relatives often
seek socially acceptable explanations and may be unaware of or unwilling to
disclose certain problems, particularly those that generate shame or put some
of the blame on themselves. It is therefore tempting to put the blame on an
impersonal thing like a disease, which cannot protest although it might never
have existed. It is a very popular belief among psychiatrists that most of
those who commit suicide suffer from depression but it is doubtful whether this
is correct – people kill themselves for many reasons other than depression.
The next argument that the DN people put forward
to prove their case that antidepressants protect against suicide isn’t any
better. They claim that more than 70% are not taking an antidepressant at the
time of death. Obviously, when people who are not depressed kill themselves,
there is no case for taking an antidepressant before they die. Furthermore,
antidepressants can cause an extreme form of restlessness called akathisia,
which predisposes to suicide10, 11 and which can make the patient stop taking the drug
before the suicide. Stopping an antidepressant abruptly, e.g. because the
patient ran out of pills, can also cause akathisia and suicide. Thus, there are
at least three good reasons why people who kill themselves might not have taken
antidepressants at the time of death.
DN’s next argument is also unconvincing. They
say that in countries where antidepressants are used properly, suicide rates
have fallen substantially. Well, in countries where cars are used properly
(causing few traffic accidents), birth rates have fallen substantially, but
that doesn’t prove anything. Scientifically sound studies have never been able
to find a relationship between increased use of antidepressants and falling
suicide rates, or vice versa (see Chapter 3).
“Some of the safest drugs ever made”
The hyperbole escalates towards the end of DN’s
article. We are told that the SSRIs are some of the safest drugs ever made and
that their adverse effects are rarely severe or life threatening. The facts are
that SSRIs kill one of 28 people above 65 years of age treated for one year;
that half of the patients get sexual side effects; and that half of the
patients have difficulty stopping antidepressants because they become dependent
on them (see Chapter 3). When silverback psychiatrists call SSRIs some of the
safest drugs ever made, I believe it is fair to say that it is unsafe for
people who suffer from something that could be treated with an SSRI to consult
a psychiatrist.
Critics “prefer anecdote to
evidence”
It is surreal to me when DN say that, “Many of
the extreme examples of adverse effects given by the opponents of
antidepressants are both rare and sometimes sufficiently bizarre as to warrant
the description of an unexplained medical symptom,” and that, “To attribute
extremely unusual or severe experiences to drugs that appear largely innocuous
in double-blind clinical trials is to prefer anecdote to evidence.” DN do not
appreciate that the main reason that SSRIs appear innocuous in clinical trials
is that the companies have manipulated the data to an extraordinary degree (see
Chapter 3).11-13
Furthermore, DN fail to listen to patients. That
an adverse effect is “bizarre” doesn’t disqualify it. Many patients have
experienced the same highly bizarre adverse effects, which have returned when
the patients were exposed to the same drug again. This is an accepted method
for establishing cause-effect relationships in clinical pharmacology, which is
called challenge, dechallenge and rechallenge. In 2010, on one of the occasions
where I lectured to Danish psychiatrists, I got nowhere with this argument in a
discussion with a US psychiatrist. He argued that the randomised trials had not
shown an increased risk of suicide, but he didn’t understand that it is not a
requirement for establishment of harms that they have been confirmed in
randomised trials. He might have listened too much to the industry, which
downplays the harmful effects of their drugs by pointing out that they weren’t
statistically significant, often after they have manipulated the data to ensure
that no significant differences would see the light of day.
DN suggest that we should ignore “severe experiences
to drugs,” which they dismiss as anecdotes and claim might be distorted by the
“incentive of litigation”. This is the height of professional denial and
arrogance. It is deeply insulting to those parents who have lost a healthy
child and those spouses who have lost a partner whom an SSRI drove to suicide
or homicide. Furthermore, members of the Council for Evidence-based Psychiatry
explained in Lancet Psychiatry that British
withdrawal-support charities report alarming numbers of people suffering disabling
symptoms for multiple years following withdrawal from antidepressants.14
“Insulting to the discipline of
psychiatry”
In their finishing remarks, DN say that my
“extreme assertions … are insulting to the discipline of psychiatry … and at
some level express and reinforce stigma against mental illnesses and the people
who have them.” I shall explain in Chapter 6 that it is the psychiatrists that
stigmatise the patients, not those who criticise psychiatry.
DN also say that, “The anti-psychiatry movement
has revived itself with the recent conspiracy theory that the pharmaceutical
industry, in league with psychiatrists, actively plots to create diseases and
manufacture drugs no better than placebo. The anti-capitalist flavour of this
belief resonates with anti-psychiatry’s strong association with extreme or
alternative political views.”
In my reply, I noted that, “This is the language
of people who are short of arguments.”15 It was pretty ironic that – of all their expostulations
– DN lamented that critics of psychiatry believe that the pharmaceutical
industry and the psychiatrists create diseases and use drugs no better than a
placebo, as if this was a self-evidently absurd proposition. As I shall explain
later, this is pretty much true. Whereas it is not true when DN say that those
who criticise the overuse of psychiatric drugs are “extreme” or “alternative.”
When I wrote to the editor of Lancet Psychiatry and
requested an opportunity to defend my academic reputation, the editor told me
that the Nutt and colleagues’ paper was given an independent peer review, as
well as being subjected to legal review. This is difficult to understand, given
its many errors, the pronounced ad hominem attacks,
and the tough UK libel law.
I addressed the worst of DN’s misconceptions in
my reply.15
I also noted that Nutt and two of his co-authors, Guy M Goodwin and Stephen
Lawrie, had between them declared 22 conflicts of interest in relation to drug
companies, and I wondered whether this explained their dismissal of
psychotherapy, although it is effective and recommended by the UK’s National
Institute for Health and Care Excellence (NICE).
After having read this, you might think that –
in their own words about their critics – these psychiatrists are “extreme,” as
they cherish so many unsustainable opinions about their own field of work. But
unfortunately they are not.
Professor David Nutt is a mainstream
psychiatrist and an influential one. He was previously the United Kingdom’s
drug czar (the main adviser to the government) until he was sacked for claiming
that ecstasy is no more dangerous than riding a horse, which he called
“equasy,” short for “Equine Addiction Syndrome.”16 Nutt won the 2013 John Maddox Prize for Standing Up for
Science. The judges awarded him the prize in recognition of the impact his
thinking and actions have had in influencing evidence-based classification of
drugs, and his continued courage and commitment to rational debate, despite
opposition and public criticism. Words fail me.
Professor Guy M Goodwin is head of Oxford
University’s Department of Psychiatry and was President of the British
Association for Psychopharmacology in 2002-2004.
Professor Dinesh Bhugra, at the Institute of
Psychiatry at King’s College in London, was previously President of the UK’s
Royal College of Psychiatry and is currently president-elect of the World
Psychiatric Association.
Professor Seena Fazel is a Forensic Psychiatrist
at Oxford University’s Department of Psychiatry; he has an interest in violent
crime and suicide.
Professor Stephen Lawrie is Head of the Division
of Psychiatry at the University of Edinburgh and is on the editorial board of Lancet Psychiatry.
These psychiatrists are at the top of their
profession and yet they hold views which are in direct contrast to the science
in their field. This illustrates that psychiatry is in deep crisis and that its
leaders suffer from organised denial.
My preference is to mention names because people
should be held responsible for their actions and arguments. If they do
something laudable, they would be disappointed if they were anonymous, but it
must work both ways. If I concealed the names when people did something
reproachable, or sustained an erroneous belief, I would be inconsistent, and my
readers would try to guess anyway who they were. Science is not about
guesswork, which is another reason why I prefer to mention names. However, it
is fair to point out that when I name a person for something he or she should
not be proud of, there are thousands of others that have done the same or share
the same beliefs.
2
What does it mean
to be mentally ill?
If we first take a look at medicine in general,
we may better understand the diagnostic problems in psychiatry. We put disease
labels on patients with similar problems to make it easier to communicate with
each other, to do research, and to treat and prevent diseases from occurring.
These diagnostic labels work best when we know what causes particular diseases.
It is very useful to know, for example, that a certain pneumonia is caused by
pneumococci, as we may then cure it with penicillin. We therefore subdivide
pneumonias according to their aetiology and may even label them this way, e.g.
we talk about pneumococcal pneumonia.
There are many different kinds of diagnoses in
medicine and some are preliminary and just describe a symptom, e.g. stomach
pain, which may become the final diagnosis, if no cause is found, or the final
diagnosis could be stomach ulcer.
Some diagnoses are syndromes, which consist of
several symptoms, signs and paraclinical findings (e.g. results of blood tests
or radiology).1 Rheumatoid arthritis is a good example. We don’t know
yet what causes it, although we suspect it is an infection. In 1975, a cluster
of cases of arthritis occurred in Connecticut that were later shown to be
caused by a bacterium, Borrelia, which is tick-borne.
Before the aetiology was known, it was a syndrome diagnosis, and the patients
could have experienced a rash, headache, fever and other symptoms and signs in
addition to the arthritis.
We can cure this disease with penicillin and
other antibiotics, in contrast to rheumatoid arthritis, which is treated with
pretty dangerous drugs. Most patients receive non-steroidal, anti-inflammatory
drugs (NSAIDs) for their pain and some die because these drugs can cause
stomach ulcers and heart attacks. Disease-modifying agents are also dangerous,
and drug treatment is therefore an important reason why these patients don’t
live so long as other people.
The level of understanding of psychiatric
diseases is pretty low compared to the rest of medicine, and the treatments are
much more harmful and deadly than those used for rheumatoid arthritis (see
Chapter 14). We don’t know much about what causes mental illnesses and the
diagnostic uncertainty is far greater than in other areas of medicine.
One of the things that is part of the syndrome
diagnosis of rheumatoid arthritis is the presence of rheumatoid factor in the
blood, which is an antibody directed against the person’s own tissues. There is
no such blood test for a mental disorder, and it hasn’t been possible to
demonstrate that people suffering from common mental disorders have brains that
are different from healthy people’s brains (see Chapter 11).
It is not easy to define what we mean by being
ill or having a disease and we are not consistent when we talk about these
issues. People with type 2 diabetes who have no symptoms are not ill, they just
have a risk factor, increased blood glucose, which predisposes them to becoming
ill. And yet we call such people patients and might even say they suffer from
diabetes, although they don’t suffer the slightest bit. As another example,
women who go to mammography screening are often called patients in information
leaflets and scientific articles although they are healthy citizens, at least
in relation to breast cancer.
Quite often, psychiatrists prefer to talk about
a mental disorder, rather than a mental illness or disease, which is because
psychiatric diagnoses are social constructs. The staff at the Mayo Clinic in
Minnesota call it an illness, however:2
Mental illness refers to a wide range of
mental health conditions – disorders that affect your mood, thinking and
behavior … Many people have mental health concerns from time to time. But a
mental health concern becomes a mental illness when ongoing signs and symptoms
cause frequent stress and affect your ability to function … In most cases,
symptoms can be managed with a combination of medications and counselling
(psychotherapy).
This is how most doctors think. As we don’t know
what a mental disease is, we define it as a constellation of symptoms, which
impair the patient’s life.
Psychiatric diagnoses are made by talking to the
patients, but the current checklist approach looks a bit too much like the
familiar parlour game, Find Five Errors. For example, we say that a person who
has at least five symptoms out of nine possible is depressed.3
If we look hard enough, we will surely find
“errors” in most people. We are very quick to form an opinion about a stranger,
which in an evolutionary sense has great survival value. If we come across a
stranger from another tribe in the forest, we decide instantly whether to run,
fight, or start talking. In a similar vein, the doctor’s intuition and
experience may suggest in a matter of seconds what the problem is for a
particular patient, and there is a considerable risk that the doctor from then
on asks leading questions, which yields the required number of error points and
leads to a misdiagnosis.
Instead of trying to understand the patients,
psychiatry has developed into a checklist exercise,4 which one could ask a secretary or the patients
themselves to carry out. Psychiatrists have told me that this is what general
practitioners often do, after which they make a diagnosis. A 1993 study in the
United States by the Rand Corporation showed that:5
Over half the physicians wrote prescriptions
after discussing depression with patients for three minutes or less.
Studies have shown that doctors quite often
don’t use the official checklists but, rather, their hunch about what might be
wrong, which increases the risk of misdiagnosis and overdiagnosis even more.
Although there are 374 diagnoses in DSM-IV (Diagnostic and
Statistical Manual of Mental Disorders), only half of people who were in
treatment met diagnostic criteria for a disorder.6
This is a very unfortunate development. Serious
mental illness is often linked to previous traumas, and childhood adversities
triple the risk of developing psychosis.7 If the medical history isn’t uncovered – which takes
time – the treatments applied will usually be pretty ineffective. Even Robert
Spitzer, who was the driving force behind the new checklist approach to
psychiatric diagnoses in his capacity as chairman of the working group for
DSM-III, now recognizes that what he introduced and believed in has had
unfortunate consequences.
About 25 years ago, I discussed with a seasoned
psychiatrist what the individual perspective means in comparison to what
randomised trials tell us about the value of our treatments. I didn’t understand
what he meant about individualising the treatment, arguing that no two patients
are alike. I said that we wouldn’t know what we were doing unless we studied
our interventions in randomised trials and treated patients with the same
diagnosis in the same way even though they were different. I was influenced in
my thinking by the failure of Freudian psychoanalysis, which was unscientific,
as its practitioners didn’t bother to test whether their theories were true.
They simply felt they were confirmed again and again by their patients.8 Science philosopher Karl Popper has written about
this way of thinking with vitriolic sarcasm:8
“As for Adler, I was much impressed by a
personal experience. Once in 1919, I reported to him a case which to me did not
seem particularly Adlerian, but which he found no difficulty in analysing in
terms of his theory of inferiority feelings, although he had not even seen the
child. Slightly shocked, I asked him how he could be so sure. ‘Because of my
thousand-fold experience,’ he replied; whereupon I could not help saying: ‘And
with this new case, I suppose, your experience has become
thousand-and-one-fold’.”
Even in contemporary psychiatry, diagnoses are
sometimes made this way.
The psychiatrist and I didn’t discuss the same
thing. What he meant was that all the individual circumstances that for a
particular patient leads to a certain diagnosis are different from those of the
next patient who gets the same diagnosis, and if we don’t take these into account,
we might give the patient the wrong treatment. I think we were both right. We
need the randomised trials but only as a starting point for considering all the
other relevant issues for a particular patient, which requires careful
listening and an open mind.
On being sane in insane places
“All the other doctors said he couldn’t
control himself. He has a disorder.”
The family to a boy wrongly diagnosed with
Asperger’s and wrongly treated with olanzapine9
My concerns about how diagnoses are made in
psychiatry are not exaggerated. It is one of the major problems in psychiatry,
and it can take surprisingly little to get a diagnosis. It can be risky, for
example, if patients mention they hear voices. In 1973, psychologist David L Rosenhan
published a famous article in Science, “On being sane
in insane places.”10 Rosenhan and seven other healthy people showed up at
psychiatric hospitals and said they heard voices. The task was to get out again
by their own devices by convincing the staff that they were sane. As soon as
they had been admitted, they therefore ceased to simulate symptoms and behaved
completely normally. Yet they were hospitalised for 19 days on average
(Rosenhan for two months before he was released), and they were prescribed
drugs they avoided swallowing, a total of nearly 2,100 pills of a wide variety,
although the pseudopatients presented with the same “symptom.” They were all
discharged with a diagnosis of schizophrenia in remission, although their only
“symptom” had been that they heard voices, which normal people can experience.
Many of the real patients suspected that the
pseudopatients were sane but the staff didn’t notice the normality. This
illustrates an important bias in diagnosis making. Once a diagnosis is made, it
is hard to reverse; it sticks to you. Rosenhan explained that the label was so
powerful that many of the pseudopatients’ normal behaviours were overlooked
entirely or profoundly misinterpreted by the staff in order to make them fit
with a popular theory of the dynamics of a schizophrenic reaction. A case
summary prepared after a pseudopatient was discharged illustrates this fallacy:
This white 39-year-old male … manifests a
long history of considerable ambivalence in close relationships, which begins
in early childhood. A warm relationship with his mother cools during his
adolescence. A distant relationship to his father is described as becoming very
intense. Affective stability is absent. His attempts to control emotionality
with his wife and children are punctuated by angry outbursts and, in the case
of the children, spankings. And while he says that he has several good friends,
one senses considerable ambivalence embedded in these relationships also.
In actual fact, nothing of an ambivalent nature
had been described in the pseudopatient’s relations, and an entirely different
meaning would have been ascribed if it were known that the man was normal.
The pseudopatients made notes and observed that
patient behaviours were often misinterpreted by the staff. When a patient had
gone “berserk” because he had been mistreated by an attendant, a nurse rarely
asked questions but assumed his upset derived from his pathology, or from a
recent family visit. The staff never assumed that it could be one of themselves
or the structure of the hospital that explained the patient’s behaviour.
Rosenhan explained that the diagnosis becomes a
self-fulfilling prophecy. Eventually, the patient accepts the diagnosis and
behaves accordingly. Rosenhan argues that we should not label all patients
schizophrenic on the basis of bizarre behaviours or cognitions, but limit our
discussions to behaviours, the stimuli that provoke them, and their correlates.
He finds that the psychological forces that result in depersonalisation are
strong and imagines what it would be like if the patients were powerful rather
than powerless. If they were viewed as interesting individuals rather than
diagnostic entities; if they were socially significant rather than social lepers;
and if their anguish truly and wholly compelled our sympathies and concerns;
would we then not seek contact with them, despite the availability of
medications? Perhaps for the pleasure of it all?
Unfortunately, these wise words have been
forgotten in present-day psychiatry where the patients’ personal histories
count for so little that the psychiatrists often fail to unravel them.
Rosenhan describes how powerlessness was evident
everywhere. The patient was deprived of many of his legal rights and was shorn
of credibility because of his psychiatric label. The pseudopatients observed
abusive behaviour, which was terminated quite abruptly when other staff members
were known to be coming; staff were credible witnesses, the patients were not.
Rosenhan concludes that we cannot distinguish
the sane from the insane in psychiatric hospitals and wonders how many sane
people that are not recognised as such in our psychiatric institutions? And how
many patients that might be sane outside the psychiatric hospital but seem
insane in it because they are responding to a bizarre setting?
A research and teaching hospital whose staff had
heard of Rosenhan’s findings doubted that such an error could occur at their
hospital. Rosenhan therefore informed the staff that at some time during the
following three months, one of more pseudopatients would attempt to be admitted
into the psychiatric hospital. Each staff member was asked to judge whether a
patient was a pseudopatient. Forty-one of 193 patients (21%) were alleged, with
high confidence, to be pseudopatients by at least one member of the staff.
However, Rosenhan had not admitted any pseudopatients!
Very many people are wongly diagnosed with
schizophrenia. A 1982 study found that two-thirds of 1,023 African-Americans
with schizophrenia didn’t have symptoms necessary for this diagnosis according
to current guidelines.11 In 1985, the chief psychiatrist at Manhattan State
Hospital reviewed the records of 89 patients with schizophrenia and concluded
that only 16 should have gotten the diagnosis.11
Erroneous diagnoses can be fatal. In one such
case, a child with Asperger was treated with antipsychotic drugs, which
triggered schizophrenia-like symptoms, including psychosis, whereby the
erroneous diagnosis became a self-fulfilling prophecy, which ultimately killed
her because of the drugs that were enforced on her against her will (see
Chapter 15, Dear Luise).12
It is not as odd as it might seem that many
people are wrongly diagnosed with schizophrenia. Psychiatry is radically
different from other areas of medicine, as normal people have similar symptoms
and feelings as patients have; it is mostly a matter of degree. Even for
schizophrenia, this is the case. Psychosis is not a biological illness like
arthritis, and many normal people have psychotic experiences – including
delusions and hallucinations – from time to time.
The demons attack you
When we have made a diagnosis, whether right or
wrong, we blow life into our social construct, e.g. the Mayo Clinic staff said
that the disorder affects you, as if it had some independent existence.
The patient’s symptoms are real, but the
diagnostic label is not real in the sense that it defines something that exists
independent of us. An elephant truly exists and may attack us if we come too
close. We also say that diseases attack us, e.g. “she had an asthma attack,”
like if asthma had some real existence in nature, like an elephant.
You may feel I am getting too philosophical, so
I shall therefore explain in Chapter 5, about ADHD, why these distinctions can
be very important. Here is another example. When a friend of mine was admitted
to hospital in her twenties with acute psychosis, the psychiatrist said: “You
are schizophrenic!” At that point, she felt she stopped existing as a person,
with autonomy and dignity. She was no longer someone that her carers needed to
respect, she was a bag of symptoms they took control over, and the following
years were devastating for her.
Subtle differences can be important. If her
psychiatrist had said: “You are a person who currently has symptoms, which we
usually call schizophrenia,” it would have indicated that the person was still
there and was so much more than her symptoms, and that the disease would not
necessarily last for the rest of her life, which, unfortunately, is often how
psychiatrists have perceived this disease. They haven’t realised that it is
them, with their antipsychotic drugs, who have made the troubles lifelong (see
Chapter 11).
Let there be disorder
“And DSM said: Let there be disorder”
KLRK, GOMERY AND
COHEN IN MAD SCIENCE13
In its fourth edition, the Diagnostic
and Statistical Manual of Mental Disorders (DSM) from the American
Psychiatric Association tried to define what a mental disorder is.14 I have highlighted in italics some of the more
problematic bits:
A clinically significant
behavioral or psychological syndrome or pattern that occurs in an
individual and that is associated with present distress (e.g., a painful
symptom) or disability (i.e., impairment in one or more important areas of
functioning) or with a significantly increased risk of
suffering death, pain, disability, or an important loss of freedom. In
addition, this syndrome or pattern must not be merely an expectable
and culturally sanctioned response to a particular event, for example,
the death of a loved one. Whatever its original cause, it
must currently be considered a manifestation of a behavioral,
psychological, or biological dysfunction in the
individual. Neither deviant behavior … nor conflicts that are primarily between the individual and society are mental
disorders unless the deviance or conflict is a symptom of a
dysfunction in the individual.
This definition is extremely elastic and
includes many judgments, also with regard to the degree of the phenomena being
described. This ambiguity results in large observer variation when independent
psychiatrists assess whether a given person has a mental disorder or not and which
one it is.14, 15
It is quite impossible to make all this
ambiguity and subjectivity operational, and it would be easy to suggest a more
meaningful and robust definition. The DSM is a consensus document, however, and
its diagnoses are unscientific and arbitrary. Real sciences do not decide on
the existence and nature of the phenomena they are dealing with via a show of
hands with a vested interest and pharmaceutical industry sponsorship.16
The claim that the extensive new diagnostic
checklist system introduced in DSM-III in 1980 is reliable has been
convincingly refuted in a book.15 The
disappointing results when two psychiatrists evaluated the same people have
been buried in a smoke of positive rhetoric in surprisingly short articles,
given the importance of the subject. The documentation is hard to find, but the
book says it all. Its two authors did a formidable job in casting light on this
issue that no one has wanted to debate in the American Psychiatric Association.
Even the largest study, of 592 people, was disappointing despite the fact that
the investigators took great care in training the assessors.17 For bulimia nervosa, which is extremely easy to
diagnose, the kappa values when two physicians interviewed the same people were
above 0.80, but for major depression and schizophrenia, two of the most
important diagnoses, the kappas were only 0.64 and 0.65, respectively.
Since we cannot say decisively what a mental
disorder is, we could try the accepted diagnostic procedures on healthy people
to see whether they also get psychiatric diagnoses. Indeed they do. I looked up
Psych Central, a large website that has been highly praised by neutral observers
and has won awards.18 We were eight normal and successful people who tried the
tests for depression, ADHD and mania, and none of us survived all three tests.
Two had depression and four had definite, likely or possibly ADHD. Seven
suffered from mania; one needed immediate treatment, three had moderate to
severe mania, and three had milder degrees.
My results have been confirmed by others, which
suggests that there is one or more psychiatric diagnoses awaiting each of us.
Rosenhan showed that American psychiatry had no clothes, which was confirmed in
another study from the 1970s:11
When researchers interviewed 463 people, they
found that all of them experienced thoughts, beliefs, moods, and fantasies that,
if isolated in a psychiatric interview, would support a diagnosis of mental
illness.
Denmark recegntly introduced a new law that
specifies that patients admitted to hospital are guaranteed a diagnosis within
four weeks. This can be helpful in reducing the stressful waiting time for
people who don’t know if they have cancer or not, but the law was much
criticised, for good reasons. For example, many ailments are selflimiting, and
as all treatments can lead to harm, it is often in the patients’ best interest not to get a diagnosis, as doctors have difficulty in not treating when they have a diagnosis. They have learned a
lot about using drugs for everything one can possibly imagine, and also for
what one cannot imagine, during their medical studies, but very little about
when it would be best to just wait and see. My own take on the new law is that
if you approach a doctor with a mental health problem, you are guaranteed at
least one diagnosis!
It’s not surprising that when therapists were
asked to use DSM criteria on healthy people, a quarter of them also got a
psychiatric diagnosis.16 Imagine if you tested healthy people for cancer
with a test that gave a quarter of them an erroneous diagnosis, which led to
treatment with chemotherapy for a cancer that wasn’t there. We wouldn’t allow
such a poor test to be used in any other area of healthcare except psychiatry.
DSM-III from 1980 was replaced by DSM-IV in
1994, which was even worse than its predecessor and lists 26% more ways to be
mentally ill.16
Allen Frances, chairman for the DSM-IV task force, now believes the
responsibility for defining psychiatric conditions needs to be taken away from
the American Psychiatric Association (APA) and argues that new diagnoses are as
dangerous as new drugs: “We have remarkably casual procedures for defining the
nature of conditions, yet they can lead to tens of millions being treated with
drugs they may not need, and that may harm them.”19 Frances noted that DSM-IV created three false epidemics
because the diagnostic criteria were too wide: ADHD, autism and childhood
bipolar disorder.
Psychologist Paula Caplan was involved with the
DSM-IV and fought hard to get the silliest ideas out.14 In 1985, when the APA decided to introduce Masochistic Personality
Disorder to be used for women who were beaten up by their husbands, Caplan and
her colleagues mockingly inventing Macho Personality Disorder that evolved into
Delusional Dominating Personality Disorder for the violent males, which they
suggested would apply if a man fulfilled 6 of 14 criteria, of which the first
was “Inability to establish and maintain meaningful interpersonal
relationships.”
A crucial question in the clinical encounter is:
Do I have a good reason to believe that it would help to give this person a
diagnosis? Some of us still remember Minimal Brain Damage Dysfunction, which
was thrown in the faces of millions of parents although it could only be
harmful, as there was nothing they could do.
Professionals other than psychiatrists are also
keen to overdiagnose and overtreat people. When my wife was pregnant for the
first time, my main role was to keep the professionals away from her, and I
demonstrated time and again for them that the interventions they suggested were
either useless or harmful, with reference to an evidence-based book based on
systematic reviews of the randomised trials.20 This was how the Cochrane Collaboration, to which I
belong, was born; it started literally with pregnancy and childbirth. Shortly
after our first daughter was born, my wife and I were visited by a nurse who
declared that our daughter would have difficulty talking, as the ligament under
her tongue was too tight. We had a big laugh after the nurse was gone. She
didn’t know what she was talking about, and even if it had been true, there was
no treatment, so why invent a false diagnosis?
Very few leading psychiatrists are willing to
admit that their specialty has spiralled out of control and when issues of
overdiagnosis and overtreatment are brought up, their standard reply is that
many patients are underdiagnosed. Of course there will always be some
overlooked patients, but the main problem is not underdiagnosis but
overdiagnosis, which those psychiatrists that are not silverbacks know
perfectly well. In a 2007 survey, 51% of 108 Danish psychiatrists said they
used too much medicine and only 4% said they used too little.21
I consider it organised denial, whose purpose is
to protect guild interests, that silverbacks all over the world ignore the
clear results of the loose diagnoses and the loose hand at the prescription
pad. Sales of drugs for the nervous system in Denmark are so high that
one-quarter of the whole population could be in treatment. In the United
States, the most sold drugs in 2009 were antipsychotics, and antidepressants
came fourth, which cannot possibly reflect genuine needs, but it gets worse all
the time.18
Our children have not avoided the disease
mongering. In the United States, 1% of children up to only four years of age
are on psychotropic drugs, although the first three years of life are a period
of rapid neurodevelopment,22 and about a quarter of the children in American summer
camps are medicated for ADHD, mood disorder or other mental health problems.18
It is psychiatry that has become insane, not our
children. Some child psychiatrists brag that they can make an initial
assessment of a child and write a prescription in less than 20 minutes, and for
some paediatricians it takes only five minutes.23
Why is it that leading psychiatrists cannot get
enough? Isn’t this behaviour so bizarre, abnormal, socially dysfunctional, and
harmful towards others, that, in accordance with the psychiatrists’ own way of
thinking, it would be legitimate to invent a diagnosis for it? An appropriate
name could be Obsessive Compulsive Disease Mongering Disorder,
OCDMD, which could also be short for Obvious Common
Desire of Money-making Diagnoses. The diagnostic criteria could be a
disturbance of at least six months during which at least five of the following
are present:
1.
Has been on industry payroll
within the last three years.
2.
Is willing to put his or her name
on ghost-written manuscripts.
3.
Believes that getting a diagnosis
cannot hurt.
4.
Believes that screening cannot
hurt, as the drugs have no side effects.
5.
Believes that people with
psychiatric disorders have a chemical imbalance in the brain.
6.
Tells patients that psychiatric
drugs are like insulin for diabetes.
7.
Believes that depression and
schizophrenia destroy the brain and that drugs prevent this.
8.
Believes that antidepressants
protect children against suicide.
9.
Believes information from drug
companies is useful.
I have come across psychiatrists who have a full
house, i.e. for whom all nine criteria apply. I am against forced treatment
(see Chapter 15), but I am in favour of forced retirement for doctors who suffer
from OCDMD in order to protect other people from harm.
You may think I am being unfair to psychiatry,
but my criteria are actually more reasonable than the criteria in DSM-III for
Oppositional Defiant Disorder in children:15
“A disturbance of at least six months during
which at least five of the following are present:
1.
Often loses temper.
2.
Often argues with adults.
3.
Often actively defies or refuses
adult requests or rules, e.g., refuses to do chores at home.
4.
Often deliberately does things
that annoy other people, e.g., grabs other children’s hats.
5.
Often blames others for his or her
own mistakes.
6.
Is often touchy or easily annoyed
by others.
7.
Is often angry and resentful.
8.
Is often spiteful and vindictive.
9.
Often swears or uses obscene
language.”
These criteria are totally subjective and
arbitrary, and “often” is part of them all. How often is “often” supposed to
be? Many children fulfil all nine criteria, and yet only five are needed for a
“diagnosis.” For what purpose? As far as I can see, this is pretty normal
behaviour.
I am sure that naivety, ignorance and the urge
to do good play a role for the silly diagnoses, but there is a darker side to
it. Many of those who develop DSM have heavy conflicts of interest in relation
to the drug industry and creating many diagnoses means money, fame and power
for those at the top.14 It is also about getting control over others, which
is inherent in our biology. Putting diagnoses on people is a powerful
instrument that makes them dependent on what their psychiatrists feel and
think, and it leads to abuse (see Chapter 15). A patient told me that when she
felt her psychiatrist behaved in a God-like manner and asked him whether he
thought he was God, he punished her by adding an additional diagnosis,
borderline personality disorder.
The most prominent American child psychiatrist,
Joseph Biederman, who has likely done more than anybody else to overdose our
children with antipsychotics through his invention of juvenile bipolar
disorder,13, 24
has also behaved in a God-like manner. At a court trial, an attorney asked him
about his rank at Harvard Medical School. “Full professor,” he replied. “What’s
above that?” the attorney asked. “God,” Biederman replied.24
Some psychiatrists cannot even resist the
temptation of putting diagnostic labels on their opponents in public debates.
Henrik Day Poulsen is probably the doctor in Denmark who collaborates the most
with drug companies. In 2013, he was an Advisory Board member or a consultant
for six companies, and “educated” other doctors for nine companies. Like his
benefactors, he didn’t like my book about deadly medicines and organised crime
in the drug industry,18 and wrote in a newspaper article that I, “in my
usual paranoid manner,” had showed off with examples how the ugly drug industry
cheats and defrauds people.25 Usual paranoia means having a chronic psychosis
characterised by delusions, i.e. being insane.
On another occasion, when a politician with a
background as a psychiatric nurse said that, given his income from the drug
industry, she was in doubt about whether he worried about the patients or provided
a sales pitch for using more pills, he called her “desperate.”26 Poulsen has more diagnoses up this sleeve; he has
published the book “Everyday’s psychopaths.”
Psychiatric drugs lead to many wrong
diagnoses
There are several reasons – but few good ones –
why many mental health patients have more than one diagnosis. First, the
diagnostic criteria are very broad and highly unspecific for the problems
patients have. Second, there is a lot of overlap between the different diagnostic
categories and a propensity of one condition to change into another over time.
This is often called high comorbidity, although the problem is not that the
patient has several “diseases” but that the diseases are so vaguely defined
that it is like a biologist looking at a shadow at a distance who says: “It is
an elephant and a wildebeest and possibly also a rhinoceros.” Third, the drugs’
side effects are often misinterpreted as new disorders. Prescribing one drug
therefore often leads to prescribing of other types of drugs in cascade
fashion. For example, an antipsychotic may cause the patient to feel lethargic
and depressed, which leads to an antidepressant; and if started on an
antidepressant, the patient may develop symptoms of mania, which leads to an
antipsychotic.9, 24
Doctors need to realise that it’s impossible to
judge whether a patient truly also suffers from these additional “illnesses,”
as long as the patient is under influence of mind-altering chemicals.9
The adverse effects can come and go, which is an important reason why people
think it cannot be the drug.27 In this way, not only routine
treatment but also attempts at withdrawing a drug – which often elicit these
side effects – can lead to more diagnoses, more drugs and more harm. Addiction
experts know perfectly well that it is futile to diagnose underlying
psychiatric disorders when a patient is abusing drugs. Drug abuse and dependence
with their cycles of intoxication and withdrawal mimic every possible
psychiatric problem. Then why don’t psychiatrists abstain from making diagnoses
when people are under influence of those brain-active chemicals we call
psychiatric drugs?27
It should be forbidden to make new diagnoses
while the patient is in treatment with psychotropic drugs, and if psychiatrists
cannot resist the temptation, they should by default call it a likely
drug-induced disorder. This will put the blame on themselves and not on the
patient, and will increase the likelihood that psychiatrists would taper the
drugs, as they would be afraid of litigation, if they did nothing after having
diagnosed a drug-induced disorder.
A fourth important reason for the far too many
diagnoses is that the diagnoses are often made at the first visit, when the
patients may turn up with sadness, stress at work, marital problems, a recent
trauma or so much else that many of us will experience from time to time.
Doctors tend to forget that the diagnosis is a snapshot, and that the patients
might be fine both before and after their visit to the doctor. Obviously, the
more a person visits a doctor, the higher the risk of getting a false
diagnosis.
Doctors should be patient and should try to
avoid putting diagnostic labels on people at their first visit, also because
diagnoses are sticky. Even when proved wrong later on, diagnoses are almost
impossible to get rid of again, and they stigmatise people (see Chapter 6) and
may have implications for employment, insurance, and many other important
issues.
Doctors should also avoid prescribing drugs at
the first encounter unless the situation is very acute. If a patient insists on
getting a drug, e.g. an antidepressant, an honest discussion of its many harms
and its doubtful benefits (see Chapter 3) should convince most patients that it
is not a good idea to rush into action.
The diagnostic labels psychiatrists use fit very
poorly with the type of patients general practitioners meet, but any challenge
to specialist perspectives on mental disorders in primary care usually
generates incredulity among psychiatrists and a reinforcement of their belief
that retraining of primary care workers is the solution.28 Retraining in what? Not in the DSM, I hope!
The Goodness Industry
Our “doing good” culture poses a major health
risk in the psychiatric field. Institutions such as kindergartens and schools
may put pressure on parents to accept dubious diagnoses like ADHD to obtain additional
funding, and other institutions may put pressure on psychiatrists to obtain a
diagnosis of post-traumatic stress disorder.
It can also be rewarding for people themselves
to play sick to get a diagnosis, which can open the floodgates for all sorts of
benefits in terms of increased social services, educational support, flex jobs,
light jobs, early retirement, disability allowance, insurance claims, and
whatever else. As an example, education benefits in Denmark can be 2.4 times
higher for people who have been diagnosed with schizophrenia, schizotypal
personality disorder, persistent psychotic condition, short-term psychotic
condition, schizoaffective disorder, unspecified psychosis of nonorganic origin
and emotionally unstable personality structure of borderline type. The
borderline diagnosis in particular is a pretty elastic one.
In the Goodness Industry, too many therapists
are too tempted to do too much for too many people, and patient representatives
– often supported by the pharmaceutical industry – are often wrong when they
claim that their members are underdiagnosed, undertreated, and
underprioritised.
I have heard several senior psychiatrists say it
cannot hurt anyone to get a diagnosis. Such people shouldn’t work as
psychiatrists. All professional interventions in citizens’ lives, including
giving people diagnoses, can cause harm. It is a paradox that public debates
and reports in the news media are dominated by the beneficial effects of
diagnoses and interventions when the first thing we know about any intervention
is that it can be harmful. If this were not the case, it could not have any
potentially beneficial effect.
Patients are not consumers
In the Anglo-Saxon tradition, patients are often
called consumers, but it is a strange term. Patients don’t consume anything; in
fact, the psychiatric drugs consume them, as they take their personality away.
Consumption was the old term for tuberculosis, which “eats” the tissues.
Similarly, psychiatric drugs “eat” the brain if taken for a long time, as they
cause chronic brain damage (see Chapter 11).
When patients with breast cancer, prostate
disease, fractures and HIV were asked, they preferred to be called patients,
not consumers, clients, customers, or anything else.29 Many alternatives to “patient” incorporate assumptions
(e.g. a market relationship), which care recipients may find objectionable. We
should respect this and drop the term consumer. It was introduced with good
intentions about empowering patients but this can be done without calling them
something they don’t want to be called and which is pretty misleading, too.
More funny and fake diagnoses
When life gets too absurd, a good laugh can
help. Two funny videos illustrate how easy it is to convince healthy people to
take drugs they don’t need for a disease they don’t have. The Australian artist
Justine Cooper invented a TV commercial that advertises Havidol (have it all),
with the chemical name avafynetyme HCl (have a fine time plus hydrochloric
acid).30, 31 Havidol is for those who suffer from dysphoric social
attention consumption deficit anxiety disorder (DSACDAD).
Feel empty after a full day of shopping? Enjoy
new things more than old ones? Does life seem better when you have more than
others? Then you may have the disorder, which more than 50% of adults have.
Havidol should be taken indefinitely, and side effects include extraordinary
thinking, dermal gloss, markedly delayed sexual climax, inter-species communication
and terminal smile. “Talk to your doctor about Havidol.” Some people believed
it was for real and folded it into real websites for panic and anxiety disorder
or for depression.
Another video featured journalist Ray Moynihan.32 A new epidemic – motivational deficiency disorder – was
first announced in the BMJ’s 1 April issue in 2006,33 and like for Havidol, some people believed the disease
existed. In its mild form, people cannot get off the beach or out of bed in the
morning, and in its most severe form it can be lethal as the sufferer may lose
the motivation to breathe. Moynihan says: “All my life people have called me
lazy. But now I know I was sick.” The drug is Indolebant, and its champion, neuroscientist
Leth Argos, reports how a patient’s wife telephoned him and was in tears. After
having using Indolebant, her husband had mowed the lawn, repaired the gutter
and paid an electricity bill – all in one week.
I showed these two videos as an introduction to
my talk about overdiagnosis and overtreatment when I lectured for over 100
psychiatrists in 2012. They laughed out loud but not when I added that what
they had just seen wasn’t far from their everyday practice.
A patient once told me she suffered from chronic
fatigue syndrome but she described many weird symptoms that couldn’t possibly
be disease symptoms. A little later, I told the company I was in about the
video with Moynihan’s motivational deficiency disorder; everyone laughed but
her. Perhaps she got my hint.
There is a cartoon where the doctor says to the
patient: “We can’t find anything wrong with you, so we’re going to treat you
for Symptom Deficit Disorder.” I also came across Disorder
Fabrication Syndrome, invented by Barry Turner, Lecturer in Medical
Ethics and Law:34
A new psychiatric condition has been observed by
psychiatrists working at the Brandt-Sievers Institute for Eugenics. The
condition, Disorder Fabrication Syndrome, is a kind of paranoid delusional disorder
where the sufferer believes in their own infallibility and superiority and is
often associated with comorbid narcissistic personality disorder. The sufferer
will incessantly classify all manner of normal human behaviour as a disorder or
syndrome.
The disorder is thought to be caused by a
chemical imbalance brought on by studying psychology and psychiatry at an
institute funded by big pharma. The constant handling of money doled out by the
drug companies seems to affect the way the psychologists and psychiatrists
process neurotransmitters. Another theory is that this might be a kind of
hysteria induced by chronic avarice.
The most effective treatment for this group of
patients is to strike them off any professional registers which makes their
craving for pharmaceutical company money remit. In extreme cases, prosecuting
them for research fraud is another alternative. This sometimes controversial
method has just been applied with great success at the University of Vermont.
It is believed that the condition is
underdiagnosed in psychiatrists and clinical psychologists and that a screening
programme ought to be introduced in this high risk population.
There are many silly diagnoses in psychiatry
that could be used to label many people, e.g. Premenstrual Dysphoric
Disorder, which is also harmful, as the diagnosis might prevent women
from getting a job or have custody of their children in case of a divorce.14
The criteria for this diagnosis are so unspecific that they cannot distinguish
between women with severe premenstrual symptoms and other women, and even men
give answers similar to women with severe symptoms,14 so I take it
that men should be treated indefinitely, as they have no periods. The FDA didn’t
care. It approved fluoxetine for this non-disease, which the US psychiatrists
had the gall to call depression!18 Eli Lilly gave the drug another
name, Sarafem, which was a repainted Prozac with attractive lavender and pink
colours. Pretty ironic colours on a pill that ruins people’s sex lives (see
next chapter). In Europe, Lilly was forbidden to promote fluoxetine for
something that wasn’t a disease, and the European Medicines Agency fiercely
criticised Lilly’s trials, which had major deficiencies. The Cochrane review of
this non-disease included 31 trials and it found antidepressants to be
effective.35
Of course. Everything that has side effects (and there were plenty)35 seems to work when the outcomes are subjective (see next
chapter), both for diseases and non-diseases.
3
Depression
Screening for depression
The diagnostic criteria in psychiatry are very
broad, and they should therefore not be applied on healthy people. Such
screening is a sure way to make us all crazy. A notorious programme in the
United States was TeenScreen, which came up with the result that one in five
children suffer from a mental disorder, leading to a flurry of discussions
about a “crisis” in children’s mental health.1
It wasn’t a crisis in children’s mental health
but a crisis in the standard of psychiatric research2 plus a chronic impairment of the intellectual
capacity or honesty of some leading psychiatrists. We usually say that a
screening tool shouldn’t lead to too many false negative findings, but for
depression, it doesn’t really matter if we overlook some cases. It is so easy
to spot the severe cases of depression. Therefore, what is being overlooked are
the mild cases, which are self-limiting and for which there is consensus that
antidepressant drugs don’t work.
What is important is that there should not be
too many false positives, i.e. healthy people who are diagnosed with
depression, but this is exactly what we get. The screening test recommended by the
World Health Organization is so poor that for every 100,000 healthy people
screened, 36,000 will get a false diagnosis of depression.3, 4 When I criticise my colleagues for using such poor
tests, I am told that they are only a guideline in the diagnostic work-up and
that additional testing will be performed. In an ideal world perhaps, but this
is not what most doctors do. Many patients report that there was no further
testing and that they got a diagnosis and a prescription in about ten minutes.5 This is expected, as 80-90% of prescriptions are
written by general practitioners,5, 6 and they don’t have much time.
That the standard of psychiatric research is
very poor is illustrated by the fact that in only 5% of the studies assessing
the false positive and false negative results of screening for depression had
the researchers excluded patients who were already diagnosed with depression.2
This flaw is inexcusable. If we want to know how good ultrasound is to pick up
cancers in the stomach of people who look healthy, we don’t study people who
have already been diagnosed with large cancers with ultrasound, the very
technique we want to test.
The Cochrane review on screening for depression
recommends firmly against it, after having examined 12 trials with 6,000
participants.7 Nonetheless, the Danish National Board of Health
recommends screening for depression.8 Our health authorities are masterminds in the sport
of eating a cake and still having it. After dutifully quoting the Cochrane
review, the authorities recommend screening for various poorly defined “risk
groups,” which are:
·
Previous depression
·
Depression in the family
·
Heart disease
·
Stroke
·
Chronic pain
·
Diabetes
·
Smoker’s lungs
·
Cancer
·
Parkinson’s disease
·
Epilepsy
·
Other mental disorders (because of
comorbidity with depression)
·
Pregnant women
·
Women who just had a baby
·
Refugees
·
Immigrants.
This impressive list of people in “risk groups”
cover a considerable part of the population. Unsurprisingly, there were many
psychiatrists in the working group that came up with these recommendations.
When I – as invited speaker at large scientific
meetings for psychiatrists – have pointed out how harmful screening for
depression is, they didn’t pay the slightest attention. This organised denial
has shocked me, particularly when the professor at my own hospital – in reply to
my remark that screening leads to treatment of many healthy people with
antidepressants – said that it didn’t matter because antidepressants have no
side effects! Really? To a substantial extent, the “risk groups” comprise those
who have lived more than five decades, and antidepressants kill many of these
(see Chapter 14).9
It is difficult to know how much overdiagnosis
of depression there is, as we don’t even know what a true diagnosis is. If we
count elephants, we don’t suddenly decide to include also wildebeests in our
count just because they are also greyish and have four legs. For depression,
however, the criteria for the diagnosis have been broadened enormously over the
years. Based on the nine criteria in DSMIV, psychiatrists have calculated that
one can be depressed in at least 1,497 different ways.10 Some of these variations are not really what most
people would call depression.
In 2010, the US Centers for Disease Control and
Prevention stated that 9% of the interviewed adults met the DSM-IV criteria for
current depression.3 However, very little is required. You are depressed
if you have had little interest or pleasure in doing things for eight days over
the past two weeks plus one additional symptom, which can be many things, for
example:
·
trouble falling asleep
·
poor appetite or overeating
·
being so fidgety or restless that
you have been moving around a lot more than usual.
This is unreasonable. A boy whose sweetheart
abandoned him will feel miserable for all fourteen days and cannot sleep or eat
much. Little pleasure in doing things will happen to most of us, no matter how
positive, active and outgoing we are, and most Americans overeat.
With such an approach to diagnosis, it is not
surprising that the prevalence of depression has increased dramatically since
the days when we didn’t have antidepressant pills.11 And there is a substantial risk of circular evidence
in all this. If a new class of drugs affect mood, appetite and sleep patterns,
depression may be defined by industry supported psychiatrists as a disease that
consists of just that; problems with mood, appetite and sleep patterns.12
I have listened to many pseudo-academic
discussions where people have tried to explain why there are more depressed
people now than previously. The usual explanation is that our society has
become more hectic and puts greater demands on people. As far as I can see, we
are more privileged than ever before, our lives are less stressful, social
security is far better, and there are far fewer poor people. It is more
reliable to estimate whether the prevalence of severe depression has increased,
and psychiatrists constantly tell me that this is not the case.13
One of the signs that US silverbacks have run
amok is the medicalisation of grief. In DSM-III, bereavement was a depressive
disorder only if it had lasted for more than a year, in DSM-IV it was two
months, and in DSM-5 from 2013 it is only two weeks. Few marriages are so bad
that the person left behind will rejoice after only two weeks that the partner
is gone. We should allow people to be unhappy at times – which is completely
normal – without diagnosing them. In clinical practice, these “limits” are
immaterial of course. A clinician will not tell a sad person to wait another
week before he fulfils the diagnostic criteria for depression and can get a
prescription.
The major change in DSM-III from 1980 was the
introduction of a symptom-based approach for diagnosis. It has been criticised
for creating diseases and for classifying normal life distress and sadness as
mental disease in need of drugs. Expected reactions to a situational context,
for example the loss of a beloved person, divorce, serious disease or loss of
job, are no longer mentioned as exclusion criteria when making the diagnosis.
These changes, which are so generous towards the drug industry, could be
related to the fact that all the DSM-IV panel members on mood disorders had
financial ties to the pharmaceutical industry.3
Public debates on overdiagnosis are frustrating,
and I wonder whether leading psychiatrists don’t understand the issues, or
whether they display organised denial in order to cover up for their failures.
We use so many antidepressants in Denmark that every one of us could be in
treatment for six years of our lives, and the increased use of these drugs
doesn’t reflect an increasing need; it is closely related to the marketing
pressure.14 This should make everybody’s alarm bells ring, but
when the TV host asked us during a panel discussion how we could reduce the
high consumption and expressly pointed out that we should not discuss whether
the consumption was too high, Professor Lars Kessing didn’t reply to the
question but said the consumption wasn’t too high because the prevalence of
depression had increased greatly during the last 50 years.
The denial seems epidemic. Another chief physician
at Kessing’s department recently told a journalist that the consumption of
antidepressants corresponds to the number of sick patients.15 Such statements that all is fine are misleading.
Although there is international agreement that antidepressants don’t work for
mild depression and shouldn’t be used, most of those treated have rather mild
depression.6
Studies have shown that more people are
overdiagnosed than underdiagnosed for depression,13 which shouldn’t
surprise anyone who is not a psychiatrist. In fact, the term “major depressive
disorder” has become contradictory in terms, as it now includes cases of mild
major depressive disorder. This is also meaningless since such cases are
neither major, nor depression, nor even a disorder.13
Antidepressant drugs don’t work for
depression
We have used antidepressant drugs for more than
50 years, but it is unlikely that they have a real and useful effect on
depression, whereas their many harmful effects are not in doubt.
Antidepressants cause more harm than good,16 which the remainder of this chapter is about.
The US Food and Drug Administration (FDA) found
in a metaanalysis of randomised trials with 100,000 patients, half of whom were
depressed, that about 50% got better on an antidepressant and 40% on a placebo.17 A Cochrane review of depressed patients in primary
care reported slightly higher benefits,18 but didn’t include the unpublished trials, which
have much smaller effects than the published ones.19
Most doctors call the 40% in the placebo group a
placebo effect, which it isn’t. Most patients would have gotten better without
a placebo pill, as this is the natural course of an untreated depression.
Therefore, when doctors and patients say they have experienced that the
treatment worked, we must say that such experiences aren’t reliable, as the patients
might have fared equally well without treatment.
It is important to understand these issues. When
I point out in public debates that antidepressants are pretty ineffective,
psychiatrists often say that they are still useful, as the patients benefit from
the placebo effect. But how large is the placebo effect? One of my senior
researchers, Asbjørn Hróbjartsson, wanted to find this out, so he collected all
trials where the patients were randomised to placebo or nothing (often called a
waiting list control group). In the most recent update of our review, we
included 234 trials investigating 60 clinical conditions in all areas of
healthcare.20 We found that placebo interventions do not have
important clinical effects, apart from a few areas such as pain and nausea.
However, we cannot know whether these effects are real or the patients just
tried to be kind to the experimenting doctor. The problem with such studies is
that we cannot blind a trial where half the patients get something that looks
like an active treatment, and the other half don’t get anything. Psychological
research has taught us that in such settings, and when the outcome is
subjective, positive effects will be considerably exaggerated.
Hróbjartsson recently published another
important study. He wanted to see to what extent observers who had not been
blinded to the treatment patients received exaggerate the effect, and he
collected all trials that had both a blinded and a non-blinded observer.21 He included 21 trials for a variety of diseases and
found that the treatment effect was overestimated by 36% on average (measured
as odds ratio) when the non-blinded observer assessed the effect compared to
the blinded observer. Most of the studies had used subjective outcomes, and as
the effect of antidepressants is also assessed on subjective scales (e.g. the
Hamilton scale), Hróbjartsson’s results are directly relevant for
antidepressant trials, as these trials have not been effectively blinded. Antidepressant
medications have conspicuous side effects, and many patients and doctors will
therefore know if the blinded drug contains an active substance or placebo. If
we assume that the blinding is broken for all patients in the antidepressant
trials, and adjust for the bias the loss of blinding causes, we will find that
antidepressants have no effect (odds ratio 1.02).3, 16
The blinding needs not be broken for all
patients, however. All that is required for the effect to disappear is that 5%
of the patients are misclassified in terms of whether they became better or
not, as the 50% effect on active drug then becomes 45%, and the 40% effect on
placebo also becomes 45%. The blinding is generally broken for many patients in
psychotropic drug trials, in some cases for all patients, as in a trial of
alprazolam versus placebo.22 The authors of a review of blinding problems ended
their paper by saying that, “The time has come to give up the illusion that
most previous research dealing with the efficacy of psychotropic drugs has been
adequately shielded against bias.”22 This was in 1993, but the
psychiatrists have chosen to totally ignore this fundamental problem in their
research on drugs. Organised denial again.
Many years ago, trials were performed with
tricyclic antidepressants that were adequately blinded, as the placebo
contained atropine.23 This substance causes dryness in the mouth and other
side effects similar to those seen with antidepressants, and the trials are
therefore much more reliable than those using conventional placebos. The mouth
can become so dry on an antidepressant that one can hear the tongue scraping
and clicking, which is an important reason that some patients lose their teeth
because of caries. A Cochrane review of nine trials (751 patients) with
atropine in the placebo, failed to demonstrate an effect of tricyclic
antidepressants.23
The measured effect, a standardised mean difference of 0.17, was not only
statistically uncertain, but also so small that even if it were true, it would
have no clinical relevance. It corresponds to 1.3 on the Hamilton scale, which
ranges from 0 to 52, and the smallest effect that can be perceived on this
scale is 5-6.24 (In the clinical study reports we obtained from the
European Medicines Agency, the median standard deviation on the Hamilton scale
after treatment was 7.5; thus, a standardised mean difference of 0.17
corresponds to 0.17 x 7.5 = 1.3.) The minimal clinically
relevant effect is of course larger than the bare minimum that can be
perceived. That you can see light at the end of the tunnel doesn’t necessarily
mean that there is enough light to read a newspaper.
Given the poor blinding and the subjective
scales used to assess the outcome, it is not surprising that everything that
numbs people or makes them euphoric seems to “work” for depression, including
antipsychotics, anti-epileptic drugs and stimulants. Three of the 17 items on
the Hamilton scale, for example, are about insomnia and this problem alone can
yield six points on the scale.25 And if a person goes from maximum anxiety to no anxiety,
eight points can be earned. Thus, alcohol would clearly “work” for depression,
but we don’t prescribe alcohol for people.
Other meta-analyses, which, like the Cochrane
review, were not financially supported by the drug industry, have also shown
disappointing results. Virtually all psychiatrists say that antidepressants
work for severe and moderate depression, but that isn’t correct. According to
the American Psychiatric Association, moderate depression has a Hamilton score
between 14 and 18, severe depression is between 19 and 22, and very severe
depression is above 22.26 A meta-analysis with individual patient-level data
from six trials (718 patients) found that selective serotonin reuptake
inhibitors (SSRIs) were ineffective for both mild, moderate and severe
depression, and even for patients with very severe depression, the effect
corresponded to only 3.5 on the Hamilton scale,26 which is well
below what is a minimal clinically relevant effect. Furthermore, these trials
were not adequately blinded, as they had used conventional placebos. If we
adjust for this bias, the small effect for very severe depression disappears.
Even if we assume that antidepressants might have a trivial effect on those who are very severely
depressed,26, 27 this is a small fraction of the patients that are
treated. A study found that only 8% of depressed patients treated in routine
clinical practice could be included in a standard efficacy trial.28 As half the patients in depression trials have very
severe depression,26, 29 and as many of the trials have been performed in
hospitals, it cannot be correct when some psychiatrists claim that
antidepressants are highly effective for the melancholic depression they treat
in their hospitals.
A highly revealing way of judging the efficacy
issue is to see how much faster people improve on an active drug than on a
placebo, and a meta-analysis of 37 industry-sponsored trials of fluoxetine and
venlafaxine showed just that.30 The patients were severely depressed to begin with
and after four weeks on the drug, they were only mildly depressed (Figure 3.1).
It took eight more days before patients on the placebo had improved to the same
extent. However, as these trials were not adequately blinded, the true
difference is likely to be a few days,23 since a Hamilton score difference
of 1.3 amounts to less than a week on the figure.
Thus, there is no good reason to use
antidepressant drugs or to claim that they work like insulin for diabetes. The
effect of insulin is instantaneous; in contrast, what we see in the figure is
the slow, spontaneous remission in both groups, plus some bias in the active
group.
Figure
3.1. Depression severity over time in 37 trials of fluoxetine or venlafaxine
versus placebo. HAM-D is the Hamilton Depression Scale. Redrawn.
These sobering facts are in stark contrast to a
2013 statement from the president of the American Psychiatric Association,
Jeffrey Lieberman, who claimed that antidepressants are highly effective and
alleviate the symptoms substantially, if not completely, in 50-80% of the
patients who suffer from major depression.31 In 2014, the medical director at the Norwegian drug
agency, Steinar Madsen, said at a meeting that antidepressants work for 50-60%
of the patients. I replied that his statement illustrated why we cannot trust
our drug regulators and reminded him that the FDA had found in their analysis
of 100,000 patients that antidepressants worked for only 10% of the patients.
These monstrous exaggerations are everywhere. A
Cochrane review of electroconvulsive therapy claimed precisely the same, that
antidepressants work for 50-60% of the patients.32 I wonder who invented these numbers and why people
are so eager to ruin their credibility by citing them?
Reboxetine is approved in Europe but not in the
United States, where Pfizer’s application was rejected.33 A German health technology assessment institute
wanted to evaluate the drug33 but, despite several requests, Pfizer
steadfastly refused to provide the institute with a list of all published and
unpublished trials.34 The institute therefore concluded that it couldn’t
assess whether the drug was of any benefit,35 but as this could lead to lack of reimbursement,
Pfizer responded immediately, now with the ludicrous claim that they had
provided the institute with sufficient data, which from Pfizer’s point of view
were “suited for a benefit assessment.” Pfizer ultimately had to hand over all
the trials, however, and the analysis showed that reboxetine produced no
significant effect. The European Medicines Agency (EMA) did nothing,36 apart from criticising the institute for having left out
a statistical outlier from its analysis, but that criticism was inappropriate.
The odds ratio for response in the seven included trials was 1.24 (95%
confidence interval (CI) 0.98 to 1.56) whereas it was 11.4 (95% CI 3.1 to 42.1)
for the excluded trial. When two confidence intervals are so far apart, we
suspect fraud, and even one of the included trials was suspiciously positive.
Patients are the best judges for deciding
whether a subjective effect of a drug outweighs its side effects, but the
trials showed no such benefit. Just as many patients stopped treatment
prematurely when they were on antidepressants as when they were on placebo.37 This shows that the patients find the drugs useless, and
it is likely even worse than this. Most patients on active drug will experience
side effects, and although they might have preferred to quit, they could have
decided to go on till the end of the trial hoping that a beneficial effect
would eventually show up. Conversely, patients who have guessed they are on
placebo might be more keen to stop, as it isn’t meaningful to take placebo and
waste time on control visits. Therefore, the fact that the patients in these
poorly blinded trials stop their trial drug just as often when it’s active as
when it’s placebo could mean that in reality they feel the drug is worse than
the disease. I find this likely.
US court cases that have temporarily opened the
companies’ archives, and also our own archive of trials submitted to the EMA,
have revealed that the industry has measured the patients’ quality of life in
many trials but has failed to publish the results.11 It doesn’t take
a genius to work out that if the results had been positive the world would have
heard about them.
An analysis of a prescription database showed
that after only two months half the patients had stopped taking the drug.38 Nonetheless, the psychiatrists love the pills and often
say they work in 70-80% of patients,39 which is mathematically impossible when only 50%
continue taking the drug after two months.
There are many reasons why the effect of
antidepressants has been overrated. It provides prestige and cool cash to claim
large effects. The psychiatrists know that if they report major benefits and
few harms in the trials, the drug companies will ask them again, which will
enhance their academic standing and income. This distortion is sometimes done
deliberately. It is very telling that psychiatrists found a positive effect of
SSRIs in eight depression trials, including 1,756 children and adolescents
(effect size 0.25), whereas no effect was reported by patients (effect size
0.05).40 The Cochrane review of newer antidepressants in children
and adolescents found exactly the same (effect sizes of 0.29 and 0.06,
respectively, calculated by me based on standard deviations from other
reviews).41
Trials in adults show the same. The clinicians’
assessments in trials of old drugs like amitriptyline showed an effect size
0.25 whereas the patients’ effect size was 0.06.42 This could be because clinicians know the side effects
better than patients and therefore are better at unblinding the trials, but it
could also simply be a matter of academic corruption.
Other important flaws in placebo
controlled trials
Virtually all trials of psychotropic agents are
flawed, not only because of the unblinding problem, but also because of their
design. This was recognised decades ago, but drug trials and reviews have
continued to pretend the problem doesn’t exist,43 likely because the psychiatrists choose to ignore
everything that threatens the myths they have built up around their profession.
The design problem is that people are being
randomised who have already been treated with the same type of drugs, which
means that harms are inflicted on the placebo group because of withdrawal
effects. Three-quarters of the depression trials have an initial placebo
lead-in period of 1-2 weeks where patients can be excluded before
randomisation,29
but this time is too short because some withdrawal symptoms come much later or
last much longer.44, 45 In nine trials of depression, patients were abruptly
switched to an inactive placebo for 1-2 weeks after they had been treated for
8-9 weeks with duloxetine, which has a half-life of only 12 hours.45
About half the patients experienced withdrawal effects, and about half had not
yet resolved after the 1-2 weeks of observation. Eli Lilly didn’t report what
happened to these patients after the formal observation period, but in the
first quarter of 2012 more reports were submitted to the FDA on serious drug
withdrawal effects for duloxetine than for any other regularly monitored drug,
including two opioids.44
There are many tricks. Some studies exclude
patients who improve in the placebo lead-in period; some studies use active
drugs in this period and exclude people who experience troublesome side
effects; and some studies have both types of “cleansing,” which was the case
for one of the very few trials of fluoxetine in children that purported to have
shown an effect.46 But even with this extremely biased design, the children
fared no better on the drug than on placebo on self-rating scales or on ratings
by their parents. The “effect” was only seen on a secondary scale filled out by
the psychiatrists who were paid by Lilly to run the trial!46
What is particularly interesting is that SSRIs
don’t work for children and adolescents.47 This might be because many of these patients were not
exposed to an antidepressant before they were recruited to the trials, which
are therefore less biased than trials in adults.48
Why do doctors treat depression with drugs? Not
to improve the score on some highly bias-prone subjective scale. What we want
to achieve more than anything else is to reduce the patients’ risk of
committing suicide, and I shall discuss this issue below. It is also important
to help people cope with their lives, e.g. getting them back to work and saving
their marriages and other social relations, but although there are thousands of
trials of antidepressants we don’t know whether drugs are helpful for this.
This means that either it hasn’t been studied, or the results have been so
disappointing that the industry has buried them. Given the drugs’ lack of
efficacy on depression and their pronounced side effects, especially their
damaging effect on people’s sex lives (see below), it seems unlikely that they
have such effects.
Fluoxetine, a terrible drug, and
bribery in Sweden
The SSRIs are pretty terrible drugs and patients
aren’t too happy taking them. But doctors choose to ignore how bad these pills
are. When the first best-selling SSRI, fluoxetine, appeared in the late 1980s,
there was no doubt about it. Senior management in Eli Lilly wanted to shelve it
after having considered to market it for eating disorders,11 but Lilly was in
serious financial trouble and had to make it a success.3
Initially, the FDA was sceptical and noted
serious flaws in Lilly’s trials. An FDA officer wrote in 1984 that patients who
didn’t do well after two weeks had their code broken, and if they were on
placebo, they were switched to fluoxeine.39 In this way, six weeks of
fluoxetine was compared to two weeks on placebo, which is a hopelessly flawed
comparison and, with the blinding broken, more bias was introduced. It also
turned out that 25% of the patients had taken an additional drug, and when the
FDA in 1985 removed patients on other drugs from Lilly’s trials, there was no
significant effect of fluoxetine. By adding benzodiazepines, Lilly broke the
rules for its trials but didn’t inform the FDA, and when the FDA later learned
about it, the agency permitted it and thereby broke its own rules.49 The public and the doctors were never informed about
this ruse.
The FDA went to extremes to make it look like
fluoxetine worked.39 Perhaps the fact that Lilly is an American company
played a role. Fluoxetine was approved when Bush senior was president and he
had been a member of the board of directors of Lilly. Vice President Dan Quayle
was from Indiana where Lilly’s headquarters are, and he had former Lilly
personnel on his own staff and sat on an FDA oversight committee.49
The German drug regulator found fluoxetine
“totally unsuitable for the treatment of depression,” and furthermore noted
that according to the patients’ self-ratings there was little or no response,
in contrast to doctors’ ratings.46
Despite the formidable odds, Lilly turned this
awful drug into a blockbuster, which contributed to making the company one of
the world’s ten biggest. It’s pretty clear to me that without the help of
corrupt psychiatrists, big pharma wouldn’t have sold many of its psychotropic
drugs.3
Corruption is widespread in American healthcare, but even in Sweden there was corruption.
When the director of Lilly in Sweden, John Virapen, showed some of the data on
the drug to Swedish psychiatrists, they laughed and didn’t think he was serious
about seeking approval for it.50 But that didn’t last long.
Virapen, who had good reasons to feel his future
career at Lilly depended on approval of fluoxetine, solved his problem with
bribery. He found out who the independent expert was who would examine the
clinical documentation for the Swedish drug agency. This expert was Anders
Forsman, forensic psychiatrist and member of the legal council in the Swedish
National Board of Health.51 Forsman didn’t like fluoxetine at all and had laughed
about it just two weeks earlier, but when Virapen asked him what was required
to get the drug approved quickly, Forsman suggested $20,000, which shouldn’t
become known to the taxman, plus a good deal of research money for his
department. Half the money to be paid at once and the other half when the mission
was accomplished, just like when the mob orders a murder.
After the deal, deaths disappeared in footnotes
and, according to Virapen, it went something like this:50 “Five had
hallucinations and tried to commit suicide, which four of the test subjects
succeeded in doing” was changed to: “Five of the other test subjects had
miscellaneous effects.” On top of this, Forsman wrote his own personal letter
of recommendation.
I have met with Virapen and his account of the
events has been confirmed by official documents. For example, the chairman for
the Institute against Bribery wrote to the Department of Justice that the
agreement was that Forsman would get the money in return for a positive report
about the drug, and that he cashed the money. Forsman didn’t cover his tracks.
While the work was ongoing, he wrote to Virapen that he hoped he would be able
to function as a sort of lubricant for the processes, “You understand what I
mean.”
When confronted with his misdeeds many years
later, Forsman lied about them.52 He claimed he had informed the director of the Swedish
drug agency verbally about his collaboration with Lilly before he got the
official assignment and that he also mentioned his conflict of interest in his
report and explained about his contacts with Lilly in detail, but that someone
at the Board of Health had erased it. This seems pretty far-fetched and the
director and another professor at the drug agency both declared that they would
never have accepted an expert with such conflicts of interest.
The approval in Germany also followed what
Virapen calls “unorthodox lobbying methods exercised on independent members of
the regulatory authorities.”
After having been so helpful to Lilly, Virapen
was fired. This is like a script from the mob. When a hitman has murdered a
well-known citizen, it is safest to leave no witnesses and kill the assassin.
The official explanation was that Lilly had certain ethical principles! Two
other people who knew about the bribery were also fired.
Virapen tried to prosecute Forsman, but it
wasn’t possible because he wasn’t an employee of the health authority. The
Swedish anticorruption law was later amended, as a direct consequence of this
affair.
Forsman’s career didn’t suffer. He came to work
for the court, as a psychiatric assessor for Sweden, and probably felt at home
there, as there is nowhere where people lie as much as in court.
There weren’t many truly depressed people in the
mid-1980s when the criteria for the diagnosis were much more stringent and
relevant than today. Fluoxetine was therefore marketed as a mood lifter. Not
much difference to street pushers here, as fluoxetine can have cocaine- and
amphetamine-like stimulant effects on some people.49 The warnings on
the labels for antidepressant drugs, such as anxiety, agitation, panic attacks,
insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia,
hypomania, and mania leave no doubt that these drugs can induce medication madness
just as street drugs can.49
Harms of antidepressant drugs are
denied or downplayed
It took some years after I started my research
on antidepressant drugs before I fully realised how dangerous they are. This is
because their most serious harms have been denied or downplayed by all the
major players in the field who have a joint interest in obscuring them. The
drug industry earns billions by selling lies about their pills; the drug
regulators won’t admit that they erred when they approved the drugs, so they
are very slow in issuing warnings and don’t withdraw the drugs from the market;
and the leading psychiatrists earn millions by dutifully defending all the
illusions the drug industry has created.
Fluoxetine quickly became America’s most
complained-about drug.46 In the first nine years, the FDA received 39,000
adverse event reports, far more than for any other drug. There were hundreds of
suicides, horrendous crimes, hostility, psychoses, confusion, abnormal
thinking, convulsions, amnesia and sexual dysfunction. Already in 1991, only
three years after its launch, fluoxetine led the harms list, and yet, at an FDA
hearing the same year, after many witnesses had told stories about
out-of-character suicides and homicides, the advisory committee members, many
of whom had financial ties to the drug makers, unanimously rejected this
proposal: “There is credible evidence to support a conclusion that
antidepressant drugs cause the emergence and/or the intensification of
suicidality and/or other violent behaviors.”
There is also widespread professional denial
among psychiatrists of the drug harms patients tell them about. This was
displayed when I mentioned on TV news that antidepressants can change the
personality. In a commentary to this, the president of the Danish Psychiatric
Association wrote it was misleading to focus on a side effect that is so scary
for patients and which was extremely rare.53 It isn’t. Six years earlier, Danish psychiatrists had
conducted a study in which approximately 500 patients told them what they
thought about their antidepressant treatment, and about half the patients
agreed that the treatment could alter their personality and that they had less
control over their thoughts and feelings.54 Four-fifths agreed that as long as they took
antidepressants, they didn’t really know if they were actually necessary.
The patients’ replies correspond closely with
what other researchers have found,55 but the Danish psychiatrists refused flatly to believe
what the patients had told them. They considered it wrong and called the
patients ignorant. They also felt that the patients needed “psychoeducation.”
However, the relatives had the same opinion as the patients about
antidepressants. Perhaps they should also be taught they were wrong?
A British study was similarly discouraging: no
less than 78% of 2,003 lay people considered antidepressants addictive, but
according to the psychiatrists who had conducted the study, the patients only
needed to be told that addiction wasn’t a problem!6
In a survey of 1,829 patients on antidepressants
in New Zealand, 62% reported sexual difficulties, 60% felt emotionally numb,
52% felt not like themselves, 39% cared less about others, 47% had experienced
agitation and 39% had experienced suicidality.55 None were told anything by their doctors about feeling less like
themselves or about possible effects on relationships with other people (other
than sexual dysfunction).
It is very strange that these terrible drugs
have become so popular but it’s likely because both patients and doctors
consider the natural remission of the depression a drug effect. For example,
83% of the patients believed that the drugs had reduced their depression.55
An international survey of 3,516 patients from
14 patient advocacy groups showed that nearly half had stopped taking a
psychotropic drug at some point in their life because of side effects, and the
main problem was agitation in a quarter of the patients.56
In the mythology of antidepressants, the
combined effects of crime, corruption, fraud, bias, substandard research,
irrational arguments and organised denial among psychiatrists have had
particularly devastating consequences for patients in relation to suicide. It
is a true horror story and the most tragic area of healthcare I have ever
encountered. Our most vulnerable patients – the children – are driven into
suicide with “happy pills” that should never have been prescribed to them, as
they don’t work for depression. And drug companies and doctors push children
into suicide while claiming that their drugs protect
them against suicide. Can anything be worse than this? And, as usual, the drug
agencies have protected the drug companies.
The FDA protects Eli Lilly
In 1990, only two years after fluoxetine came on
the market, Martin Teicher and colleagues described six patients who had become
suicidal and reacted in bizarre ways on fluoxetine, which was something
completely new to them. Teicher’s observations were very convincing, but Lilly
lied to Teicher telling him that no data existed confirming his observations of
suicidality.49
Internal Lilly documents revealed that the FDA worked with the company on the
suicide issue, and at the subsequent 1991 FDA hearing, Lilly’s scientist left
out information that demonstrated that fluoxetine increases the risk of
suicide.57 Earlier, Lilly had submitted data to the German drug
agency showing that suicide attempts almost doubled on fluoxetine compared to
placebo. But at the hearings, the chair of the FDA committee, psychiatrist
Daniel Casey, brutally interrupted Teicher so that he couldn’t present his
findings. He was allowed to present a few slides while Lilly staff presented
many. A few years later, Teicher’s wife was offered a top job at Lilly without
having applied, which was hardly a coincidence. The standard procedure is to
blacklist and haunt critical people and if that doesn’t work, to buy them or
their close relatives. Teicher’s wife divorced him and went to work for Lilly.
In 1989, a man shot eight people dead, wounded another
12 and killed himself one month after he started fluoxetine.3 Lilly won a jury
verdict and claimed it was “proven in a court of law … that Prozac is safe and
effective.” However, the trial judge suspected a secret deal had been struck
and pursued Lilly and the plaintiffs, eventually forcing Lilly to admit that it
had made a secret settlement with the plaintiffs during the trial. Infuriated
by Lilly’s actions, the judge ordered the finding changed from a verdict in
Lilly’s favour to one of “dismissed as settled with prejudice,” saying, “Lilly
sought to buy not just the verdict but the court’s judgment as well.” Peter
Breggin was an expert in support of the family, but his own attorney betrayed
him and presented a weak case, as he knew about the secret deal.49 After this deal,
Breggin’s attorney sent back the revealing documents to Lilly where they
disappeared against the law impeding other lawsuits. Incriminating documents
also disappeared at the FDA.
Lilly bought FDA panel members, too. An FDA
advisory panel concluded in 1991 that fluoxetine was safe despite concerns
raised by FDA’s safety officer David Graham and others, which led critics to
point out that several of the panellists had financial ties to Lilly.
Throughout the 1990s, while swearing publicly
that fluoxetine didn’t increase the risk of suicide or violence, Lilly quietly
settled lawsuits out of court and kept the incriminating evidence hidden by
obtaining court orders to seal the documents. Lilly’s internal papers indicate
that the company had an explicit strategy to blame the disease and not the drug
for violence and suicide, and Lilly excluded 76 of 97 cases of suicidality on
fluoxetine in a post-marketing surveillance study it submitted to the FDA. In
relation to lawsuits, David Healy found early drafts of fluoxetine’s package
insert that stated that psychosis might be precipitated in susceptible
patients; the warning wasn’t included in the package insert for the United
States but the German drug agency required it.
By 1999, the FDA had received reports of over
2,000 suicides associated with fluoxetine, and a quarter of them specifically
referred to agitation and akathisia. A severe form of agitation, akathisia, is
extreme restlessness that some patients describe as wanting to jump out of
their skin. These people behave in an agitated manner which they cannot control
and can experience unbearable rage, delusions, and disassociation.49
Akathisia was likely much underreported in the trials and misdiagnosed as
nervousness, agitation or “agitated depression.”39
The FDA said it would not have allowed a company
to put a warning about akathisia or suicide on the label; it would have
considered it mislabelling! This was a red herring, however, as drug companies
can change the labelling without prior approval by the FDA if they feel it is
needed for safety reasons.58 In a court case of sertraline, a judge called Pfizer’s
arguments “perverse” and another judge said that it would be “inconceivable to
argue that an additional warning regarding suicidality would be false or
misleading” and that the law “allows, even encourages, manufacturers to be
proactive when learning of new safety information related to their drug.”59 The court case was about a 15-year old girl, Shyra
Kallas, who was prescribed sertraline by her primary care doctor for warts –
yes for warts – and shot and killed herself. Daniel Troy of the FDA filed an
FDA brief that claimed that the agency’s authority pre-empts state drug safety
requirements, which Pfizer used to its advantage to fend off lawsuits involving
suicides. Interestingly, Troy counted Pfizer as one of his clients in the year
before he took public office.
FDA’s expert on safety matters, David Graham,
noted that fewer than 10-20% of fatal effects were reported for fluoxetine, but
the data nevertheless showed relatively more suicidality among patients on
fluoxetine than among those on tricyclic antidepressants or placebo.59
However, the safety officers’ admonitions were largely ignored by FDA top
brass, and although the FDA had been aware of an apparent seven times greater
rate of suicidal behaviour in children taking sertraline since 1996, the agency
did nothing about it. At long last, in July 2005, the FDA issued an advisory to
healthcare professionals stating that antidepressant drugs increase suicidal
thinking or behaviour in about one out of 50 children.
Lilly concealed the increased risk of suicide
and violence and kept suicides from public view.3 In 2004, a
healthy 19-year-old student who had taken duloxetine in order to help pay her
college tuition hanged herself in a laboratory run by Lilly.60 It turned out that there had been 41 deaths and 13
suicides among people taking duloxetine but missing in FDA’s files was any
record of the college student and at least four other volunteers known to have
committed suicide. Lilly admitted that it had never made public at least two of
those deaths, and anonymous sources told a journalist that duloxetine caused
suicidal tendencies in patients who took the drug for urinary incontinence and
weren’t depressed.
The FDA said that federal regulation prohibited
it from releasing study data for a drug that fails to win FDA approval, and the
FDA didn’t approve duloxetine for incontinence. This is absurd, as duloxetine
was approved for depression. The FDA’s argument for secrecy is that, “failed
efforts at drug development need protection lest entrepreneurs suffer a
competitive disadvantage when other companies aren’t forced to expend the same
time and money exploring dead ends.”60 FDA’s disregard for research
ethics means that patients will die in drug trials because other companies
won’t know that a particular type of drug is lethal. The FDA says it’s
compelled to maintain secrecy by law, but there is no such law.61
It is also unethical to allow the same molecule
to be sold under two different trade names (Yentreve and Cymbalta), as it leads
to overdosing. As many doctors and patients wouldn’t know it’s the same drug,
it might be prescribed twice, for two different illnesses.
Later, the FDA announced that 11 of 9,400 women
on duloxetine in the stress urinary incontinence trials had a suicide attempt.62 These studies show that SSRIs increase the risk of
suicide also in middle-aged people, as the suicide attempt rate was 2.6 times
higher than for other women of similar age.62
Drug regulators in Europe also protected Eli
Lilly. When we contacted the UK drug regulator in 2011 to get data on
fluoxetine, which the EMA didn’t have, as the UK was the EU Reference Member
State for fluoxetine, we were told the agency had destroyed the files! The UK
agency destroys the files after 15 years, “unless there is a legal, regulatory,
or business need to keep them, or unless they are considered to be of lasting
historic interest.”3 So does that mean there is no legal or historical
interest for unpublished clinical study reports on a drug that is still on the
market and kills many people?
Massive underreporting of suicides
in the randomised trials
There are many reasons why the randomised trials
have seriously underestimated the risk of suicide and suicidal events from
antidepressant agents. Above all, almost all placebo controlled trials have
been conducted by drug companies, which have a profound interest in hiding that
their drugs push people into suicide. This became particularly clear when, in
2004, the BMJ received a series of internal Lilly
documents and studies on fluoxetine from an anonymous source, which had been
available ten years earlier in a litigation case.63
These documents revealed that Lilly had known
since 1978 – ten years before fluoxetine came on the market – that fluoxetine
can produce in some people a strange, agitated state of mind that can trigger
in them an unstoppable urge to commit suicide or murder. In 1985, two years
before fluoxetine was approved, the FDA’s safety reviewer noted under the
headline “Catastrophic and Serious Events” that some psychotic episodes had not
been reported by Lilly but were detected by the FDA by examining case reports
on microfiche. The reviewer noted that fluoxetine’s profile of adverse effects
resembled that of a stimulant drug.
The documents also showed that Lilly was keen to
root out the word “suicide” altogether from its database and its headquarters
suggested that, when doctors reported a suicide attempt on fluoxetine, Lilly
should code it as an “overdose.” This is highly misleading, as it is hardly
possible to kill oneself by overdosing fluoxetine and as the suicides occur on
normal doses. Lilly wasn’t alone with this misconduct. Independent
investigators that looked at UK regulator data found that several companies had
coded suicide attempts as overdoses.64
Lilly’s instructions furthermore were that
“suicidal ideation” should be coded as “depression.” But two internal Lilly
researchers in Germany were unhappy with these directions, and one of them
wrote in 1990: “I do not think I could explain to the BGA [the German
regulator], to a judge, to a reporter or even to my family why we would do
this, especially on the sensitive issue of suicide and suicide ideation.”65 Already in 1985, an in-house analysis of placebo
controlled trials found 12 suicide attempts on fluoxetine versus one each on
placebo and a tricyclic antidepressant, but after the code was broken, Lilly’s
hired consultants threw out six of the attempts on fluoxetine!49
One of the leaked documents noted that 38% of
the fluoxetine-treated patients reported new activation in the clinical trials,
compared to only 19% of placebo-treated patients. This means that fluoxetine
causes activation in one of five patients treated with the drug (as the difference
to placebo is about 20%). Akathisia is a severe form of agitation, so this was
bad news for Lilly, as akathisia increases the risk of suicide. Early on, Lilly
therefore recommended that such patients should also take benzodiazepines,
which reduce the symptoms. The FDA approved fluoxetine based on four pivotal
studies, but three of them permitted the use of concurrent psychotropic
medication, and one-quarter of the enrolled patients took benzodiazepines or
chloral hydrate.66 Other companies adopted the same strategy, and minor
tranquillisers were permitted in 84% of placebo controlled trials of
antidepressants.29
This means not only that suicides and suicide
attempts on antidepressants have been seriously underestimated in the trials;
it also means that we don’t know what the true effect on depression is, as
benzodiazepines have an effect on depression.
Further obfuscating the suicide risk, at least
three companies, Glaxo-SmithKline (GSK), Lilly and Pfizer, added cases of
suicide or suicide attempts to the placebo arm of their trials, although they
didn’t occur while the patients were randomised to placebo. Some of these
events occurred in the run-in period, before the patients had been randomised,
other events happened in the active drug group after the randomised phase was
over.67 These fraudulent manoeuvres can be important for the
companies in court cases. For example, 60-year old Donald Schell murdered his
wife, daughter and granddaughter and committed suicide after two days on
paroxetine, but in its defence, GSK said that its trials didn’t show an
increased risk of suicide on paroxetine.68
The FDA continued to protect the companies.3
In 2003, FDA officials noticed a curious thing while examining the results of a
trial with youngsters on paroxetine.69 GSK had reported that substantially more kids had shown
“emotional lability” on the drug than on a placebo, but what was that? When the
FDA officials asked GSK, it turned out that almost all of these events were
related to suicidality. So what did the FDA do about it? The FDA bosses
suppressed this information!
When FDA’s safety officer Andrew Mosholder, a
child psychiatrist, concluded that SSRIs increase suicidality among teenagers,
the FDA prevented him from presenting his findings at an advisory meeting and
suppressed his report. When the report was leaked, the FDA’s reaction was to do
a criminal investigation into the leak. Drug companies react in the same way
when an employee leaks information about drug harms that the company has buried
in its archives.70
David Healy noted in 2002 that, based on data he
had obtained from the FDA, two suicides and three suicide attempts that were
ascribed to the placebo group in a paroxetine trial had occurred in the run-in
period, before the patients were randomised.71 This wasn’t denied by GSK, but the company stated that
Healy’s analysis – which was the correct one – was scientifically invalid and
misleading. GSK also masqueraded as wounded patients when it pompously stated
that, “Major depressive disorder is a potentially very serious illness associated
with substantial morbidity, mortality, suicidal ideation, suicide attempts and
completed suicide. Unwarranted conclusions about the use and risk of
antidepressants, including paroxetine, do a disservice to patients and
physicians.”72
Psychiatrist Joseph Glenmullen studied these
documents for the lawyers and said that it’s virtually impossible that GSK
simply misunderstood the data, and Martin Brecher, the FDA scientist who
reviewed paroxetine’s safety, said that this use of the run-in data was
scientifically illegitimate. But GSK was right about one thing: “Unwarranted
conclusions about the use and risk of antidepressants, including paroxetine, do
a disservice to patients and physicians.” GSK has done exactly what they warn
against. Even in 2011, GSK denied that paroxetine can cause people to commit
suicide.68
FDA’s meta-analysis of suicides in
trials with 100,000 patients is deeply flawed
Though we cannot trust the randomised trials of
antidepressants, they can still be of value, e.g. it would be highly convincing
if they demonstrated an increased risk of suicide events despite all the bias
and fraud.
The pressure on drug agencies to find out if
SSRIs cause suicide began in 1990, but although it mounted during the following
years, very little happened. It took 16 years before the FDA published a
meta-analysis addressing this issue. The FDA’s analysis included 372 placebo
controlled trials of SSRIs and similar drugs involving 100,000 patients.17
It showed that up to 40 years of age, the drugs increased suicidal behaviour,
and in older patients they decreased it (see Figure 3.2.).
However, it is far worse. Although the FDA knew
that the companies had cheated on them earlier in relation to suicidal events,
the agency asked them to adjudicate possibly suicide-related adverse events in
their trials and send them to the FDA. This is weird. Why would the companies
not continue cheating when they knew the FDA wouldn’t check their work? If they
didn’t cheat this time, it would be too obvious how much they had cheated
earlier. And why didn’t the FDA behave as we do in other walks of life? The
police wouldn’t ask a criminal to go back to the scene of the crime and look
for evidence while being assured that the judge would believe him. The FDA’s
official excuse was that the companies knew best and that the large number of
participants was also a reason to let the sponsors adjudicate the events.73 It was very convenient for the FDA to accept that the
evidence it would get would very likely be flawed, as it would lessen the risk
of accusations that the agency had failed earlier.
Figure
3.2. FDA’s meta-analysis of 372 placebo controlled trials of SSRIs and similar
drugs involving 100,000 patients. Odds ratios for suicidal behaviour for active
drug versus placebo by age. Redrawn.
Another major problem with the FDA’s approach
was that, although it was widely known at the time that any dose change
increases the risk of suicide,74 suicidal events that occurred later than one day after
stopping randomised treatment were not registered. As stopping an SSRI may
increase the risk of suicide for weeks, this approach seriously underestimates
the suicidal effects of SSRIs.
The actual data demonstrate that the FDA’s
analysis grossly underestimates suicide risk. In trials on certain drugs
included in the FDA’s analysis, there were sometimes more
suicides than in the whole FDA analysis of all the drugs. There were only five suicides in FDA’s
analysis of 52,960 patients on SSRIs (one per 10,000 patients), but an internal
Lilly memo from 1990 described nine suicides in 6,993 patients on fluoxetine in
the trials (13 per 10,000).75 In a 1995 meta-analysis, there were five suicides on
paroxetine in only 2,963 patients (17 per 10,000; this meta-analysis wrongly
reported two suicides on placebo, which had occurred in the washout period).76 Adding the suicides on both drugs, we get 14 suicides in
only 9,956 patients. Other data are equally disturbing. In 1984, the German
drug agency described two suicides among only 1,427 patients on fluoxetine in
the trials (14 per 10,000).77
An analysis of prescriptions written by general
practitioners in the UK immediately after the drugs came on market is similarly
revealing.78 The patients had an average age of 50 and 79% had
depression, but although the follow-up was only about six months, there were 90
suicides among patients receiving fluoxetine, sertraline or paroxetine, which
was 24, 17 and 27 suicides per 10,000, respectively.
The data I found are remarkably consistent and
show, based on the randomised trials alone, that:
There are likely to have been 15 times more
suicides on antidepressant drugs than reported by the FDA in its meta-analysis
of 100,000 patients in 2006, which is an error of 1,400%!
What I get out of this colossal underreporting
of suicides is that SSRIs likely increase suicides in all ages. One would have
thought that suicide is a hard endpoint but in drug trials, it is highly
subjective how many suicides there are. Thomas Laughren was responsible for the
FDA’s meta-analysis of 100,000 patients from 2006, and he published a paper
using FDA data in 2001 where he reported 22 suicides in 22,062 patients
randomised to antidepressants, which is 10 per 10,000,79 or 10 times as many as he reported five years later.17
There were only two suicides in 8,692 patients on placebo, which Laughren
interprets thus: “There is obviously no suggestion of an excess suicide risk in
placebo-treated patients.” No, there surely isn’t, but why didn’t Laughren
comment on the fact that hits us in the face, namely that there were four times
as many suicides on antidepressants as on placebo, which was statistically
significant (P = 0.03, my calculation)?79
In its large analysis, the FDA found that
paroxetine increased suicide attempts significantly in adults with psychiatric
disorders, odds ratio 2.76 (95% CI 1.16 to 6.60).17 GSK limited its
analysis to adults with depression, but it also found that paroxetine increases
suicide attempts, odds ratio 6.7 (95% CI 1.1 to 149.4).80 GSK USA sent a “Dear Doctor” letter that pointed out
that:81
The risk of suicidal behaviour was increased
also above age 24.
In contrast, the FDA has claimed that it is only
in those below 24 years of age that these drugs are risky.73
In GSK’s analysis, there were 11 suicide
attempts on paroxetine (3,455 patients) and only one on placebo (1,978
patients). Five of the 11 suicide attempts were in patients aged 25 to 30
years, which illustrates how dangerous it is to operate with age limits when we
are dealing with suicides on antidepressants. I really wonder why GSK reported
no suicides, as there were five suicides in the 1995 meta-analysis of
paroxetine in fewer patients, as just mentioned. But there is so much that
doesn’t add up in this “creative” area where 2 + 2 is not necessarily 4.
Table
3.1. Sertraline trials in adults; n: number of suicides and suicide attempts;
N: number of patients; follow-up: time after the randomised phase ended; RR:
relative risk; CI: confidence interval.
A 2005 meta-analysis conducted by independent
researchers of the published trials included 87,650 patients and all ages and
they found double the suicide attempts on drug than on placebo (odds ratio
2.28, 95% CI 1.14 to 4.55).82 They also found out that many suicide attempts must have
been missing; some of the investigators responded that there were suicide
attempts they had not reported in their trials, while others replied that they
didn’t even look for them. Further, events occurring shortly after active
treatment was stopped were not counted.
The bias this omission causes has been
demonstrated in meta-analyses of sertraline used in adults (Table 3.1). The
FDA’s meta-analysis didn’t find an increase in suicide, suicide attempt or
self-harm combined, relative risk = 0.87 (FDA’s Table 30), whereas Pfizer’s own
meta-analysis suggested a halving of this, relative risk = 0.52, when all
events that occurred after 24 hours were omitted.83 When Pfizer included events occurring up to 30 days
after the randomised phase was over, there was an increase in these suicidality
events of about 50% (relative risk = 1.47). A 2005 meta-analysis conducted by
independent researchers using UK drug regulator data found a doubling in
suicide or self-harm when events after 24 hours were included (relative risk =
2.14, 95% CI 0.96 to 4.75, my calculation).84 These researchers noted that the companies had
underreported the suicide risk in their trials, and they also found that
non-fatal selfharm and suicidality were seriously underreported compared to the
reported suicides.
In a meta-analysis conducted by GSK,85 suicide-related events occurred more often on paroxetine
than on placebo in children and adolescents (odds ratio 3.86, 95% CI 1.45 to
10.26), whereas suicide items on rating scales like Hamilton’s didn’t show this
difference. A meta-analysis carried out by the FDA in children and adolescents
found the same; suicide items on depression scales misleadingly showed a
slightly less risk of suicidality with SSRIs (relative
risk 0.92, 95% CI 0.76 to 1.11) whereas company data showed a doubling of this
risk (relative risk 1.95, 95% CI 1.28 to 2.98).86
In absolute terms, two out of 100 children
experience suicidality because of the drugs they take.
Robert Gibbons and colleagues used individual
patient data obtained from Eli Lilly and they claimed that fluoxetine didn’t
increase suicide risk in children and adolescents with major depressive
disorder,87 but this only illustrates that it is misleading to use
too small samples. The FDA researchers found that fluoxetine increased the risk
of suicide, suicide attempt or preparation for suicide in people under 25,
relative risk 2.32 (95% CI 0.78 to 6.87) and when all drugs were included, this
increased risk was the same but it was now statistically significant, relative
risk 2.35 (95% CI 1.35 to 4.09).17 Gibbons declared in his paper that
he had served as an expert witness for Wyeth and Pfizer in cases related to
antidepressants and suicide. I am sure Gibbons improved his chances of also
becoming an expert witness for Lilly and I shall say more about this remarkable
man later.
It is clear that the risk of suicide caused by
SSRIs has been grossly underestimated in the trials, and there are many reasons
for this:
Fraud.
The investigators didn’t report suicide attempts
or didn’t even look for them.
Many suicidal events have been coded as
something else.
By only recruiting people at very low risk of
committing suicide for their trials, the drug industry has taken great care not
to get in trouble.
The companies have urged investigators to use
benzodiazepines in addition to the trial drugs, which have prevented some of
the violent reactions that would otherwise have occurred.
Some trials have run-in periods on active drug, and
patients who don’t tolerate it aren’t randomised.
Most patients were in antidepressant treatment
before they were randomised, which leads to withdrawal symptoms in the placebo
group that predispose to suicide.
Events occurring shortly after active treatment
is stopped were rarely registered.
Many trials are buried in company archives and
these are not the most positive ones.
Patients are carefully monitored in trials and
drug intake is likely to be stopped before a serious problem develops. In
clinical practice, patients may not be monitored at all, and may miss doses,
which increases the risk of suicide because of withdrawal effects. A study of
prescription refill data indicated that 30% of patients on SSRIs may miss 4-15
days of therapy between prescription refills.88
Patients in trials have contact with other
people and get hope, therefore the risk of suicide is less than in real life.
The FDA failed us again. Despite the vast number
of missing suicide events, its meta-analysis showed an increase in suicidal
behaviour up to age 40, but when the FDA published its results in 2009, it had
used 10-year age groups and now claimed that the risk was only increased in
people under age 25.73 In contrast, the 2005 meta-analysis conducted by
independent researchers mentioned above82 found that the risk of a suicide
attempt in those below 60 years of age was 2.4 times larger in the SSRI group
than in the placebo group, and when they took length of treatment into account,
they found that for every 1,000 patients treated for one year, there were 5.6
additional suicide attempts on active drug compared to placebo.82 Thus, by
treating only 180 patients for a year with an SSRI, one additional patient will
attempt suicide.
My deep mistrust of the FDA is shared by FDA’s
own scientists and is based on solid evidence of FDA’s inappropriate actions in
other matters of great importance for public health.3 Thomas Laughren,
who was in charge of FDA’s misleading meta-analysis of 100,00 people,
established the Laughren Psychopharm Consulting in 2013 with himself as
director.89 He says:
“I have 29 years of experience at the FDA
protecting the public health by assuring the safety and efficacy of psychiatric
drugs. I accomplished this goal in part by working with pharmaceutical
companies to help shape their development programs in order to meet FDA’s goals
for assuring the development of safe and effective psychiatric drugs. I also
worked to advance public health by helping to speed innovations to make
psychiatric drugs safer and more effective.”
Laughren furthermore says his goal is to help
pharmaceutical companies so that they can “meet the high standards of FDA and
other regulatory agencies.” He certainly knows how to speak like a drug
company.
The pervasive scientific misconduct has led to a
research literature where one has to dig deeply to find the few gems among all
the garbage. A 2004 UK systematic review of trials in childhood depression
showed that, when unpublished trials were included, a favourable harm-benefit
profile changed to an unfavourable one for several SSRIs.90 None of the companies (Eli Lilly, GSK, Pfizer, Lundbeck
and Wyeth) was forthcoming when asked for unpublished data, so the authors got
them from a drug agency. Unfortunately, this review was highly misleading for
fluoxetine, which was praised as being the only drug that had a “favourable
risk-benefit profile.” It hasn’t. We are supposed to believe that fewer serious adverse events occurred on fluoxetine than on
placebo (less than 1% versus 3.6%)! And also that the rate of discontinuation
because of adverse events was similar (5·7% versus 6·3%). Given what we know
about SSRIs, this is impossible and only tells us how deeply flawed the
fluoxetine trials are. Another major blunder in the review is that the authors
only included suicidal behaviour if it was a serious adverse event (causing
death, permanent damage, or hospitalisation).
The Dutch drug agency had a more sober view on
these trials.91 They defined suicidality as suicide, suicide attempt or
suicide thoughts and found that there was a signal for all the drugs, with no
difference between them. They also pointed out that the UK review had excluded
a large trial of fluoxetine that found that this drug also increases
suicidality. The Dutch were strangely secretive; they didn’t name the drugs but
it is clear from their table that fluoxetine was one of them, and which one it
was.
Even the EMA finally woke up. It announced in
2006 that parents and doctors should carefully monitor children and youth being
treated with fluoxetine and watch out for suicidal tendencies.3 A fake fix. It’s
impossible for parents to monitor their children closely. Children leave home
virtually every day, so what would a monitoring schedule look like? And
children have hanged themselves next door while their parents watched TV,
shortly after they appeared totally normal and said everything was okay. I once
discussed this with a child psychiatrist on TV and told her it didn’t make
sense to me that psychiatrists treated depressed children with a drug that
doubled their risk of suicide. Her reply was that the children should be
monitored closely, particularly in the beginning. What then about children who
forget to take a couple of pills or who stop taking their drug because of its
side effects? It just cannot be done. Suicides on SSRIs can occur totally
unexpectedly.
Numerous studies have shown that SSRI can be
deadly at any age. Many people, also in the later decades of life, have changed
their personality completely upon taking an SSRI and have killed themselves,
others, or both. This raises an interesting hypothesis that the authors of the
FDA meta-analysis also mentioned.73 Antidepressant drugs could have
two separate effects: an undesirable effect in some patients that promotes
suicidal behaviour (and violence towards others), and a therapeutic effect in
some that decreases suicidal behaviour. Clinical and animal studies provide
support for this hypothesis. A review of 84 animal studies showed that reduced
aggression upon treatment with SSRI was most common, but sometimes the animals
became more aggressive.92
In 1994, a trial showed that 18 of 54 patients
made a suicide attempt on fluoxetine and 18 of 53 made one on placebo.93 The included patients did not have major depression but
had nonetheless made at least two previous suicide attempts. We are not told
whether some patients already were on an antidepressant drug and therefore went
cold turkey when randomised to placebo, or what age the patients had, but they
were likely adults, as researchers almost always say if their patients were
children. Thus, the trial showed that fluoxetine doesn’t protect adults against
suicide attempts.
Fluoxetine should never have been approved for
children, or indeed for any creature. It is FDA-approved for “separation
anxiety” in dogs, which is when dogs howl too much when their owner leaves
home. Perhaps this is not such a fantastic idea. Eli Lilly showed in 1978 that
cats who had been friendly for years began to growl and hiss on fluoxetine and
became distinctly unfriendly.94 After cessation of fluoxetine, the cats returned to
their usual friendly behaviour in a week or two.
These drugs quite seriously impair normal
development. The package insert for fluoxetine mentions that after only 19
weeks of treatment, children had lost 1.1 cm in height and 1.1 kg in weight
compared to children treated with placebo.
I assume the FDA had an off-day in 2007 – or all
the bosses were away at the same conference – when it admitted that:
SSRIs can cause suicide at all ages.
The FDA humbly “proposed” to the drug makers
that they update their black box warning:95
“All patients being treated with antidepressants
for any indication should be monitored appropriately and observed closely for
clinical worsening, suicidality, and unusual changes in behavior, especially
during the initial few months of a course of drug therapy, or at times of dose
changes, either increases or decreases. The following symptoms, anxiety,
agitation, panic attacks, insomnia, irritability, hostility, aggressiveness,
impulsivity, akathisia (psychomotor restlessness), hypomania, and mania, have
been reported in adult and pediatric patients being treated with
antidepressants.”
The FDA also noted that, “Families and
caregivers of patients should be advised to look for the emergence of such
symptoms on a day-to-day basis, since changes may be abrupt.”
The FDA finally admitted that SSRIs can cause
madness at all ages and that the drugs are very dangerous; otherwise daily
monitoring wouldn’t be needed. But since this is a fake fix, the FDA, instead
of “proposing” label changes, should have taken the drugs off the market.
Particularly since the problems are much worse in clinical practice than what
is reported in industry sponsored trials. Peter Breggin reports that of 184
patients in hospital starting fluoxetine, sertraline or paroxetine, 11
developed mania and eight became psychotic, and in Yale, 8% of 533 consecutive
admissions were for mania or psychosis caused by antidepressants, and two
patients heard voices commanding them to kill themselves.49 Breggin also
notes that two of the three most common adverse reactions to fluoxetine were
depression and abnormal thoughts, but the FDA scratched out depression from its
prominent place in the label and it went from being frequent to being
non-existent, and abnormal thoughts became abnormal dreams, which is not quite
as bad.
Some of our drug regulators appear to be smarter
than others, though. As far as I know, Australia is the only country that has
refused to approve any SSRI for use in children.6 Some countries
have approved fluoxetine based on deeply flawed trials, but it’s very unlikely
that any SSRI works for children, and in the large TAD trial there were six
suicide attempts in the fluoxetine groups and one in the other groups.96 Hardly a drug you would want to expose your child to.
It is totally reprehensible, outright
dangerous and disrespectful towards all those who have lost a child or a spouse
to an antidepressant drug that leading psychiatric professors and the drug
companies continue to deny97-99 – in direct contrast to the most reliable data we have –
that antidepressants increase the risk of suicide among children and
adolescents.
Another dirty trick: using
patient-years instead of patients
In their submissions to drug agencies, several
companies obscured the suicide risk by using patient-years as the denominator
instead of the number of randomised patients. This introduced considerable bias
because several of these trials had a follow-up phase where all patients could
receive the active drug. As those who continue with the drug for a long time
are those who tolerate it, patient-years are added “for free” to the drug group
in terms of suicidality.
Based on FDA documents David Healy has obtained,
it is possible to see how large this bias is. In Pfizer’s submission on
sertraline, there was a 26% decrease in suicide attempts on active drug
compared with placebo.100 However, three of five suicide attempts ascribed to
placebo happened in the wash-out phase before randomisation, and when the FDA
excluded these, sertraline caused a 29% increase in suicide attempts. Using
patients as the denominator, the increase in suicide attempts on sertraline was
73%. For paroxetine, suicide attempts decreased by 52% using patient-years, but
increased by 25% using patients.101 David Graham reported in an internal FDA document that
the suicidality rate on fluoxetine was 0.52% versus 0.18% on placebo, i.e.
almost three times higher on drug.102
These dirty tricks were not harmless, as it
appears they contributed to convincing the FDA that it should not worry about a
suicide risk with SSRIs.103
Psychiatrists on company payrolls also use these
dirty tricks. In 1995, Stuart Montgomery and colleagues examined paroxetine in
a series of meta-analyses and came up with the astounding result that there
were 5.6 times fewer suicides on paroxetine than on
placebo!104
Case stories of suicide on SSRIs
Thousands of people have committed suicide
because of the antidepressants they took and many of them have been reported in
scientific articles, in newspaper reports and on websites.
The tragic loss of a loved one can influence
people’s memories and could make them forget about any significant
psychological problems preceding the suicide, which would move some of the
self-blame from the family to the doctor. However, although such recall bias
can occur, we also know that antidepressants can cause healthy volunteers to
become suicidal. Furthermore, people close to the victim have in many cases
noticed a fundamental change in personality, which is so bizarre that they
don’t have the slightest doubt that the pills caused it.
We owe it to those who died because of a greedy,
criminal and fraudulent drug industry, assisted by overly industry-friendly
drug regulators and corrupt psychiatrists, to tell some of their stories. A
thousand deaths are a faceless statistic. But there are real people behind the
numbers and when we describe what happened to real people, other people tend to
take notice.
Here are eight of the tragic deaths I know about
at a personal level because I have met with the parents or spouses left behind.
They all wished me to tell their story to alert other people to the dangers of
SSRIs and also wanted me to show photos of those they lost (see photos). I met
four of them in Los Angeles at a scientific meeting on the theme that
biological (drug-based) psychiatry does more harm than good (see photos) (see
Chapter 14). Their determination in publicizing their own tragedies has spared
others from experiencing the same, as they realised before it was too late that
their loved one was heading for disaster.
Unfortunately, many doctors and other people
believe that when our authorities have issued a warning against using a drug up
to a certain age, it is safe to use the drug above that age. In Denmark, the
package inserts warned against the increased risk of suicide up to age 18, although
there never were any data to suggest that the risk wasn’t increased in people
slightly older than this. Such misleading recommendations have had tragic
consequences.
Danilo Terrida
Danilo Terrida was only 20 when he hanged
himself in a crane at a shipyard in 2011, two hours after having assured his
family on the phone that he was fine and had small-talked with them. A month
earlier, he had celebrated his birthday and everything apparently went well.
Two weeks later, he made contact with the emergency medical service because he did not feel well psychologically and was sent home with
tranquillising pills and was advised to see a doctor the next day. The local
doctor he contacted refused to see him and asked him to call his family doctor
several hundred kilometres away. This he did, and after eight minutes on the
phone, he was prescribed sertraline, although he wasn’t depressed, and with no
follow-up. A few moments before he killed himself, Danilo talked to a friend
and said he didn’t know what was happening to him, but he didn’t mention
anything about suicide. This is rather typical of an SSRI-induced suicide, and
the timing is also typical. Many people kill themselves early on. The involved
doctors have been officially criticised for amending Danilo’s files, up to a
year after his death, so that it looked more plausible that he killed himself
because of a depression, which wasn’t true (see www.daniloforlivet.dk).
At least 11 other people, 10 of them adults, who
have committed suicide in Denmark on antidepressants have acquired economic
compensation from the Patient Insurance Association.105
Toran Bradshaw
Maria Bradshaw’s son Toran who was her only
child was prescribed fluoxetine in January 2007 despite having been assessed as
being a healthy adolescent who had an expected reaction to a stressful life
event, which was a breakup with his girlfriend. A
month later, Toran experienced a severe cluster of adverse reactions including
suicidal behaviour, self-harm, aggression, hostility, hallucinations, lack of
concentration and impaired functioning. The symptoms were so severe that he
dropped out of school. His psychiatrist’s response was to increase his dose,
which worsened the adverse reactions. Toran withdrew from fluoxetine and from
mental health treatment of his own volition.
The following year, a psychiatric registrar
prescribed fluoxetine to him again, against his mother’s wishes. The registrar
recorded no diagnosis after having conducted a mental state exam and finding no
evidence of depression, anxiety or any other mental disorder. The next day, a
multi-disciplinary team reviewed Toran’s file and recorded “diagnosis deferred”
noting that there was no evidence of a mental disorder. Toran initially refused
the prescription on the basis that fluoxetine should not be taken with alcohol,
but the registrar recorded that he had reached an agreement with Toran that he
would stop taking the fluoxetine on a Friday, could drink up to six bottles of
beer a night over the weekend and restart his fluoxetine on Mondays. Given
fluoxetine’s long half-life in the body, 2 to 4 days for the drug and 7 to 15
days for its active metabolite norfluoxetine, this was a foolish
recommendation. Toran followed this regime but suffered a repeat of the former
adverse reactions and suddenly hanged himself after 15 days on fluoxetine. He
was only 17 years old.
After Toran’s death, Maria had genetic testing
conducted, which confirmed that Toran metabolised drugs slowly and had
therefore been overdosed. Maria also established CASPER, an organisation where
those bereaved by suicide help others bereaved by suicide (http://www.casper.org.nz/).
Maria has told me that the national media have credited CASPER with a 20% drop
in youth suicide and that it means more to her than anything else that her son
continues to do good in the world despite not being here physically.
Maria wrote to the District Health Boards in New
Zealand and found out that 8% of those who died and who had gotten a recent
prescription for an antidepressant, had no diagnosis of any mental disorder. In the district responsible for Toran’s care, 75% of those under 18
who died had no diagnosis.
In New Zealand, psychiatrists and suicidologists
have managed to convince the government that publishing information on suicides
causes copycat suicide. She has reviewed the evidence for this, which is
extremely weak, but it’s nonetheless a criminal offense for Maria to tell
Toran’s story, punishable by a fine of up to $5,000 each time and a fine for
the media of up to $20,000. These threats have not stopped Maria and she has
had support from the media.
Maria sold her home to pay for Toran’s inquest
when the doctors dragged it out over 18 days of hearings, thinking she would
walk away because of the cost. She now lives in Dublin, in the home of another
mother who lost her child to SSRI-induced suicide, Leonie Fennell, and has
everything she owns in two suitcases.
There have been ten government enquiries into
Toran’s death but, as in all such cases, the issue is not whether the child
received a good standard of care but whether the psychiatrist departed from
generally accepted practice. And of course, since the usual practice in psychiatry
is terribly poor, most of the investigations found that Toran’s care was not a
departure from usual practice. However, both the government and Mylan
Pharmaceuticals have resolved that it is probable that fluoxetine caused
Toran’s suicide.
Maria is still fighting to achieve justice and
has persuaded the police to review Toran’s file to see whether manslaughter
charges can be laid. She hopes that her efforts will be a deterrent, which
could make other doctors consider that their patients may have a stroppy mother
like her and be more careful. Maria has spent seven years on meticulously
documenting Toran’s case learning everything she could about
psychopharmacology, psychiatry, neurochemistry, genetics, randomised trials and
anything else that could help not only her but also all the other parents that
have stories similar to hers.
When I gave a lecture at the Department of
Psychology at the Manooth University outside Dublin, to which Maria had invited
me, another bereaved mother was in the audience, Stephanie McGill Lynch, who
also lost her child to fluoxetine. Maria wrote to me:
“I know you agree with me that this has got
to stop.” Yes, and this is why I have written this book. I won’t accept that
doctors and drug companies push our children into suicide with drugs that have
no benefits for them. I cannot see it’s any different to killing our children
by pushing narcotic drugs in the street.
Jake McGill Lynch
Jake’s mother, Stephanie, describes her son as a
beautiful, bright 14-year old boy. In late 2011, he was diagnosed with
Asperger’s syndrome in an extremely mild form (the diagnosis of Asperger’s was
eliminated in 2013 in DSM-5 and replaced by a diagnosis of autism spectrum
disorder).
Jake started counselling with a psychologist in
2011 due to some dark thoughts that had appeared in an essay he wrote in
school. In January 2013, he had counselling again, for
anxiety, and his psychologist decided to refer him to her colleague, a
psychiatrist, as she felt his anxiety would be heightened when he was to sit
his state exams. Jake’s parents didn’t even know what a psychiatrist was but
just thought it was the psychologist’s colleague.
Jake’s dad took him to his appointment because
no big deal was made of it, and they met with the psychiatrist for ten minutes,
after which they left with a prescription for fluoxetine. Jake had never been
on medication before, but the family was not given any literature or any
description from the psychiatrist or the pharmacist, and they didn’t even know
what sort of drug Prozac was but simply trusted the psychiatrist.
Six days later, Jake had his first reaction. He
walked out of an exam half-way through it and cried for about 2-3 hours that
night, saying, “You don’t know what it’s like in my head.” His parents thought
this was from the stress of the exams. They never imagined that a drug could do
this to a person.
About a week later, they got Jake back to the
psychiatrist and told her all about what happened, but she said that it would
wear off after three or four weeks and that Jake would be fine. But Jake was
not fine, and on day 46 he was a bit restless after school and looked a bit
flush in the face, although he never had a colour in his cheeks. His parents
thought he had a row with his little online girlfriend.
The family had a legally held rifle in the
house, as Jake and Stephanie were members of a shooting club. They would often
take the gun down, and Jake asked if he could take it down that night, which
was nothing out of the ordinary, so his request was granted. Stephanie forgot to
take the box from his room with bolt and ammunition.
Jake placed the gun in his mouth and pulled the
trigger. He had no history of suicide ideation or self-harm, and no diagnosis
of anything but Asperger’s. However, the National Health Service in Ireland is
now trying to say he had severe anxiety – although this isn’t true – and it
fights the parents from every corner with this. It is the same story all the
time: put all the blame on the disease, never on the drug. The parents asked
David Healy to do a second opinion based on Jake’s medical files, which he did.
Stephanie and her husband have attended their
son’s inquest three times so far and are still in the middle of a legal
argument about which medical expert the Coroner’s court will allow them to
consult. The court has refused their request to use David Healy, as he is
considered to be not impartial due to his papers and books about the relation
between SSRIs and suicide!
Stephanie finds the whole thing absolutely
disgusting. This was a 14-year old child who had plans for the future. He had
no illness, he had a condition that no medication would fix, and he was living
quite happily with just counselling for his anxiety. Stephanie and her husband
were never told about the dangers of drugs like fluoxetine. Had they known
about them, they would never have kept a firearm in the house.
Shane Clancy
Shane was 22 years old when he
broke up with his girlfriend.106 He found it difficult without her and was prescribed
citalopram. He became agitated and rang the doctor four days later, as his
tongue felt very swollen (a recognized side effect of citalopram). He left a
message but got no response, and five days later he took the remainder of the
tablets in an attempted suicide.
His mother brought him back to the clinic where
he saw a different doctor who continued the prescription for citalopram.
Ten days later, Shane called his ex-girlfriend,
who was in her new boyfriend’s house, and asked her to send her boyfriend
outside, as Shane was hurt and needed help. Shane stabbed the boyfriend fatally
and also stabbed his ex-girlfriend and her boyfriend’s brother who emerged from
the house to find out what was going on. Shane was later found dead in the
garden having stabbed himself about 20 times.
The case was all over the media for several days
and every scrap of evidence that pointed to pre-meditation was a nail in
Shane’s coffin. At first there was no mention of antidepressants, but Leonie
Fennell, Shane’s mother, feeling guilty for having engineered her son onto
citalopram, raised the issue. The Irish College of Psychiatrists responded that
there was absolutely no evidence that antidepressants could cause problems and
to say so was dangerous and irresponsible.
Before the inquest, an extraordinary letter to
the national newspapers was sent from all professors of psychiatry in Ireland
(or so they said), stating that there was no evidence that antidepressants
could cause harm.
The jurors were asked to recommend whether the
verdict should be suicide or an open verdict. An open verdict means that there
is no clear evidence that the act was planned, but could, for example, have
happened under the influence of a substance like LSD. In European countries, an
open verdict is not an initial step to suing a pharmaceutical company, as it is
almost impossible to sue a pharmaceutical company in Europe.
Returning an open verdict in England or Ireland
does not blame the drug. It simply means in this case that the jurors have
decided that the killings and the events did not permit a straightforward
answer. But even so, the pharmaceutical companies sent academics such as
Professor Guy Goodwin from Oxford (see Chapter 1), along with several
high-powered lawyers to ensure the coroner or the jury would return a suicide verdict.
It didn’t. David Healy provided expert testimony and the jury returned an open
verdict.
Just like the American Psychiatric Association
(APA) before and since, The Irish College of Psychiatrists went into overdrive
issuing statements left, right, and centre that there was no evidence that
citalopram could cause suicide or violence. This led a retired professor of
psychiatry, Tom Fahy, send this letter to the Irish College:
“I am afraid the College is plain wrong.
There is no such thing as a college statement which is circulated to the
membership simultaneous with its publication, without opportunity for comment
or vote and ‘in unison’ with a body 100% financed by drug companies, and with
personal hostile references to expert testimony at an inquest with families
still in grief. And this on the heels of a dreadful multiprofessorial letter
even before the inquest began. Extraordinary and outside my experience. If I
were not retired I’d dissociate and publicly resign.”
Stewart Dolin
Stewart Dolin had the perfect life.107 He was married to his high school sweetheart for 36
years. He was the father of two grown children with whom he had a very close
and meaningful relationship. He was a senior partner of a large international
law firm, managing hundreds of corporate lawyers. He enjoyed his work and
derived satisfaction from cultivating relationships with his clients, as well
as helping them achieve the results they desired. He enjoyed travel, skiing,
dining, joking around with his family and friends and an occasional cigar. He
was 57 years old and high on life.
In the summer of 2010, Stewart developed some anxiety regarding work. He was prescribed
paroxetine. Within days, Stewart’s anxiety became worse. He felt restless, had
trouble sleeping and kept saying, “I still feel so anxious.”
Six days after beginning the medication,
following a regular lunch with a business associate, Stewart left his office
and walked to a nearby train platform. A registered nurse later reported seeing
Stewart pacing back and forth and looking very agitated. As a train approached,
Stewart took his own life. This happy, funny, loving, wealthy, dedicated
husband and father who loved life left no note and no logical reason why he
would suddenly want to end it all. The package insert for paroxetine did not
list suicidal behaviour as a potential side effect for men of Stewart’s age.
Stewart’s wife did not know it then, but Stewart
was suffering from akathisia. She started MISSD (The Medication-Induced Suicide
Education Foundation in Memory of Stewart Dolin), which is a non-profit
organisation dedicated to honouring the memory of Stewart and other victims of
akathisia by raising awareness and educating the public about the dangers of
akathisia so that needless deaths are prevented.
Candace Downing
Candace was a happy 12-year-old girl who had
never been depressed or had suicidal ideation.108 She was prescribed sertraline because she suffered from school anxiety. Her mother Mathy found her
beautiful little girl hanging, her knees drawn up. Her father knew the minute
he saw her that it was too late but tried to administer CPR, which continued
for another 45 minutes at the hospital but in vain.
“Do you know what that’s like, to see your happy
little girl hanging? There was no note, no warning, not for her, not for us.”
When Candace entered middle school, she began
having problems on tests and frustration over certain homework assignments. She
would block on answers she knew on tests, or write so illegibly that some
answers were marked incorrect, even if she had them correct. Because of her
parents’ concern, she saw her paediatrician, who recommended that she see a
child psychiatrist. He immediately wanted to give her sertraline. Mathy was
opposed, but he reassured her that it was safe and that he would recheck her in
three weeks. After three weeks, he wanted to double the dose, from 12.5 mg to
25 mg, which Mathy opposed. Because of her vehemence, the medication was not
increased at that time.
Right before school started following summer
vacation, Mathy and Candace returned to the child psychiatrist, who once again
wanted to increase the dose. When Mathy voiced concern, he stated, “What are
you worried about? Kids take 100-200 mg of Zoloft a day without any problems.”
“Why was so much hidden from us? Why were we not
ever informed about the contraindications or adverse reactions of Zoloft, or
for that matter, antidepressants in children? Didn’t we have the right to be
informed? … Shouldn’t it have been our choice to place Candace on medications
that involved risk rather than the pharmaceutical companies or the FDA?”
Candace had many friends. Everybody loved her
and when she died, more than a thousand people attended her service. Candace
was everybody’s little girl, and if it could happen to her, it could happen to
anyone’s child.
After Candace’s death, the Downings became aware
that an abrupt withdrawal from an antidepressant can prove fatal, as it can
create psychotic states, with decreased powers of reasoning. No one ever told
them that their daughter was going in and out of psychotic states and needed to
be watched closely every second.
“If we had been able to make our own choices, if
we had been aware of the risks, this would never have happened, as we would
never have allowed Candace to be placed on such a risky and controversial
medication,” said Andrew Downing.
“What happened to our daughter and so many
others like her is a travesty. We have since met other families who have lost
their child after Zoloft was prescribed for test anxiety. Those in a position
to create positive change can go home to their children at night. We will never
have that opportunity with Candace again. Our therapist referred to what
happened to Candace as abduction. She was taken away from us with no warning
and died in the process. What gave them that right?” Mathy stated tearfully.
The Downings, and other families, charge that
drug makers knew from premarketing studies that these drugs made some children
and teens suicidal but hid the study results.
“This is about the right of the American people
to make their own decisions. I can’t sit back as an American citizen and watch
children continue to die. And that is why we hope the documentary
‘Prescription: Suicide?’108 will help to get that message out
where it counts: among the American families whose biggest concern is to
protect and nurture their children,” said Mathy.
The Downings have testified at FDA hearings and
are lobbying Congress to make all research public. Mathy has also addressed the
US Drug Safety Systems Committee, which is reviewing the numerous allegations
against the FDA’s inadequate handling of policy regarding antidepressants.
The Downings’ psychiatrist had not told them
that he was on Pfizer payroll making speeches touting Zoloft. Pfizer said in a
statement for CBS News that “it’s paid consulting work with doctors helps the
company learn how to reduce adverse reactions.”109 No condolences were apparently offered.
People have called the Downings and said that
because of Candace their child is alive, as they knew what to look for.
Cecily Bostock
Cecily Bostock was a musician, an artist, an
over-achiever in almost everything she did.110, 111 She was having a lot of trouble
sleeping, had racing thoughts, was over-analysing, and was overly
sensitive. This prompted a prescription of paroxetine.
Her mother Sara said that within three weeks of
taking Seroxat, Cecily became a totally different person.
“The last two days she was just a complete
zombie I have to say. She was just agitated, jumping at every noise and not
making sense. I was very concerned. We were very close to Cecily. I just loved
her deeply.”
Sara found her daughter lying on the kitchen
floor. There was a large chef’s knife on the floor by her and just a trickle of
blood from her chest. Cecily had stabbed herself twice through the heart. Her
autopsy revealed she had a very high blood level of paroxetine, which reflects
poor metabolisation and is a feature common to many of these suicides.
Cecily killed herself about 20 days after she
had started taking Seroxat. She was just 25 years old.
Since her daughter’s death, Sara has been
campaigning and creating awareness about the dangers of antidepressants. She
spoke at a charity conference in 2008 about her experience and knowledge from
years of research, which is on video (http://vimeo. com/16727219). Sara has also given testimony
at an FDA hearing and has co-founded www.ssristories.com, which is a collection of over 5,000
stories that have appeared in the media.
Woody Witczak
In 2003, Tim, known to most as Woody, died of a
sertraline-induced suicide at age 37.112 He was not depressed, nor did he have any history of
mental illness. He died after taking the drug for five weeks with the dosage
being doubled shortly before his death. He was given the antidepressant
by his general physician for “insomnia.”
Woody loved life and all that this world has to
offer. He had endless energy, a constant smile and truly cared for others. He
had a successful career in sales and was active in the community, socially and
politically, always willing to fight against injustice. Woody truly inspired
others to be the best they could be.
Woody went to his regular internist because he
was having trouble sleeping, in part because he had just started a new position
as vice president of sales with a start-up company about two months earlier. He
was excited about this dream opportunity to make his mark on the business
world. Along with this excitement came some stress and difficulty sleeping.
This was the first time he’d ever gone to a
doctor for this sort of issue. Woody’s doctor gave him three weeks’ worth of
sertraline samples and told him to come back for a follow-up appointment after
the samples were finished. There was no discussion about the risks or the need
to be closely monitored because of this mind-altering drug. The first three
weeks Woody was taking sertraline his wife was out of the country on business
and no one was monitoring him. Within a couple of days, he experienced many of
the known side effect of sertraline, e.g. night sweats, diarrhoea, trembling
hands, and worsened anxiety.
One of the most significant side effects Woody
had was akathisia. He was very restless, which caused him not to sleep, and
irritable and felt he always needed to keep moving.
Shortly before his death, Woody came home crying
after driving around all day. He sat in a foetal position on the kitchen floor
profusely sweating with his hands pressing around his head saying, “Help me.
Help me. I don’t know what’s happening to me. I am losing my mind. It’s like my
head is outside my body looking in.” The next day, Woody called his doctor to
tell him what happened and was told to be patient because it could take four to
six weeks before the drug worked.
Over the course of the next week, in typical
Woody fashion, he was looking for ways to “beat this feeling in my head all
while still running three to four miles a day. Two weeks later, when sertraline
should have worked according to his doctor, Woody was found hanging from the
rafters in the garage. Woody’s family and friends only wish they knew then what
they know now. It wasn’t Woody’s head. It was the drug.
Never once did Kim, Woody’s wife, or Woody
question the drug. Why would they? It was FDA approved, heavily promoted as
safe and effective, and it was given by his doctor. People trust their doctors,
who assume the FDA and the drug companies did their job to ensure that the
drugs they prescribe are safe and effective.
The day Woody died, the front page of the local
newspaper had an article that people in the UK had found a link between
antidepressants and suicide in teens. Kim’s quest for the truth has led her to
testify about the dangers of SSRIs at hearings in the US Senate, at the FDA,
the Health Department, Congress and the courts. Together with other
campaigners, she was active in getting black box warnings added to
antidepressants.
Through my work, I have met with relatives of
many more people killed by SSRIs than those described here. It makes me
particularly angry that most of those who died or killed others shouldn’t have
had a prescription for an SSRI. This is true for all of the eight victims I
have mentioned, as the “indications” were:
anxiety regarding work or school work (3)
break up with girlfriend (2)
trouble sleeping (2)
didn’t feel well psychologically (1).
Here are brief accounts of additional tragedies,
which I have described before.3 Again, in none of the cases was
there a reasonable indication for an antidepressant.
Matt Miller had moved to a new neighbourhood and
a new school and was prescribed sertraline and told to call his doctor in a
week. After taking his seventh pill, Matt went to his bedroom closet and hanged
himself, having to lift his legs off the floor and hold himself there until he
passed out. He was only 13 years old.
Jeremy Lown was a teenager with Tourette’s
syndrome. To treat his uncontrollable tics and verbal outbursts, his
neurologist prescribed fluoxetine. Three weeks later, Jeremy hanged himself in
the woods behind his house.
Vicky Hartman was given a sample pack of
sertraline by her child’s doctor. She didn’t suffer from any mental disorder
but mentioned she needed a “pick-me-up” to help with stress. Soon after
starting the medication, she shot her husband and herself.
A man hanged himself after taking fluoxetine,
which his cardiologist had prescribed for chest pain, and a woman shot herself
after taking the fluoxetine her family doctor had prescribed for migraine.
Twenty-year-old student Justin Cheslek had
trouble sleeping and was prescribed sleeping pills. When he complained to the
doctor that the pills made him groggy and “depressed,” the doctor gave him
paroxetine, on which he developed akathisia. Two weeks later, the doctor gave
him venlafaxine, and after three weeks on antidepressants, he hanged himself.
Brennan McCartney went to his family doctor with
a chest cold and mentioned he felt sad over breaking up with a girl. He left
with a script for an antibiotic and a sample pack of citalopram. On the fourth
day, Brennan seemed agitated when he left the house and failed to come home. He
hanged himself in a local park, only 18 years old.
Caitlin Hurcombe, a teenager, had visited
relatives in the United States where she saw an ad for fluoxetine and wanted to
try it. She went to her local doctor and it took her eight minutes to get the
prescription. She descended into unprecedented chaos, including neural
twitches, violent nightmares and self-harm, and hanged herself 63 days later.
As this story shows, advertising prescription drugs to the public, which is
legal only in the United States and New Zealand, can kill healthy people who
don’t need them. Caitlin’s story is particularly tragic, as the name Prozac was
developed for Eli Lilly by a branding agency.113 Prozac suggested positive and professional and zappy,
and conveyed the idea that taking antidepressants did not have to mean you were
mentally ill. Instead, you could be young and troubled by the world, in need of
an aspirin for an existential hangover. Prozac was eagerly grasped as the
embodiment of a dream, the idea that an antidote to the pain of modern living
could exist in a simple pill. This marketing killed Caitlin.
Akathisia is the main culprit
It is a longstanding belief that the “activating
effect” antidepressants cause in some patients gives them the energy to follow
through on suicidal impulses before the mood improvement takes effect. This
myth should have been scrapped ages ago, but the drug industry has perpetuated
it, as it has been useful for their storytelling. According to Lundbeck,114
“When the leaflet says that suicidal thoughts
may worsen when you first start taking antidepressants, it is because … it can
take some time before the drug works (sometimes up to two weeks). Therefore,
the disease is not necessarily attenuated at once, and it may therefore trigger
enhanced suicidal thoughts, but this is because of the disease, not the drug.”
This information is totally misleading. The
disease is never attenuated at once; it doesn’t take two weeks before the drug works – the patients
slowly become better whether they are treated or not (see Figure 3.1); and it
is not the disease that triggers enhanced suicidal
thoughts, it is the drug.
The many proofs that this is a myth come from
several types of research, e.g. data show that both the incidence of akathisia
and deliberate self-harm increase with dose, unlike the effect on the
depression.115 Further, people kill themselves or others without being
depressed; even healthy people can do it when they are exposed to these drugs.
We also know what the mechanism of action is. In addition to akathisia,
drug-induced psychosis and emotional blunting play a role; people act in an
out-of-character fashion.
In 2000, David Healy published a study he had
carried out with 20 healthy volunteers – all with no history of depression or
other mental illness – and to his big surprise two of them became suicidal when
they received sertraline.11 One of them was on her way out the
door to kill herself in front of a train or a car when a phone call saved her.
Both volunteers remained disturbed several months later and seriously
questioned the stability of their personalities. Pfizer’s own studies of sertraline
in healthy volunteers had shown similarly deleterious effects, but most of
these data are hidden in company files.11 We have collected around 150
healthy volunteer studies from the literature and from the EMA and they show
that SSRIs double the incidence of effects that can predispose to suicide.116
There are numerous accounts of suicides in
healthy people and in people who had minor problems with their lives that
should never have caused their doctor to prescribe an antidepressant for them.
When I discuss this with leading psychiatrists, very few admit that the drug
can cause suicide. Most display their specialty’s organised denial and have
typically used these arguments:
The suicides are just anecdotes (in my opinion,
they are tragic losses for the families and they don’t see them as
“anecdotes”).
The randomised trials didn’t show a
statistically significant increase in suicides (the psychiatrists reward the
drug industry for all its frauds).
The trials only showed an increase in suicidal
behaviour, not in suicides (I shall debunk this argument below).
The randomised trials were not designed to
detect suicide and suicide attempts (which is correct, but the effect of this
is that the true risk has been much underestimated).
Observational studies have shown that
antidepressants protect against suicide, e.g. suicides increased when the usage
of the drugs went down (all reliable studies have rejected this relation, see
next section).
Those who killed themselves suffered from an
unrecognised depression (this is a tautology, a bit like Freud’s postulate that
we are all homosexuals and those who deny it are latent homosexuals).
Prior to its meta-analysis of 100,000 patients,
the FDA held a meeting with public representation.117 Understandably, the families were outraged that they
had not been informed of the increased risk of suicide and said that such a
notification would have led them to refuse such dangerous treatment, preventing
their tragic, unnecessary losses. Here are two of the testimonies.
Lisa van Syckel mentioned that: “The FDA and the
pharmaceutical industries have repeatedly stated that it is the disease, not
the drug, that causes our children to become violent and suicidal. It wasn’t
the disease that caused my daughter to viciously mutilate herself; it was the
drug. It wasn’t the disease that caused my daughter to become violent and
suicidal and out of control. It wasn’t the disease that caused her to scream
the words ‘I want to die.’ And, it sure as hell was not the disease that caused
Christopher Pittman to kill the two people he loved the most, his grandparents.
He had been on Zoloft just three weeks and he was 12 years old. Christopher is
now facing life in prison as an adult. Pfizer refers to me and others as a
detractor of SSRIs and that I am misinforming legislators with oversight
responsibilities. As an adult, I am considered fair game for verbal attacks
but, ladies and gentlemen, Pfizer crossed the line the day they attacked a dead
child. They viciously attacked a dead child and you all know it. And you,
ladies and gentlemen, as adults, need to tell Pfizer that they need to stop.”
Mathy Downing (see above) noted that little
Candace’s death was “entirely avoidable, had we been given appropriate warnings
and implications of the possible effects of Zoloft. It should have been our
choice to make and not yours. We are not comforted by the insensitive comments
of a corrupt and uncaring FDA or pharmaceutical benefactors such as Pfizer who
sit in their ivory towers, passing judgments on the lives and deaths of so many
innocent children. The blood of these children is on your hands. To continue to
blame the victim rather than the drug is wrong. To make such blatant statements
that depressed children run the risk of becoming suicidal does not fit the
profile of our little girl.”
Lundbeck: Our drugs protect children
against suicide
Lundbeck sells five antidepressants
(amitriptyline, nortriptyline, citalopram, escitalopram and vortioxetine) and
the company should therefore know a lot about such drugs. However, in 2011 its
CEO, Ulf Wiinberg, claimed in a radio programme that SSRIs reduce suicides in
children and adolescents. When the stunned reporter asked him why the package inserts
warned against suicide attempts, also for Lundbeck’s drugs, he replied that he
expected the leaflets would be changed by the authorities!
The radio interview took place while Lundbeck’s
US partner, Forest Laboratories, was negotiating compensation with 54 families
whose children had committed or attempted suicide under the influence of
Lundbeck’s antidepressant drugs.
The head of the Institute for Rational
Pharmacotherapy in the Danish drug agency, Steffen Thirstrup, mentioned in the
programme that he was surprised that Lundbeck contested the facts about the
products in the package inserts that authorities both in the EU and the United
States had decided the industry must disclose. Wiinberg replied that Thirstrup
talked about suicide thoughts and behaviours whereas he himself talked about
suicides, to which the interviewer pointed out that Thirstrup didn’t talk about
suicide thoughts and behaviour but about the increased risk of suicide and
suicide attempts.
Wiinberg argued, as companies and silverback
psychiatrists always do, that it is the depression and not the drugs that
increase the risk of suicide.11
I had already seen and heard much nonsense about
psychiatric drugs but felt this was so much over the top that I published an
open letter to Lundbeck.118 The next day, Lundbeck’s research director, physician
Anders Gersel Pedersen, responded in a way that looked like an acute attack of
industry pomposititis.114 His reply begins thus:
We have – with regret – read Peter Gøtzsche’s
open letter, which unfortunately seems characterized by a limited professional
insight into the complicated and extremely important issue of suicide and
suicidal behaviour associated with depression in children and adolescents, and
a possibly increased suicide risk in relation to treatment of depression with
antidepressants … In our view, any dialogue on this important topic should be
evidence-based and not just take the form of superficial polemic on an
insufficient basis.
Pedersen argued that it had never been shown
that there is a clear relationship between suicidal behaviour, suicide attempts
and suicide. Such arguments are utterly stupid. A suicide starts with a thought
about suicide, which leads to preparations for suicide, a suicide attempt and
suicide. It should surprise no one – apart from the pill pushers, including
corrupt psychiatrists who say the same as Lundbeck – that the risk factors for
serious suicide attempts are very similar to those for suicide.119, 120
Totally misleading observational
studies of suicide
Pedersen wrote that untreated depression leads
to more suicides and mentioned that epidemiological studies in the United States
and the Netherlands had shown that suicides among children and adolescents had
increased after the usage of antidepressant drugs went down.114 He stated that
suicide rates went up by 14% and 49%, respectively, and that the rates doubled
among boys in the Netherlands.
Pedersen’s references do not provide any support
to his opinion. He quoted a 2007 paper by Robert Gibbons for an increase in
suicide rates after the FDA and the EMA warned against using antidepressants in
young people in 2003 and 2004.121 However, critics quickly pointed out the dishonest
science Gibbons had employed to make his case.122 He didn’t use the same calendar years for SSRI
prescriptions as for suicides! In fact, the number of suicides for persons ages
five to 24 declined when there was a significant
decrease in the prescribing of SSRIs to youth. In other words, the data
indicated that SSRIs cause suicide.122
This is not the sort of error a scientist
accidentally makes. It looks like a deliberate attempt to tell a story that
fits a preconceived end.122 In the Netherlands, the academics
were incensed with Gibbons and his statistical antics (Gibbons is actually a
statistician, which is hard to believe) and they noted that the increase in
suicides in the Netherlands was so small that it wasn’t statistically
significant. They described Gibbons’ conclusions as “astonishing” and
“misleading” and stated that he and his co-authors had been “reckless” to
publish such claims.122
Gibbons has published at least ten papers
telling stories that just aren’t true, e.g. that the FDA’s warnings have
increased suicides, that antidepressants are highly effective in youths, and
that the randomised placebo controlled trials of fluoxetine and venlafaxine
didn’t find evidence of an increased suicide risk in youths.122 Critics
submitted letters to Archives of General Psychiatry
pointing out that Gibbons’ claim about fluoxetine and venlafaxine were based on
inappropriate data selection, opaque methodology, obvious arithmetic errors,
methodological errors, misinterpretation of the data, deceitful presentation,
and misleading conclusions, and that, if properly analysed, Gibbons would have
found the same harmful effects as the FDA did. However, the editor-in-chief
Joseph Coyle refused to publish the letters but relegated them to the journal’s
website where few people will ever find them.
Gibbons’ dishonest research has received a lot
of media attention and the silverbacks love to cite it. This is how societal
delusion and organised denial is created. Gibbons isn’t honest about his
conflicts of interest either. In 2012, he published a paper about the
development of a computerised test for depression, but he and his four
co-authors failed to inform the readers that Gibbons is the president and
founder of a commercial company that owns the rights to the test and several
related tests and that they all owns shares in this company.123
Pedersen’s other references are similarly
disastrous. A study from 2006 only included data between 1992 and the first
half of 2003, and did therefore not cover the period after FDA’s warning.124 This study found that the risk of suicide attempt was
highest in the month before starting antidepressant treatment and declined
progressively after this. This shouldn’t surprise anyone, as a suicide attempt
may precisely be the reason for initiation of treatment, which the authors also
acknowledged. The authors also noted that there were few adolescents in their
study and that they accounted for only three suicides and 17 serious suicide
attempts. They therefore resolved that their “data contribute nothing to the
debate regarding the efficacy or clinical appropriateness of antidepressant
treatment for adolescents.” Perhaps Pedersen hadn’t read the paper he cited, as
my discussion with Lundbeck was about suicides in children and adolescents.
Pedersen’s third reference was to an absurd
study by Göran Isacsson from 2005.125 It was about forensic toxicological screening of 14,857
suicides in Sweden from 1992 to 2000. Already the premise for the study was
wrong: “If treatment with SSRIs increased the suicide risk in depressed
individuals, they should be found in suicides more often than otherwise
expected.” Patients committing suicide might very well have stopped their
treatment because of development of akathisia, which predisposes to suicide,
and they might therefore not have traceable drug in the blood post mortem.
Isacsson actually admits this in the Discussion section of his paper (as this
admission contrasts sharply with his premise, I assume the editors forced him
to write it).
Just like Gibbons, Isacsson has also published a
long series of papers that I won’t characterise as honest attempts at finding
out whether SSRIs can cause suicide; in fact, other researchers have noted that
both Gibbons and Isacsson conclude the opposite of what their data show.126
Five years later, Isacsson published a similar
paper with the declarative title, “Antidepressant medication prevents suicide
in depression.”127 Most of the data were the same but he now included
three more years, up to 2003. This article was retracted two years later in a
non-transparent manner. It wasn’t clear who requested the retraction but I
doubt the initiative was Isacsson’s. Furthermore, readers weren’t informed what
the errors were, which is bizarre. A Swedish reporter submitted a Freedom of
Information request to the Karolinska Institutet in Stockholm where Isacsson
worked but was told it was confidential information and that no data could be
released. It took five months of legal process to get access to the correct
data. In its final statement to the court, Karolinska Institutet claimed that
the correct figures didn’t exist at the time of the reporter’s request, but that
they had now been produced.
Isacsson had made much of his finding that only
15% of patients admitted for psychiatric care for depression had measurable
amounts of antidepressants in their blood at the time of suicide, but it turned
out that the correct number was 56%, which leads to the opposite conclusion
about the effect of antidepressants than the one Isacsson reached.
The correct number appeared in a short statement
to the court in Stockholm, which researchers won’t find again. The reporter
therefore wrote to the Karolinska Institutet again requesting the document
where the 56% was listed, but was now told that, “The data were produced owing
to the request from the Administrative Court of Appeal and are not saved in any
document. As the requested documents do not exist at Karolinska Institutet they
cannot be released.”
Not only was the cover-up bizarre, Isacsson’s
paper is, too. It is close to impossible to understand, and I found several
contradictions in it. It was published in the same journal as his 2005 paper
but this time the editors appeared to have woken up, as there were many more
caveats, some of which are rather amusing and tell us that studies like
Isacsson’s are worth absolutely nothing and only increases the scientific
pollution. For example: “Definitive conclusions cannot be drawn,” “Individuals
prevented from suicide cannot be identified, only their absence among suicides
can be estimated,” ”A limitation of the study was that we lacked information on
diagnoses and other possibly confounding variables,” and the best one, “Since
individuals characterized by a non-event cannot be identified, a definite proof
is impossible.”
Although Isacsson’s papers were both published
in Acta Psychiatrica Scandinavica, and 79% of the
suicides were likely the same, there was no reference in the 2010 paper to the
2005 paper. Many would regard this as scientific misconduct. Isacsson quoted,
however, two other of his papers, also from Acta Psychiatrica
Scandinavica,128, 129 which were very similar to his 2005 and 2010 papers.
Isacsson’s pollution of the literature is
substantial. A PubMed search on his name and “suicide” in the title yielded 41
references in November 2014. The retraction of his 2010 paper from Acta Psychiatrica Scandinavica wasn’t a hindrance for
publishing more of the same in this journal. In 2013, for example, he published
another forensic analysis and again claimed that the warning may have led to an
increase in suicides.130 In this paper, Isacsson has a section called
“Comparison with other studies” where he cherry-picks references to Gibbons’
work and to other unreliable studies and claims that suicidality is not
necessarily a risk factor for suicide. Of course it is.119, 120
Isacsson has not restrained himself in the media
either. In 2013, he wrote in a Swedish newspaper that those people who could
have reduced their suicide risk with SSRIs were excluded from the randomised
trials, which included people who were more suicide prone.131 Total nonsense. The truth is that only people at low risk of suicide were recruited for the trials.
Pedersen had four more references in his article.
One was to a study of suicides in Danish children by Professor Lars Kessing, a
psychiatrist on the Lundbeck payroll, and others.132 It found that none of 42 children aged 10-17 was
treated with SSRIs within two weeks prior to suicide, but since SSRIs were not
approved for use in children in the study period, this isn’t surprising. There
was also a five-year follow-up, and now some of those who committed suicide
were on SSRIs. Those treated had a “highly statistically significant and
strongly increased rate of suicide compared to those not treated with SSRIs”
(rate ratio 19.21; 95% CI 6.77 to 54.52). This result didn’t look good for
Lundbeck’s drugs, and the authors presented another analysis where they had
corrected for psychiatric hospital contact. The rate ratio was still increased,
4.47, but bingo, it “was no longer quite significant (95% CI 0.95 to 20.96).”
It is terribly misleading to correct for
psychiatric hospital contact, as such contact in itself
increases the risk of suicide for psychiatric patients 44 times.133 A correction will therefore spuriously attenuate a true
relationship. The authors found that SSRIs dramatically increase the risk of
suicide in children, but they concluded the opposite:
“Not treating severely depressed children and
adolescents with SSRIs may be inappropriate or even fatal.” What may be fatal
for children are psychiatrists who conclude like this and use SSRIs in
children. The study was funded by The Lundbeck Foundation.
These researchers made other inappropriate
statements. They acknowledged that the large FDA analysis found that treatment
of non-depressive children and adolescents with SSRIs
led to a higher risk of attempted suicide, but argued that, “in such analyses,
it cannot be excluded that the suicidal ideations among children and
adolescents with depression might reflect confounding by indication, i.e.,
those treated tend to have more serious conditions.” This is nonsense, as the
FDA analysis was based on randomised trials. There cannot be confounding by
indication in randomised trials.
Another paper cited by Pedersen argued that the
FDA had not found an increase in suicides and that suicidal behaviour (which was increased) should not count, as it is a poor surrogate
marker.117
But the author of the paper contradicted himself, as he also wrote that, “A
history of a prior suicide attempt is one of the strongest predictors of
completed suicide,” and that the rate of suicide is 30 times greater in
previous attempters than in non-attempters.
Pedersen also quoted an unsystematic review by
Robert Goldney who had cherry-picked those studies that supported his idea that
antidepressants protect against suicide.134 The paper is a classic example of how one should not do a review. Both Gibbons and Isacsson featured there,
including Isacsson’s meaningless 2005 study,125 without the slightest critical
comment. Goldney cited studies in the Nordic countries that linked
antidepressant prescribing with a reduction of suicide, but these studies are
unreliable. Other researchers, e.g. Per-Henrik Zahl and colleagues, have showed
that there is no statistical association (P = 1.0) between the increase in sales
of SSRIs and the decline in suicide rates in the Nordic countries.135 These authors reported that the decline in suicides in
Denmark and Sweden pre-dated the introduction of SSRIs by ten years or more. I
have great confidence in Zahl’s research. He is both a doctor and a
statistician and I have published several pivotal papers with him on
mammography screening. Zahl and colleagues declared that they had no conflicts
of interest while Goldney had “received honoraria and research grants from a
number of pharmaceutical companies.” Of course he had. With such reviews, he
lives up to his name and must be worth his weight in gold for them. Other
authors have confirmed Zahl et al’s findings in the Nordic countries and found
that a large fall in autopsy rates could entirely account for the observed
changes in suicide rates.136
Pedersen’s last reference was to a paper
published in a journal called Expert Opinion on Drug Safety.137 I had never heard of this journal before and would
never read anything in a journal with such a name. We already know we cannot
trust scientific papers about drug safety, and on top of that we have experts
who opine something about drug safety. If the journal had been called Systematic Reviews of Drug Harms, I would have been more
keen to read it. The article leads absolutely nowhere. It mentions FDA’s
warning and the subsequent decline in the usage of antidepressants in children,
which the author finds alarming without any justification whatsoever for the
alarm. Truly an “expert opinion.” Then there was also the usual criticism of
using suicidality as a surrogate for suicides, which I suppose is listed in
some User’s Guide to Eternal Happiness on the Antidepressant
Drug Market, and an alarming touch of wishful thinking:
“Most studies examined excluded patients at high
risk for attempting suicide. Had such high-risk patients been included in the
analyses, it is possible that antidepressants would have been found to confer a
protective effect.”
Remember that we are talking about children
here. And yet this author has the nerve to suggest that antidepressants might
have protected children from suicide if only we had done the randomised trials
better! The advice of such “experts” is lethal.
Pedersen isn’t just anybody. He is the research
director in one of the major drug companies selling antidepressants. I have
therefore dissected his seven references, as they tell us a lot about how
people in drug companies and their paid prostitutes among academics actually
think. Industry propaganda talks about a research-intensive industry but those
responsible in the companies aren’t interested at all in research. They are
only interested in pushing drugs and they do this by selling lies about their
drugs, with no respect for science, human suffering and deaths, as evidenced by
the fact that they prefer junk science that supports sales for true science.
Science to them is just window dressing.
Silverbacks all over the world claim that
antidepressants protect against suicide,97-99 and some of them
struggle hard to convince the FDA to remove its black box warning against
suicide in young people. The junk science they refer to seems endless. The most
recent study was published in the BMJ in 2014,138 but as all the previous ones, it was so flawed that
nothing could be inferred from it.139 The US researchers didn’t even study their primary
endpoint, suicide attempts on SSRIs, but used a poor surrogate, poisoning with
all psychotropic substances. People on SSRIs who attempt suicide don’t usually
poison themselves (and cannot really do so with SSRIs), they tend to use
violent methods like hanging.49, 140 The researchers also ignored the fact that any dose
change with SSRIs increases the risk of suicide. Thus, the risk of suicide
increases if people suddenly stop taking SSRIs because of the warning, but this
would be due to withdrawal symptoms and not a sign that SSRIs protect against
suicide. The researchers’ assertion that FDA’s warning had been harmful was
completely refuted by other researchers with real data on suicide attempts from
five different databases, also from the United States.141
Some studies are involuntarily comical. For
example, a study of trends in use of antidepressants and suicides claimed that
there was a clear protective effect from the drugs when it was obvious by
looking at the graphs that there wasn’t.142
As just noted, properly performed observational
studies have dispelled the myth that antidepressants protect against suicide.135, 141, 143
Such a study from Sweden, where people were their own controls,143 found a three-to-four times increased risk of suicide
after starting an SSRI, with the greatest risk in the second week of treatment
(odds ratio 9.7, 95% CI 3.0 to 31.7). This is exactly what we would expect,
based on other studies.
It is worth remembering that, with all the
randomised trials we have, it wasn’t really necessary to look at the next best
evidence, the observational studies, because the trials, despite all their
flaws that tend to obscure the relationship, nonetheless showed that the use of
antidepressants doubles the number of suicide attempts.82
One of the reasons drug companies give for using
their drugs is that untreated patients may commit suicide. Therefore, according
to drug company logic, abruptly stopping what they believe is a lifesaving
drug, which drug companies do when they perform placebo controlled trials,
increases the patients’ risk of suicide. This must mean that the companies’
trials are unethical. Drug companies obviously don’t take seriously their own
arguments; they merely use the argument that fits the situation and don’t care that
their arguments are contradictory.
Antidepressant-induced homicides
That antidepressants can cause homicide is
beyond doubt.3, 11, 49, 144, 145 We should ignore people who tell us
otherwise. Some say that the randomised trials didn’t show this, but the drug
companies have a keen interest in hiding if anyone committed homicide while on
their drug. Furthermore, homicide caused by drugs is rare, which could also be
a reason why we don’t see them in the trials.
As stated earlier, we know what the main
mechanism of action is for suicide and homicide, the extreme form of
restlessness we call akathisia. There are three strong indications that it is
the drug and not some unrecognised fault with the person that leads to these
violent actions: They occur for people who by all objective and subjective
measures were completely normal before the act, with no precipitating factors;
they were preceded by clear symptoms of akathisia; and people returned to their
normal personality when they came off the antidepressant.146
Antidepressants are not safe in any age group.
There are numerous reports in the literature and on websites that middle-aged
and even old people have killed themselves or others after having experienced
akathisia. Many of these people were healthy and took the drug for
non-disease-related reasons, e.g. for fun, stress, insomnia, being bullied or
marital problems.3,
11, 145, 147
I describe here briefly a detailed Australian
report on ten forensic cases.145 All patients had mutations in their CYP450 genes that
changed their drug metabolism; none had been violent before; all developed
akathisia; and all were able to stop taking antidepressants – frequently
against medical advice – and to return to their normal personalities after the
violent action. None of them had any history of mental illness, and the
indications for treatment with antidepressants seemed to be non-existent:
Female, 35 years, nortriptyline, distress due to
husband’s drinking, killed teenage daughter in toxic delirium after three days.
Male, 18 years, fluoxetine, sister was comatose
after a car crash, violent akathisia for 14 days, killed his father four days
after he ran out of pills.
Male, 35 years, paroxetine, distressed by “on
and off” relationship with mother of his child, stabbed former partner 30+
times to death after 11 weeks of akathisia.
Male, 46 years, paroxetine, anxiety about not
making enough money to support the family, killed his son in a manic-shift
akathisia and delirium after 42 days.
Male, 16 years, sertraline and fluoxetine,
depressed, struggled at school, and the girlfriend left him, attempted suicide
on both drugs, killed therapist in hospital after 11 weeks.
Male, 50 years, venlafaxine, distress over
divorce, shot a stranger four days after stopping drug.
Male, 24 years, escitalopram, anxiety and
illicit substance use, several suicide attempts and assaults, nearly killed
partner, 12 years in jail for attempted murder.
Female, 26 years, several SSRIs, difficulties
with in-laws, two attempts to kill her two children.
Female, 52 years, paroxetine and citalopram,
harassment at work, suicide attempt and tried to kill her two children.
Female, 25 years, citalopram and venlafaxine,
marital distress, several suicide attempts on both drugs, jumped in front of a
train with her child while on citalopram.
Some of these patients received other drugs or
substances, e.g. cannabis, but it is highly likely that the violence was caused
by the SSRIs. In several cases, the treatment provided by the psychiatrists was
grossly inadequate and contributed directly to the violent actions.
An example of this is the 26-year old woman who
tried to kill her two children on two occasions. She was prescribed paroxetine
for stress but experienced an episode of rage and attempted suicide by
inhalation of carbon monoxide, and then stopped taking the drug. Despite this, she was prescribed paroxetine again and reassured about its safety
two years later. This time she experienced intense restlessness, surges of rage
and anger, panic attacks, impulsive spending sprees, and constant suicidal
ideation. She reasoned that her low self-esteem, insomnia, and suicidal
behaviour were due to difficulties with her in-laws. She overdosed and was admitted to hospital where paroxetine was increased. She
tried to kill herself again and was diagnosed with an “adjustment disorder.”
She was switched to venlafaxine, which was
increased over three months until the dose was eight times higher than the
initial dose. Each dose increase occasioned a week spent in bed with
exhaustion, as she was unable to get up (akinesia). Her mental state
deteriorated and violent outbursts and suicidal ideation became frequent and
severe. Unable to stay in one place, she drove several hundred miles with her
children and tried to kill them and herself by car exhaust. A few days later
she tried to kill her children and herself again.
There were no interacting drugs in her regimen
and many of the harms described in the FDA-approved product information for
venlafaxine fit well with her experiences,145 e.g. intentional injury, malaise,
suicide attempt, depersonalization, abnormal thinking, akathisia, apathy,
ataxia, CNS stimulation, emotional lability, hostility, manic reaction,
psychosis, suicidal ideation, abnormal behaviour, adjustment disorder (which
became a psychiatric diagnosis for her, although it was a side effect), akinesia,
increased energy, homicidal ideation, impulse control difficulties.
In contrast to the FDA-approved product
information, citizens in Australia were kept in the dark about these serious
harmful effects of venlafaxine, which could drive people into committing
suicide and homicide. But that doesn’t pardon the psychiatrists who treated her
so badly; they should have known better.
Akathisia homicides have been defended as
instances of involuntary intoxication both with and without genetic evidence,
and some people have succeeded in receiving damages from the manufacturers for
failure to warn.145
Other forensic cases are also convincing,147
and the documentary evidence in a legal case on paroxetine against SmithKline
Beecham included an unpublished company study of incidents of serious
aggression in 80 patients, of which 25 resulted in homicide. These cases
confirm that there is no upper age limit where antidepressants are safe. A man
aged 74 strangled his wife, and another was 66 when he became delusional on
fluoxetine and killed his wife who was found with 200 stab wounds.
According to internal company documents, 0.65%
of the patients in clinical trials became hostile on paroxetine compared with
0.31% on placebo, and in healthy volunteer studies, three of 271 people (1.1%)
became hostile on paroxetine and none of 138 on placebo.147 As noted above, we found in our healthy volunteer
studies that SSRIs double the incidence of effects that can predispose to
homicide.116
And an analysis of the 1,374 e-mails the BBC received after its Panorama
programme about paroxetine (see below) showed that the self-reports of violence
from patients with no apparent background of violent behaviour were clearly
linked with dosage.147
In 2001, for the first time, a jury found a
pharmaceutical firm liable for deaths caused by an antidepressant. Donald
Schell, aged 60, had been taking paroxetine for just 48 hours when he shot and
killed his wife, his daughter, his granddaughter and himself.148 Central to the case were SmithKline Beecham internal
documents showing the company was aware that a small number of people could
become agitated or violent from paroxetine. Despite this knowledge, paroxetine
packaging did not include a warning about suicide, violence or aggression,
which made the company liable. The internal documents, stamped “confidential,”
list the results of tests involving more than 2,000 healthy volunteers taking
either paroxetine or placebo. Some volunteers experienced anxiety, nightmares,
hallucinations and other side effects – definitely caused by the drug – within
two days of taking it. Two volunteers attempted suicide after 11 and 18 days,
respectively.
The blatant lies of GSK, which took over
SmithKline Beecham, just continued. Even in 2011, ten years after the verdict,
GSK denied that paroxetine can cause people to commit homicide and suicide and
that there are withdrawal problems.68 GSK’s director of US regulatory
affairs insisted that David Healy – who testified as an expert witness – had
not seen all the data and said there was “no credence” to the 25% agitation
rate that he gave in court. However, Healy had examined every one of the
healthy volunteer studies carried out before the drug was licensed except for
some material that was unaccountably not there. Furthermore, GSK contradicted
itself. During Healy’s deposition for the court case, the company conceded he
had seen a representative sample.
In sertraline paediatric trials, eight of 189
patients (4%) discontinued the drug because of aggression, agitation, or
hyperkinesis (a coding term for akathisia), compared with none in 184 patients
on placebo.147
On the Internet, there is a collection of over
5,000 media stories of massacres, homicides, suicides, and school and college
shootings dating back to 1966 that involve antidepressants and ADHD drugs, in
some cases detailing the drugs and legal defences.149 The violent actions have often been linked to
akathisia, emotional blunting, and manic or psychotic reactions,147 also in court
cases. In 2011, for example, a Canadian judge ruled that fluoxetine induced a
16-year old boy to commit murder; he knifed a friend to death.146
The organised denial in psychiatry also clouds
this issue, however. It is very tragic that leading psychiatrists opine that
homicidal ideation and behaviour is something entirely different from homicide.
It is particularly dangerous to take
antidepressants in the United States. As mentioned above, Christopher Pittman
became manic and shot his two grandparents to death two days after his dose of
sertraline had been doubled.150 Despite being only 12 years old when he did this, he
was sentenced to 30 years of prison.
David Crespi was on fluoxetine and three other
drugs, which he had taken for a couple of weeks, when he killed his two twin
daughters with a knife.151 He pleaded guilty to avoid the death penalty and got a
life sentence with no chance of parole, although he became his old self after
coming off the drugs.
Canadians seem to be less inhumane than
Americans. David Carmichael, who killed his 11-year old son while on
antidepressants, was ruled “not criminally responsible on account of a mental
disorder,” and today, Carmichael is a free man who writes and speaks on the
dangers of antidepressants.
Kurt Danysh didn’t have the luck to live in
Canada. He was 18 years old when he was prescribed fluoxetine by a general
practitioner who failed to perform any psychological testing.152 He became restless and violent and shot his father, the
person he loved the most, 17 days later in a totally out-of-character mood.
Kurt had no history of violence prior to fluoxetine, but in 1996, he was
convicted of murdering his father and sentenced to 22.5 to 60 years in prison.
Eli Lilly lied in court, claiming that fluoxetine would not cause aggressive
behaviour. However, it was revealed in 2004 that Lilly had concealed data from
1988, which linked fluoxetine to violence, and the FDA recognised that SSRIs
can cause violent behaviour, particularly in children and adolescents. Even
though more than 70 cases of homicide linked to fluoxetine have now been
reported to the FDA, the judge has dismissed all appeals, referring to a rule
that requires evidence of innocence to be presented within 60 days. In official
documents and letters, the prosecution’s own expert stated that Kurt’s criminal
actions were based on insanity caused by a mind-altering drug, which should
have provided Kurt a concrete defense.61 The state itself, however, forced
Kurt to take more of these drugs before and during his confession. Kurt has
gained a paralegal degree whilst incarcerated and has launched the SAVE
campaign (Stop Antidepressant Violence from Escalating) in the hope of saving
other children from his fate. It was later found out that Kurt is a poor
metaboliser of SSRIs.
This is as absurd, tragic and unfair as it can
possibly get. People have been released from prison decades after their confinement
when a DNA test showed that they couldn’t possibly have been the killer. Kurt’s
family cannot afford a new trial and therefore try to raise funds to make it
happen.152
Why isn’t there a lawyer who offers to take on this trial for free? Eli Lilly
executives should have been put behind bars for decades, not Kurt, but the real
villains always go free in healthcare.
I often wonder why Americans are so cruel to
their own people. Where is the societal benefit in locking people up for life
who wouldn’t have killed if they hadn’t been on drugs? It is important to
realise, as few psychiatrists do, that although a misdeed may look entirely
rational and planned in cold blood, this can be a totally wrong interpretation
because the drug may remove the usual inhibitions people have.146 We cannot say
in an individual case beyond reasonable doubt that the drug didn’t
play a role. The American way of handling these killings is inhumane to the
extreme. The Crespi family, for example, has three other children. Why not let
the father come home to them, which the mother wants and fights for? And why
not release Kurt Danysh and the other victims of drug harms?
The pills that ruin your sex life
Antidepressants are often called happy pills,
but there isn’t much happiness in pills that ruin your sex life. As this might
be their most common effect, they should have been called unhappy pills and
marketed as a formidable disrupter of your sex life, but that wouldn’t have sold
many pills.
The drug companies have kept pretty quiet about
this sales-threatening effect. An FDA scientist found out that they had hidden
sexual problems by blaming the patients rather than the drug, e.g. female
anorgasmia was coded as “Female Genital Disorder.”3
The companies have claimed that very few
patients become sexually disturbed, e.g. only 1.9% in the registration
application for fluoxetine,66 but the true occurrence is 30
times higher. A Spanish study designed to look at this problem found that
sexual disturbances developed in 59% of 1,022 patients who all had a normal sex
life before they started on drug.153 For the five most commonly used drugs (fluoxetine,
paroxetine, sertraline, citalopram and venlafaxine), I calculated the weighted
average occurrence of sexual problems:
|
57% |
experienced decreased libido |
|
57% |
experienced delayed orgasm or ejaculation |
|
46% |
experienced no orgasm or ejaculation |
|
31% |
experienced erectile dysfunction or decreased
vaginal lubrication. |
About 40% of the patients considered their
sexual dysfunction unacceptable. Some patients yawn during orgasm, which isn’t
the most fantastic way of starting an intimate relationship. In another survey,
of 3,516 members of patient advocate groups, sexual dysfunction was cited among
the most common (51%) side effects leading to treatment drop out.153
Imagine what it is like for a boy to encounter
problems with erections the first time he is going to have sex. And that he
wasn’t told it was due to the drug. He will think there is something wrong with
him, and so will his sweetheart, particularly when the
problem returns next time they try. This is cruel, and a child psychiatrist in
Brisbane told me about three boys who had attempted suicide for this reason.
The delayed orgasm is being used therapeutically
by men who have premature ejaculation. However, the randomised trials that have
shown an effect on this don’t appear to be fully reliable, as they didn’t
report on other sexual harms.154, 155 For example, a large randomised trial from Iran with
only one author reported no cases of impotence in 138 patients on escitalopram,
but in three of 138 patients on placebo.155
Sexual problems are easily overlooked if the
clinical interview is not directed towards revealing them. Patients aren’t
likely to bring them up spontaneously and might not even think they could be
drug-related; e.g. in the Spanish study, only 20% of the patients reported
their sexual dysfunction spontaneously.153
Some men become impotent on SSRIs but Eli Lilly
has the answer.156 The company sells tadalafil (Cialis) against erectile
dysfunction and recommends to take it not on demand but every day “so that the
sexually active can obtain constant spontaneity.” As the scouts say: “Be
prepared!” Your eternal erection, which may give your wife eternal headache, is
just a pill away. “Ask your doctor whether an erection is right for you.”
Damage to the foetus
As already noted, the Danish National Board of
Health recommends routine screening of pregnant women for depression and
treatment with antidepressant drugs, although the available data do not support
these recommendations.8 It acknowledges that SSRIs increase the occurrence
of spontaneous abortions, decrease the birth weight, likely increase the
occurrence of birth defects, increase neonatal complications such as
irritability, tremor, hypertonia and difficulty sleeping or breast feeding, and
increase the risk by a factor of five for developing pulmonary hypertension,
which is a lethal harm estimated to occur in 6-12 newborns per 1,000.8
Given these facts, the Board’s recommendation is
so absurdly harmful that I wrote a little sketch about it. In 2013, I listened
to a brilliant lecture by a former patient with schizophrenia, Olga Runciman,
who told us how she had found her way out of psychiatry, abandoned the drugs
and now lived a normal life. My lecture came right after hers, and I had never
met her before but was so impressed that I asked if she would be interested in
playing the part of the young pregnant woman in my sketch. She accepted and we
read it aloud from my computer as an introduction to my lecture, which is on
you tube with English subtitles (https://www.youtube.com
watch?v=i1LQiow_ZIQ/). I must have hit something essential, as it
was seen by over 10,000 people in two weeks:157
“How’s the pregnancy going?”
“Fine, I don’t have any problems.”
“And you’re not worried about whether you can
manage to look after the baby?”
“No, not at all. I am a housewife and have time
to take care of it.”
“Are you aware that it’s possible to have
depression without knowing it?”
“No, I didn’t know that, but I’m fine.”
“Yes, but … uhmmm … well … you see … if you are
suffering from a depression, it would be good to find out.”
“But I’m perfectly fine.”
“I still think you should undergo this test for
depression.”
“So what if it’s positive?”
“Then you may get a drug that will help you.”
“Well … I … There is nothing wrong with me, so
why should I undergo this test?”
“The National Board of Health recommends it.”
“Can’t you just unsubscribe from the Board of
Health? Sorry, that was a joke!”
“No, we are obliged to follow the Board’s
recommendations.”
“But a test like that is a screening test, is
there a Cochrane review about it?”
“Yes, and it recommends that one shouldn’t
screen healthy people for depression.”
“Then why on earth does the Board of Health
recommend screening pregnant women like me who are healthy?”
“I cannot understand this either, but the Board
of Health has consulted experts in psychiatry who think it’s a good idea.”
“And how many of those who are healthy will get
a wrong depression diagnosis with this screening test?”
“About one third.”
“Holy smoke! How does the drug work?”
“It works like amphetamine. It’s also difficult
for the patients to quit, just like for amphetamine and other narcotic drugs;
half the patients have difficulty stopping.”
“And what do these experts say about the side
effects of the drug? What is the most common side effect?”
“Sexual problems. They occur in half the
patients. It can be lack of sex drive, impotence and lack of orgasm, even for
the man if he receives the drug.”
“And how about suicide? Depressed people are at
high risk of committing suicide, and I assume that this medication will prevent
that from happening?”
“No, on the contrary, for someone as young as
you, the drug increases the risk of suicide. It can also cause birth defects.
The risk is small but it is clearly increased.”
“My goodness! Many thanks for all this
information, doc. Count me out. You don’t need to give me that test. I don’t
want to risk getting a wrong diagnosis of depression and get treated. My
husband and I love sex. And I have no wish to get a narcotic on prescription,
or to commit suicide, or to give birth to a deformed child.”
In my opinion, this contrived dialogue, with its
fortunate outcome, requires three things: The doctor needs to be exceptionally
well informed about the facts; the woman needs to ask relevant questions; and
the doctor needs to reply adequately to them. The clinical reality is not like
this very often. On the other hand, some doctors will not settle for a
questionnaire but will ask clarifying questions and possibly use an additional
instrument. Obviously, the use of additional instruments will reduce the
proportion of false positives, but they are also very uncertain. Screening
healthy people will therefore inevitably lead to many false positive diagnoses,
and many healthy people will be treated with antidepressants that harm them.
Birth defects have been studied in a large
Danish cohort study of 500,000 children, which showed that the risk of heart
septum defect is doubled.158 This is not a trivial harmful effect, as 1% of the
foetuses treated will get a septum defect. Cardiac birth defects are exactly
what we would expect to see because serotonin plays a major role for the
functioning of the heart. We have seen deadly valvular defects and pulmonary
hypertension in adults who took diet pills that increase serotonin levels, and
these drugs have been withdrawn from the market.3
It is of great value for people with vested
interests to spread doubt about whether SSRIs cause birth defects, and many substandard
studies claim they don’t. It is often wise to read the critical letters that
are subsequently published, e.g. those related to a 2014 study from the New England Journal of Medicine claiming there was no
problem. 159
There is no doubt that SSRIs cause birth
defects. A lawyer in Houston sent me a 56-page expert report prepared for a
court case by epidemiologist Nicholas Jewell who meticulously went through the
scientific literature. It is superb work that demonstrates that cardiac birth
defects are a class effect of SSRIs.160 Confounding by indication was ruled out, which means
that depression in itself doesn’t cause birth defects (which would also have
been very strange, but there seems to be no limits as to what psychiatrists are
prepared to suggest to avoid incriminating their drugs). Animal studies support
the human studies and show a dose-response relationship. SSRIs also double the
risk of preterm birth.161 The conclusion is inescapable:
Under no circumstances should pregnant women
be screened for depression or treated with antidepressant drugs.
The fraud and lies of
GlaxoSmithKline
GlaxoSmithKline (GSK) is one of the most
criminal drug companies in the world.3 It has committed numerous offences
that fulfil the criteria for organised crime under US law, and in 2011, GSK
pleaded guilty to having marketed a number of drugs illegally for off-label use
and was to pay $3 billion, the largest healthcare fraud settlement in US
history. Many of the crimes that have been most harmful for the patients and
have caused many deaths have involved psychotropic drugs, but GSK has also
killed many patients with rosiglitazone, a diabetes drug, which the company
touted had cardiovascular benefits although it increases cardiovascular
mortality and was taken off the market in Europe for this reason.3
The criminal activities seem to have involved
making false statements to state officials, obstructing a federal investigation
into illegal marketing, lying to the FDA about illegal promotion, withholding
incriminating documents, paying kickbacks to doctors, and misreporting prices
to Medicaid.
SmithKline Beecham, later merged into GSK, started
marketing paroxetine in 1992. The company falsely claimed for the next ten
years that paroxetine isn’t habit-forming despite the fact that it led to
withdrawal reactions in 30% of the patients in the original licence
application.3
In 2001, the World Health Organization had found paroxetine to have the hardest
withdrawal problems of any antidepressant drug and in 2002, the FDA published a
warning. A year later GSK quietly and in small print revised its previous
estimate of the risk of withdrawal reactions in the prescribing instructions
from 0.2% to 25%,162 a 100 times increase.
Our drug regulators did absolutely nothing to
protect patients for ten years, although the rate of withdrawal reactions was 100
times larger in the registration material than in the material GSK presented to
patients and doctors.
From 2002 onwards, the BBC presented four
documentaries about SSRIs in its Panorama series, the first one called Secrets of Seroxat. They are very good. The journalist,
Shelley Joffre, showed that the GSK spokesperson, Dr Alastair Benbow, lied in
front of a running camera. He denied, for example, that paroxetine could cause
suicidality or self-harm while he sent data to the drug regulator one month later
that showed exactly this, and which immediately led to a ban on using
paroxetine in children. The UK drug regulator also lied to the public and
covered up for GSK, which is based in the United Kingdom, when it said that
this information was completely new to the company (which had known about it
for around ten years). Worst of all:
The head of the UK drug agency echoed the
drug companies’ untruthful assertion that it was the disease, not the drug,
that increased the suicide risk.
Later, when US senator Charles Grassley asked
GSK for how long the company had known that paroxetine increases the suicide
risk, the company lied again. GSK replied that they detected no signal of any
possible association between paroxetine and suicidality in adult patients until
late February 2006. However, government investigators found that the company
had the data back in 1998 and David Healy found evidence in internal company
documents that 25% of healthy volunteers experienced agitation and other
symptoms of akathisia while taking paroxetine.
Other studies have shown similar results.163 Peter Breggin was an expert witness in a case where a
man drowned his two children and himself under influence of paroxetine, but in
2001, GSK prevented Breggin from publishing his findings about suicidality and
violence, which showed that GSK had been negligent.49 The judge
contributed to the absurdity by calling this proprietary information. GSK
listed suicide attempts as emotional lability and disguised cases of akathisia
by using many subcategories for overstimulation such as nervousness and
anxiety.
The BBC asked the public to submit emails about
their experiences with paroxetine, and 1,374 emails were read by clinical
pharmacologist Andrew Herxheimer and researcher Charles Medawar, cofounder of
Social Audit. Though GSK had fiercely denied that SSRIs cause dependence and
can lead to suicide, it was clear that both claims were wrong, and that,
furthermore, the drugs can lead to hostility and murder, e.g. “After 3 days on
paroxetine, he sat up all night forcing himself to keep still because he wanted
to kill everyone in the house.”162
The richness of the patients’ own reports was
impressive. Many described electric shock sensations in the head and visual
problems when they tried to stop, but such reactions had been coded by the
authorities as dizziness or paraesthesia. Because of these revelations, drug
agencies in many other countries now accept adverse events reports submitted
directly by patients, without needing to pass the doctors’ obstacles first.
In 2004, a researcher used the comprehensive
internal reports of GSK’s trials, made available on the internet as a result of
litigation, and found that paroxetine increased significantly suicidal
tendencies, odds ratio 2.77 (95% confidence interval 1.03 to 7.41).164 He included the unpublished trial 377, which didn’t
find an effect of paroxetine and which GSK had stated in an internal document
that there were no plans to publish.165 He also included the infamous trial 329.
Trial 329 of paroxetine in children
and adolescents
GSK published trial 329 in 2001.166 The paper falsely stated that paroxetine was effective
in children and adolescents and had minimal side effects, and GSK also lied to
its sales force, telling them that the trial had shown remarkable efficacy and
safety.167
The trial was widely believed and cited,3
but it was fraudulent. What it showed was remarkable inefficacy and harms, but
after extensive manipulations, the ghost-written paper, which had 20 doctors as
“authors,” ended up being positive.167, 168 The statistical alchemy created four statistically
significant effects after splitting the data in various ways, and many
variations were tried before the data confessed to the torture.
The paper falsely stated that the new outcomes
were declared a priori, and for harmful effects, the
manipulations were even worse. The internal, unpublished study report showed
that at least eight children became suicidal on paroxetine versus one on
placebo (P = 0.035). In the published paper only one headache was considered to
be related to paroxetine treatment. Cases of suicidal thoughts and behaviour on
paroxetine were called emotional lability, hospitalisation, exacerbated
depression or aggression,3, 164 and at least
three adolescents who threatened or attempted suicide weren’t described in the
paper whose first author, Martin Keller, wrote that they were terminated from
the study because of non-compliance.57 When the FDA demanded the company
to review the data again, there were four additional cases of intentional
self-injury, suicidal ideation or suicide attempt, all on paroxetine.
Keller seems to be the typical sort of guy we
find at the top of the much touted public-private “partnerships.” He
double-billed his travel expenses; the psychiatry department he chaired
received hundreds of thousands of dollars to fund research that wasn’t being
conducted; Keller himself received hundreds of thousands of dollars from drug
companies every year he didn’t disclose; and a social worker found a list of
adolescents who indicated they had been enrolled in a study, which wasn’t true.3
It seemed they were made up, which would have been tempting, given that $25,000
was offered by the drug company for each vulnerable teenager Keller delivered.
Keller’s misdeeds didn’t harm his career, likely
because his department had received $50 million in research funding. This isn’t
a printing error: $50 million! A spokesperson from Brown, where Keller worked,
said that Keller’s research on paroxetine complied with their research
standards. Fraudulent research that has contributed importantly to pushing
thousands of children and adolescents into suicide all over the world is said
to live up to a US hospital’s research standards. Welcome to America!
The Journal of the American
Academy of Child and Adolescent Psychiatry, which published the fraud,
refused to convey to their readers that the article misrepresented the science
and refused to retract it.168 An explanation for this passivity
can likely be found by following the money that goes to the journal’s owner.
GSK pushed its drug for use in children,
although it didn’t work, was immensely harmful, and wasn’t approved for use in
children. The illegal marketing involved withholding trials showing paroxetine
was ineffective,169 and the fraud was deliberate: “It would be commercially
unacceptable to include a statement that efficacy had not been demonstrated, as
this would undermine the profile of paroxetine.”168
The fraud and lies paid off, which is why there
is so much of it. From 1998 to 2001, five million prescriptions a year were being
written for paroxetine and sertraline for children and adolescents.170 Even in 2013, hundreds of suicides later, GSK had the
audacity to state: “GSK does not agree that the article is false, fraudulent or
misleading.”171
Why does anyone pay attention to what drug
companies or their hired allies among doctors say about anything?
Unfortunately, publicly funded studies can be just as deceptive as those funded
by the drug industry. The huge STAR*D study is one such example.
The STAR*D study, a case of consumer
fraud?
This STAR*D study was highly relevant. The
set-up and entry criteria reflected normal clinical practice and real patients
seeking care were included.172 It was the largest antidepressant effectiveness study
ever conducted. Funded by the NIMH at a cost of $35 million, it was designed to
test whether a multistep, flexible use of medications, including add-on drugs
to augment the effect of the antidepressant, would help people recover and stay
well, also in the year after recovery.
The investigators announced that the study would
produce results with “substantial public health and scientific significance.”
It surely did, but not in the way the investigators had imagined. It didn’t
show the expected positive results, and all the initial brouhaha ended as a
story of a scientific scandal and dishonest science.173
There was no placebo group, and all patients
started on citalopram. This was motivated by citalopram’s “absence of
discontinuation symptoms” and “safety” in elderly patients.174 It defies belief that some of the prominent
psychiatrists in America chose to display this level of ignorance about the
drugs they use, considering that the trial protocol was from 2002.
When the study was over, NIMH announced that,
“about 70% of those who did not withdraw from the study became symptom-free.”
NIMH repeated this false claim 36 times in various press releases,175 and the investigators also made numerous false claims,
e.g. that the patients who scored as remitted had “complete absence of
depressive symptoms” and had “become symptom-free.”176 The truth was that a “remitted” patient could have a
Hamilton score of 7. The only Hamilton suicide question, “feels like life is
not worth living,” is scored as 1, and other symptoms that are scored as 1
include “feels he/she has let people down” and “feels incapable, listless, less
efficient.” No professional would describe such patients as having become
symptom-free; in fact, each of these symptoms are used in diagnosing major
depression.176
The researchers noted in their abstract that,
“The overall cumulative remission rate was 67%.” In the main text, however,
they acknowledged that this was a “theoretical” remission rate assuming that
those who exited the study would have had the same remission rates as those who
stayed in the protocol. That assumption is extremely unlikely to be true. There
are usually many more treatment failures among those who drop out than among
those who continue. Furthermore, the investigators cherry-picked the data they
reported. Instead of using the Hamilton scale as planned, they used a scale
that added another 152 patients to the remitted group.172 They also
included 607 patients with mild depression and 324 patients with no baseline
Hamilton score who, according to their own protocol and a flow chart they
published,172, 174
should have been excluded from their analyses, and which further inflated the
number of remitted patients. If the study protocol had been followed and the
results honestly reported, the researchers would have announced that 38% of the
patients remitted during the four steps of treatment, and that the remaining
62% either dropped out or failed to remit.172
The investigators stated that most of the
remitted patients stayed well also throughout the final year of “continuing
care” where the physicians could change the patients’ medications, alter
dosages, and add new medications.173 Science journalist Robert
Whitaker did his best to figure out the precise number of patients who remitted
and stayed well throughout the study, but the data were presented in such a
confusing manner that he gave up. Ed Pigott and colleagues succeeded in
cracking the nut and reported that only 108 of the 4,041 patients174
had a “sustained remission,”174 which means that only 3% of the
patients who entered the trial remitted, stayed well and stayed in the trial
during the year of follow-up.
Even this low percentage is likely exaggerated.172
Many of the 108 stay-well patients must have come from the group of 607
patients with mild depression that shouldn’t have been included in the
analysis. Furthermore, the investigators took great care to deliver an optimal
treatment, so the success rate in routine clinical care must be lower than 3%.
Pigott and colleagues advised that, in light of
the meagre results of STAR*D, we should not use the term “treatment-resistant
depression.”172
We should focus on what is wrong with our treatment rather than using language
that wrongly implies that there is an exceptional subgroup of patients with an
exotic form of depression who are refractory to an otherwise effective
treatment.
This publicly funded study bombarded the doctors
and the public with the monstrously misleading message that antidepressants
enable about 70% of depressed outpatients to recover, and the medications were
said to be “far more effective” than placebo,173 which is
equally untruthful, and apart from this there was no placebo group to compare
with! A journalist asked one of the investigators, Maurizio Fava, a prominent
psychiatrist from Massachusetts General Hospital in Boston, whether the
analysis by Pigott and colleagues172 was correct. “I think their
analysis is reasonable and not incompatible with what we had reported,” Fava
said.173
This is a remarkable admission. Fava acknowledged that the 3% success rate is
accurate and also, at least indirectly, that this is the real result. He also
acknowledged that the investigators knew this all along, and that this
information was in their published reports. However, it is not honest science
to play hide and seek to such an extent that it is close to impossible for
others to unravel the truth.
The STAR*D study results show that the practice
guideline of the American Psychiatric Association that advise that “following remission,
patients who have been treated with antidepressant medications in the acute
phase should be maintained on these agents to prevent relapse” is harmful.
Antidepressants don’t cure depressions and don’t prevent them; they cause them.
They are depressogenic agents when used long term (see Chapter 11). The STAR*D
study provides convincing evidence of the drug-induced tardive dysphoria other
investigators have described.177, 178
Psychiatrists often respond to Whitaker’s talks
by quoting the fake STAR*D results, which they take as evidence that
antidepressants – if you just keep trying them – work for most people. This
collective delusion is terribly harmful.
The many STAR*D papers display highly selective
reporting of outcomes, numerous false claims, contradictory statements, and
even pure fiction.176 As of mid-2011, despite over 100 papers having
been published, 11 prespecified outcomes had still not been reported!179 One paper stated in the abstract that suicidal ideation
was seen in only 0.7% of the patients, and the authors said that their study
“provides new evidence to suggest little to no relation between use of a
selective serotonin reuptake inhibitor and self-reported suicidal ideation.”
This misleading statement was contradicted by some of the
same authors who, in other papers, mentioned suicidal ideation in 6.3%
and 8.6% of those on citalopram in STAR*D, i.e. 10 times more.
Is the STAR*D study so fraudulent that all its
100+ papers should be retracted? Ed Pigott says about this:176
“In my five plus years investigating STAR*D, I
have identified one scientific error after another. Each error I found
reinforced my search for more … These errors are of many types, some quite
significant and others more minor. But all of these errors – without exception
– had the effect of making the effectiveness of the antidepressant drugs look
better than they actually were, and together these errors led to published
reports that totally misled readers about the actual results. As such, this is
a story of scientific fraud, with this fraud funded by the National Institute
of Mental Health at a cost of $35 million.”
As already noted, all patients tried citalopram
first, and its remission rate was inflated by 45% in the summary article. In
their disclosure statements, ten of STAR*D’s authors report receiving money
from Forest, Lundbeck’s partner in the United States. In 2011, Pigott filed a
whistleblower complaint that alleges that Forest bribed a principal
investigator to fix the results in favour of citalopram.180 The complaint alleges that because of this bribe,
citalopram was the only antidepressant employed in the first part of the study,
and it led to falsification and overstatement of the drug’s effectiveness.
I searched PubMed for STAR*D in January 2015 and
got 290 hits, so I really appreciate that Pigott and others did the detective
work for me. It is scandalous that a hugely expensive study funded by taxpayers
can be so shamelessly misleading, but it illustrates once again that top
psychiatrists are prepared to defend their organised illusions, whatever the
costs in terms of money, deception, dishonesty, lack of public trust in their
specialty, and harm to the patients. In my opinion, the STAR*D papers should be
retracted and an independent group of scientists who are not psychiatrists
should be funded to write a paper that explains what this study really showed:
That antidepressants are ineffective and harmful.
4
Anxiety
We all get anxious from time to time, which
means a huge market potential for drugs. Because of ineffective blinding in
trials (see Chapter 3), we would expect almost anything to “work” for anxiety.
We would also expect psychological interventions to work, but for better
reasons. It is obviously a good idea to teach people how to cope with their
anxiety.
In terms of the balance between benefits and
harms, psychotherapy is far better than drugs (see Chapter 10), but drugs are
much more commonly used. So much that our citizens are drugged to about the
same extent today as 50 years ago, as a large decline in the use of
benzodiazepines has been compensated by a similar increase in the use of SSRIs,1 which are used for many of the same conditions.
Psychiatrists now say, pretty conveniently, that much of what they previously
called anxiety – when it was still okay to use benzodiazepines – in reality was
depression, so that they can now use SSRIs for the same patients.
It is true that there is much overlap in
symptoms between anxiety and depression, but the change in treatment of anxiety
disorders has happened despite the fact that a benzodiazepine is likely the
better option. A systematic review from 2013 found that the trials were
generally of poor quality, but benzodiazepines were more effective and better
tolerated than tricyclic antidepressants, and they had similar or better effect
than SSRIs, with fewer harmful effects.2 The main reason for abandoning benzodiazepines is
that there is very little money to be earned from drugs that ran out of patent
ages ago.
Another systematic review, of 48 placebo
controlled trials in patients with generalised anxiety disorder, found similar
effects of benzodiazepines (effect size 0.32), azapirones (0.30) and
venlafaxine (0.33).3 For depression, the effect sizes were 0.28 for
benzodiazepines and 0.22 for azapirones (there were no data for venlafaxine,
although this drug is an antidepressant). The effect decreased as the trials
got bigger, but the results were reasonably robust.
The authors wondered why azapirones worked for
depression, as these drugs are not usually considered effective for depression,
but that’s not surprising. A drug that reduces anxiety will also be expected to
reduce anxiety-related depression, as there is less to be depressed about when
your anxiety is gone. In addition, some of the items on Hamilton’s depression
scale are about anxiety, and the relatively small effect of the drugs could be
explained by unblinding bias (see Chapter 3). According to the published trials,
which exaggerate the effect in comparison with the unpublished trials,4 the effect size is 0.37 for the newer antidepressant
drugs for depression,4 which is about the same as their effect
for generalised anxiety disorder,3 and this effect can be
explained by unblinding bias. Whether the patients are helped by the drugs to
get on with their lives is totally obscure, not only because of this bias, but
also because we are only told about the effect on scales with uncertain clinical
relevance.
A 2008 systematic review found only one trial
comparing benzodiazepines with an SSRI whereas there were 22 comparisons with
older antidepressants. Again, the antidepressants were not better than
benzodiazepines.5
An additional problem with these trials is that
some of them have included patients on benzodiazepines, and when they are
switched to placebo, some of them may go through the horrors of benzodiazepine
withdrawal, which can be extremely anxiety-provoking.6, 7 Such trials are fatally wounded from the start, but
the FDA approved alprazolam (Xanax) – one of the worst of all benzodiazepines7
– for panic disorder even though a very large trial of 526 patients was carried
out this way, with only a one-week run-in period without drugs.8, 9 After the eight-week double-blind phase was over, the
medication was tapered over four weeks, but many patients on alprazolam
tolerated this so poorly that they were likely on their way to a lifetime
addiction, and the patients had more panic attacks five weeks after having
stopped alprazolam than when they entered the trial, whereas those on placebo
continued to fare well.
This horrible drug became the fifth most
prescribed drug in the United States, which is remarkable, as it causes panic in long-term use and has led to many suicides
and homicides.7
I shall mention a few other meta-analyses. A
Cochrane review of anxiety disorders in children and adolescents had included
21 trials of antidepressants and two of benzodiazepines, but, as I believe none
of these drugs should be used in children, I find the reported short-term
results uninteresting.10
I am also sceptical of a Cochrane review that
assessed the effects of adding an extra drug (or placebo) when anxious patients
had not responded adequately to first-line drug therapies.6 Twenty of the 28
trials were in patients with obsessive compulsive disorder (OCD), but the
trials were very heterogeneous, and much of the data were based on
antipsychotics. The authors didn’t make firm conclusions, and I agree:
antipsychotics are far too dangerous to be used for OCD (see Chapter 6). A
similar Cochrane review wasn’t limited to patients who hadn’t responded to the
antidepressant;12 no positive recommendations were made.
It’s too much for me that psychiatrists are
willing to give people with OCD both antidepressants and antipsychotics. These
patients should get psychotherapy. OCD isn’t deadly, but the drug cocktail is.
A Cochrane review of social phobia included 37
trials,13 but I consider it invalid. Some of the effects
reported were surprisingly large, around 0.6, given the moderate effect sizes
of around 0.3 usually reported for SSRIs, and one of the problems was that all
the scales appeared to have been rated by clinicians and not the patients,
which creates a large bias (see Chapter 3). Further, the trials were of very
poor quality, and the effect decreased so dramatically with the number of
patients in the trial that any meta-analysis of these data would be grossly
unreliable. The authors reported a relative risk of nonresponse of 0.64 (95% CI
0.57 to 0.73) on the Global Impression Scale, but they also showed in a figure
that the largest trials found an effect close to zero! The review also reported
an effect in relapse prevention studies, but such trials are highly unreliable
because abstinence symptoms are introduced in the placebo group when the
patients come off their drug cold turkey (see Chapter 11).
Although psychotherapy is highly effective for
social phobia (see Chapter 10), patients haven’t been spared all sorts of
trials of dangerous drugs, including anticonvulsants and antipsychotics.13
Luckily for the patients, a Cochrane review of antipsychotics wasn’t positive,
although the review was very large (11 trials and 4,144 participants).14 Seven trials of quetiapine found the drug to be
better than placebo for generalised anxiety disorder, but more patients dropped
out due to adverse events, and more patients gained weight and suffered from
sedation and extrapyramidal (muscular) side effects. There were two small
studies of olanzapine and two studies of add-on treatment with risperidone, and
they didn’t find an effect.
Sleeping pills
One of the classic uses of benzodiazepines is as
sleeping pills, but this usage also does more harm than good. The trials are
biased, and a meta-analysis found that after adjustment for this, patients at
least 60 years of age with insomnia slept 15 minutes longer on benzodiazepines
or similar drugs than on placebo.15 Adverse cognitive events were five times more
common, adverse psychomotor events three times more common, and daytime fatigue
four times more common than if the patients received placebo. After a few
weeks, the pills don’t work any longer and all that is left are the harmful
effects.
Patients who took such drugs had a higher risk
of falls – which cause many deaths because of hip fractures – and motor vehicle
crashes. A study showed that benzodiazepines doubled the risk of injurious
falls in people at least 80 years of age; these falls cause almost 1,800 deaths
every year in France.16 In another large cohort, benzodiazepines or Z drugs
doubled the death rate.17
The measured short-term effects in these trials
are likely exaggerated. It is highly subjective to record sleeping times and
sleeping quality, and the side effects of the drugs must have compromised the
blinding, e.g. in a trial of alprazolam versus placebo for panic attacks, the
blinding was broken for all patients.18
Why would anyone take such dangerous drugs
instead of reading a book until falling asleep naturally? Psychotherapy is also
a better option than pills (see Chapter 10).
5
ADHD
Childhood ADHD
This diagnosis was invented for DSM-III in 1980
but what is it? At a 1998 consensus conference, the chairman asked a leading
ADHD expert in America, Mark Vonnegut, but although he talked for two to three
minutes, Vonnegut couldn’t explain what ADHD is:1
“They cannot sit still … they are difficult and
they aggravate their parents … the diagnosis is a mess but there is, there is,
uhm, we all have a belief that we are dealing with a very serious core problem
and that we have a diagnosis that allows us to communicate and gives us
research, uhm, generates, uhm, sort of ideas for research, and I think, you
know, we, uhm, I, I do, I think, part of the problem is that the profession
keeps changing the diagnoses.” Vonnegut’s we-are-all-in-the-dark-together
utterings taught us something, namely that the psychiatrists don’t know what
they are doing.
Vonnegut also explained that a teacher might say
that a kid was two standard deviations different from the other kids in the
classroom. But hold on; 5% of us are by definition beyond two standard
deviations from the average of everything that follows the normal distribution,
but this doesn’t mean we are sick. If we take a group of normal people and
measure their height, 5% are beyond two standard deviations from the average
height, but we don’t invent some “disorder” for those 5% who are small or tall.
NIMH also gets into trouble when it uses 15
pages to tell us what ADHD is.2 On the first page, we are told that ADHD is one of
the most common childhood brain disorders and that imaging studies have shown
abnormalities in the brain. But this is totally wrong. ADHD is not a “brain
disorder” and the brains of these children are not different from the brains of
other children (see Chapter 11). The first page also says:
“Inattention, hyperactivity, and impulsivity
are the key behaviors of ADHD. It is normal for all children to be inattentive,
hyperactive, or impulsive sometimes, but for children with ADHD, these
behaviors are more severe and occur more often. To be diagnosed with the
disorder, a child must have symptoms for 6 or more months and to a degree that
is greater than other children of the same age.”
This is about as weak as it can get and it
certainly doesn’t justify calling ADHD a brain disorder. The children are
normal variants of normal behaviour, and we cannot all have average behaviour
or average height. Many children qualify for the diagnosis simply because they
are talented and therefore bored and cannot sit still in poorly disciplined
classrooms, or because they have emotional problems generated at home.
Since we are talking about degrees of
development and not a brain disease, we would expect more of those children
born in December to have an ADHD diagnosis and be in drug treatment than those
born in January in the same class, as they have had 11 fewer months to develop
their brains. This is exactly the case. A Canadian study of one million school
children showed that the prevalence of children in treatment increased pretty
much linearly over the months from January to December,3 and 50% more of those born in December were in drug
treatment. This study shows that if we approach the children with a little
patience that allows them to grow up and mature, fewer would receive drugs.
However, the diagnosis arises primarily from
teacher complaints and parents are often told that their kid cannot come back
to school unless he or she is on an ADHD drug. A general practitioner told me
that a schoolmistress had sent most of her pupils for examination on suspicion
of ADHD; clearly, she was the problem, not the kids. As soon as the kids are
branded with ADHD, it relieves everyone of any responsibility or incentive to
redress the mess they have created. We have decided as a society that it is too
laborious or expensive to modify the kid’s environment, so we modify the kid’s
brain instead. This is cruel.
NIMH says that, “With treatment, most people
with ADHD can be successful in school and lead productive lives,” but NIMH has
proved itself in a very large trial that the statement is wrong (see below).
Doctors can expect to get complaints if they don’t diagnose ADHD, particularly if they decide not to use
any of the silly checklists that abound for the diagnosis. My stepfather was a
school psychologist and his attitude was that we shouldn’t put diagnostic
labels on kids. I wish it were so, but unfortunately ADHD has become yet another
false disease epidemic.
Names create what they describe. Parents or
school teachers who have experienced that a boy is troublesome and disturbing
may feel the ADHD diagnosis gives them an explanation. It can also lead to
greater acceptance in the boy’s surroundings of his behaviour, as he cannot
help it because he has this particular “disorder.” However, it is circular
evidence to argue this way. We have merely given the boy’s behaviour a name,
ADHD. With the same violation of the rules of logic we might say that Brian
behaves badly, and because his name is Brian he behaves badly. ADHD is not an explanation, it is only a name given to a clustering
of symptoms.
It is ironic that “attention deficit” is part of
the name, as it can be an attention deficit in the children’s social
surroundings that is the real problem. If these children got more attention,
there would be fewer diagnoses, which is why Peter Breggin has called it DADD:
Dad Attention Deficit Disorder. As early as in the 1990s, a quarter of the children
in an elementary school in Iowa were on ADHD drugs and in California the
diagnosis rates increased sharply as school funding declined.4
Some parents contribute to the epidemic by
seeking out a diagnosis for their children to obtain social benefits.
Institutions such as kindergartens also contribute by putting pressure on
parents to accept dubious diagnoses to obtain additional funding.
It’s a tragedy and a fraud to take entirely
normal children and make patients out of them while telling their parents that
the children suffer from a chemical imbalance. But unfortunately many
clinicians find it easier to tell parents their child has a brain disorder than
to suggest parenting changes.
In 2011, an enterprise – evidently working on behalf
of an anonymous drug company – sent a most bizarre invitation to Danish
specialists treating children and adolescents for ADHD.4 The doctors would
be divided into two groups for an exercise called Wargames where they should defend
their product (two different ADHD medicines) with arguments and a visual
presentation. Their efforts would be filmed and the company’s anonymous client
might be watching from another room. This Orwellian “Big brother is watching
you” exercise was illegal. Danish doctors are not allowed to help companies
market their products.
Also in 2011, my wife and I got very angry when
our youngest daughter told us that a big ADHD bus had visited her school and
distributed brochures to “raise awareness of the ADHD disorder in children.” It
wasn’t about raising awareness but about pushing pills. The ADHD bus is owned
by the Danish ADHD Association, which receives financial support from companies
selling ADHD pills and other psychotropic drugs, and four of the pill brochures
were produced by a company that sells methylphenidate (Ritalin), the most
commonly used ADHD drug.
One of the brochures called “Girls and ADHD” had
a section about treatment, but only drugs were mentioned. A journalist asked
the president of the ADHD Association why the association distributes materials
from a pharmaceutical company to schoolchildren, but despite a promise to call
back, this didn’t happen. A press release about the appointment of the
association’s new director earlier the same year stated that the association
“needed a director who is commercially oriented” and who should “focus on
creating partnerships with private companies.” The principles for such
collaboration were listed on the association’s homepage and the partnerships were
about establishing an “advantageous and binding, often lengthy business
relationship between the ADHD association and a business, built on shared
expectations about input and output.” Sponsorships involved a “commercial
agreement between the ADHD Association and a company, with an expected return,
often in relation to marketing or social responsibility perspectives.” Total
corruption to the detriment of our children.
The media also distort the issues. Two ADHD
studies showed obvious discrepancies between the results and the conclusions,
which were that ADHD patients lack dopamine and that stimulants improve
long-term school outcomes. But only one of 61 media articles adequately
described the results and thus questioned the conclusion.5 The erroneous conclusion about lack of dopamine as
the cause of ADHD was uncritically propagated also in subsequent scientific
papers.5
Similarly, a survey of the 10 most cited ADHD
papers in the media showed that the media paid virtually no attention when the
findings were later shown to be false.6 Only one newspaper article of 57 describing
subsequent studies mentioned that the previous finding had been refuted.
Figure
5.1. Test for Adult ADHD.
Adult ADHD
A journalist from the Danish Broadcasting
Corporation who had been diagnosed with ADHD in childhood tried the screening
test recommended by the World Health Organization on eight of his colleagues
and found that seven of them had the “disease.”
The test is hopeless. Two members of my close
family tried it and got the diagnosis, one with a full house, as she
consistently chose the gray boxes in both the A and B test (see Figure 5.1).
Try it yourself.7 Successful, pioneering and energetic people, who
don’t like wasting their time on unproductive meetings listening to unfocused
people who talk endlessly, might end up getting the diagnosis. All that is
required in order to have “symptoms highly consistent with ADHD in adults” is
to have four marks in the gray boxes for the first six questions in part A of
the test.
If a dynamic person sometimes
has trouble wrapping up the final details of a project, once the challenging
parts have been done; and sometimes has difficulty getting
things in order when he or she has to do a task that requires organization; and
sometimes has problems remembering appointments or
obligations, then this is already three of the four points needed for the
diagnosis. Don’t many overworked people fit these descriptions? Some of the
most talented and wonderful people I know are like that and they can get the
last point if they often avoid or delay getting
started when they have a task that requires a lot of thought; or if they often fidget or squirm with their hands or feet when they
have to sit down for a long time; or if they often
feel overly active and compelled to do things, as if driven by a motor.
In 2004, the New York University School of
Medicine Adult ADHD programme offered a free screening day for adults at a
hotel, announcing that, “Despite wide recognition as a children’s disorder,
ADHD … affects millions of adults who are undiagnosed and untreated.”8 Yes, what a catastrophe that a few people are still
wandering around freely who are not medicated for a
conduct disorder! Two years later, an article reported that 85%
of those who attended screened positive for ADHD.9 The researchers surveyed 51 of these people who had
all been given a list of doctors to contact to help treat their so-called
illness, but 27 of them admitted they never followed through. The director of
the programme, Dr. Lenard Adler (yes, the surname was
Adler), interpreted the results this way: “This data shows that people with
ADHD need help to get help.” The Goodness Industry has no limits. I assume that
people who won’t accept the help to get help will then be exposed to do-gooders
who want to help them understand that they need help to get help so that they
can help themselves. Help!
Of course there are caveats in the adult ADHD
checklist that advises that further investigation is warranted and that we
should consider work, school, social and family settings. However, this is not
how clinical practice usually is. These additional investigations take time and
may never be carried out, and even if they were, there is a high risk that
leading questions will yield results that “confirm” the diagnosis. We are told,
for example, to “look for evidence of early-appearing and long-standing
problems with attention or self-control,” also in childhood, which could be
many years back. Such explorations will suffer from recall bias and
confirmatory bias tending to “validate” the provisional diagnosis, somewhat
like the scandals related to alleged sexual abuse in childhood that turned out
to be nothing other than false memories caused by the interviewer. Here is an
account of what this can lead to, which I received from a psychiatrist:
I sit with the files from a woman whom I and my
staff nurse assess as immature and disturbed. The patient was referred from a
general practitioner for a possible ADHD diagnosis. A psychologist has
described the patient as girlish, with emotional and identity-related problems,
regressive social behaviour, and an unbalanced relationship with her mother who
seems cold and irritable. The infamous ADHD tests were carried out, but
amazingly, she scored very low on both inattention and hyperactivity as a child
(only 1 of 9 symptoms was positive). When the psychologist told her that an
ADHD diagnosis cannot be made, she and her boyfriend reacted very negatively,
and the patient cried, very discouraged and demoralized, in a somewhat
dramatizing and theatrical way, and proclaimed she had nothing left to live
for. Then the psychologist wrote in her files that “it has only been concluded
that it is doubtful whether the diagnosis ADHD can be made … and I will examine
whether in this case one can make an exception and pay more attention to
symptoms in childhood (although this involves a risk of a distortion, as there
may now, if possible, be even stronger forces at play than before to get the
diagnosis).” This is discussed with a psychiatrist and it is decided to give
the patient the benefit of the doubt and do a new test. Now 6 of 9 symptoms are
considered positive for both hyperactivity and inattention in childhood, and
suddenly the overall result suggests that the patient meets the criteria for
the diagnosis of ADHD in childhood. And then comes the finale: “This concludes
the diagnostic process and the patient will be transferred for drug treatment
of the attention deficit by the ADHD team’s psychiatrist”.
This surrealistic tragedy could appropriately be
called: How to weep to get a false diagnosis. In the psychiatric supermarket,
there are diagnoses on all shelves with no expiry dates. It’s better not to
visit and better to resist letting tears become decisive.
The checklist for adult ADHD is only fives page
long, but its authors, two professors from Harvard Medical School and one from
New York University Medical School, tell us that adult ADHD can have “a
significant impact on the relationships, careers, and even the personal safety
of your patients who may suffer from it.” They provide four references related
to this statement, which are all irrelevant. One is to the DSM-IV, another is
to a textbook, the third is to a review that contradicts what the professors
say, as it notes that few studies have examined the status of core symptoms
beyond 14 months of treatment and recommends longer-term studies.10 The fourth paper is an interview study of 84 people
with adult ADHD.11 This is my usual experience with psychiatric
research. I get disappointed almost every time I look up references to
statements I find interesting. The quoted papers don’t support what is being
claimed. It is as if the veracity and relevance of the references don’t matter
the slightest bit; it’s only window dressing.
What isn’t said directly – but implicitly understood
– is that the idea of diagnosing people with adult ADHD is to treat them with
drugs: “Because this disorder is often misunderstood, many people who have it
do not receive appropriate treatment and, as a result, may never reach their
full potential.” The professors’ statement smells like a drug ad, and it has
never been shown either that drug treatment has any impact on what they call
“the relationships, careers, and even the personal safety of your patients who
may suffer from it.”
The questions in the checklist are consistent
with DSM-IV criteria and are said to address the manifestations of ADHD in
adults. Yet again, the psychiatrists have blown life into a social construct
that is nothing but a variation of normal behaviour and have given this construct
a name, as if it existed in nature and could attack people.
ADHD drugs
Drugs used for ADHD are amphetamine derivatives,
or have effects like amphetamine and cocaine. They are stimulants and can cause
mania, other psychoses, brain damage and death.12, 13 Use of amphetamines may lead to drug dependence and
people treated with methylphenidate are much more likely to abuse cocaine in
young adulthood compared to those diagnosed with ADHD without drug exposure.14 This is not surprising, as stimulants are known to
cause alterations in the reward centres of the brain.
The most used drug is methylphenidate (Ritalin);
another is atomoxetine (Strattera), which is a noradrenaline reuptake
inhibitor. Eli Lilly failed to get it approved for depression but sells it as
“non-stimulant” treatment for ADHD, which is a lie. It causes dangerously
stimulating symptoms in many children and the package insert has a black box
warning.14
It warns that suicidal ideation was seen in 5 of 1,357 patients receiving
atomoxetine versus none of 851 patients receiving placebo. Many children have
developed suicidal and homicidal impulses on atomoxetine, which can also cause
liver failure.15
As always, it is far worse in clinical practice
than companies have reported in their trials. In a consecutive cohort of 153
children treated with atomoxetine, 51 children (33%) developed extreme
irritability, aggression, mania, or hypomania.16
Which parents would want their child to take
atomoxetine, methylphenidate, or any other ADHD drug, if they were honestly
informed about the lack of any long-term benefits and all the serious harms?
ADHD drugs for children
Psychiatry has … become pharma’s goldmine,
with a simple business plan. Seek a small group of specialists from a
prestigious institution. Pharma becomes the professional kingmaker, funding
research for these specialists. Research always reports underdiagnosis and
undertreatment, never the opposite. Control all data and make the study
duration short. Use the media, plant news stories, and bankroll patient support
groups. Pay your specialists large advisory fees. Lobby government. Get your
pharma sponsored specialists to advise the government. So now the world view is
dominated by a tiny group of specialists with vested interests. Use celebrity
endorsements to sprinkle on the marketing magic of emotion. Expand the market
by promoting online questionnaires that loosen the diagnostic criteria further.
Make the illegitimate legitimate.
DES SPENCE, GENERAL PRACTITIONER, GLASGOW17
Spence mentions that a small Harvard group of
world specialists admitted undisclosed personal payments from drug companies
totalling $4.2 million. A review of 43 drug trials in ADHD, of which 39 were
sponsored by the companies, confirms Spence’s kingmaker tale. Very few drug
reactions were called serious, although many children dropped out of the
studies because of serious adverse drug reactions.18 Moreover, adverse drug reactions were only reported
if the incidence was above 2% or 5%. Many studies were conducted by the same
core group of authors and we worked out how much inbreeding there was: 21
papers (49%) came from Harvard Medical School or Massachusetts General
Hospital, both in Boston, and Joseph Biederman was the great fertilizer,
co-authoring no less than 13 of the papers (30%).
Many of the studies are also rigged, either by
dropping all children who improve on placebo before the trial starts, or the
opposite, studying only children who have tolerated the drug before they are
randomised to drug or placebo,19 or both.20
ADHD drugs are popular with school teachers, as
they make their work easier. But it is bad medicine to drug children in order
to make them less disturbing and the children pervasively dislike stimulants,20
which is easy to understand if one reads the long list of harmful effects in
the package inserts. To outweigh the harms, benefits would therefore need to be
substantial, but this is not the case.
A 2013 systematic review included 43 trials, of
which 37 assessed the effect of methylphenidate compared with placebo.21 The review’s results are obscure, however. They were
only reported as percentages on an undefined scale without standard deviations.
Furthermore, the quality of the trials was poor. Two-thirds couldn’t be
included in the meta-analysis, and most had problems with missing data and
didn’t report an adequate randomisation method. There was a huge scope for
reporting bias, and there must have been unblinding bias, as the drugs have conspicuous
side effects. Finally, an unreported number of trials were biased by design, as
they had only included participants known to have responded to stimulants. I
wouldn’t dare conclude anything based on these drug company trials.
A systematic review from 2002 done by people
from the McMaster University in Canada with a senior author whom I trust, was
also pretty negative.22 It included 14 trials of at least 12 weeks’ duration
but only five were of adequate methodological quality and no less than 25
different outcomes and 26 different rating scales had been used. Stimulants
reduced ADHD symptoms but didn’t improve academic performance. The trials
didn’t address outcomes that are important. These authors also assessed other
systematic reviews and found that they had extensive flaws due to poor
description of the methods used to find, select, assess, and synthesise the
information.
The FDA approved these drugs with absurdly
little documentation.23 Only 32 clinical trials were conducted for the
approval of 20 ADHD drugs; the median number of participants studied per drug
was 75; and the median trial length was four weeks.
The adverse effects of stimulants include tics
and twitches and other behaviours consistent with obsessive compulsive
symptoms, which can be quite common.24, 25 Stimulants also reduce overall spontaneous mental
and behavioural activity, including social interest, which causes apathy or indifference,
and many children – in some studies more than half – develop depression and
compulsive, meaningless behaviours.12, 14 Numerous animal
studies have confirmed this.14 The compulsive behaviour is often
misinterpreted as an improvement at school, although the child may obsessively
just copy everything shown on the board without learning anything. Some
children develop mania or other psychoses.12, 13
When these adverse drug effects are mistaken for
a worsening of the “disease,” the children are often given additional
diagnoses, e.g. depression, OCD or bipolar, and additional drugs, leading to
chronicity.14
But as explained in Chapter 2,
It is bad medicine to come up with additional
diagnoses when a person is under influence of a brain-active chemical, as the
symptoms are most likely drug-induced.14
There seems to be no long-term benefits from
ADHD drugs, only harms. I have heard psychiatrists argue that the drugs improve
occupational outcomes and reduce the risk of committing crime, but there are no
reliable data in support of this wishful thinking. Accord ing to Whitaker, the
American Psychiatric Association’s Textbook of Psychiatry
stated already in 1994 that, “Stimulants do not produce lasting improvements in
aggressivity, conduct disorder, criminality, education achievement, job
functioning, marital relationships, or long-term adjustment.”20
In 1999, NIMH published 14-month results of the
first longterm trial, the Multimodal Treatment study of ADHD (MAT), in which
579 children were randomized to methylphenidate, behavioural therapy, both, or
routine community care.26 Many scales and outcomes were used, with no less
than 19 primary outcomes, but the only differences between drug and behavioural
therapy were that the children were less hyperactive or impulsive and paid more
attention when on drug. Combined treatment was no better than drug alone for
core ADHD symptoms.
What I find most interesting is that the
improvement in symptoms over time in all four groups was sometimes considerably
larger than the differences between the treatments, e.g. for inattention and social
skills.
The patient sample was probably biased in favour
of drugs, as patients who had previously been on an ADHD drug were excluded if
they had not tolerated the drug. The authors considered ADHD a chronic disorder
and advocated ongoing treatment, which agreed poorly with the improvement in
all four groups, and with the Canadian study of schoolchildren where the risk
of being on the drug depended on the month the child was born (see above).
It is difficult to know what to make of all
these scores in the MAT trial. Did the reported differences translate into
anything important for the children? They actually didn’t, as judged by the
long-term results, which the psychiatrists weren’t eager to publish. It took
another eight years before the three-year results were published!27 The investigators now revealed their financial
conflicts of interest, which were astonishing. Sixteen authors listed a total
of 214 drug companies, or 13 per author. These relationships were mostly
described as research funding, “unrestricted grants” (a euphemism for
corruption),4
consulting and being on speakers’ bureaus and advisory boards. Not exactly a
bunch of people we would entrust to give us an unbiased view of the value of methylphenidate.
The four treatment groups didn’t differ
significantly for any of the numerous ADHD outcomes. The investigators partly
ascribed this to the fact that many children in the two non-drug groups took
drugs, so the treatment contrast was low. But they also mentioned that the
results were possibly due to an age-related decline in ADHD symptoms.
A companion paper is close to impossible to
interpret, as the findings were drowned in advanced statistics, but the limited
relevant data showed a lower rate of substance abuse in the behaviour therapy
group than in the drug group after three years.28 Methylphenidate didn’t protect against delinquency
and substance abuse; if anything, it caused them.
The results after six and eight years were also
discouraging.29 The treatment groups didn’t differ significantly for
grades earned in school, arrests, psychiatric hospitalizations, or other
clinically relevant outcomes. Medication use decreased by 62% after the
14-month controlled trial, but adjusting for this didn’t change the results.
These follow-up papers are also difficult to
grasp, as they confuse readers with unnecessarily complicated statistics. I
shall take it all down to earth by quoting one of the investigators:30 “I think that we exaggerated the beneficial impact
of medication in the first study … The children had a substantial decrease in
their rate of growth … there were no beneficial effects – none … that
information should be made very clear to parents.”
It wasn’t. The public was duped, seduced and
lied to.31 A news release issued by NIMH presented the negative
results in a favourable light; the title was: “Improvement following ADHD
treatment sustained in most children.” One of the authors on the payroll of
many drug companies, Peter Jensen, said, “We were struck by the remarkable
improvement in symptoms and functioning across all treatment groups.” And
rather than saying that the growth of children on medication was stunted, the
press release said that children who were not on medication “grew somewhat
larger.”
The drug industry uses the same dirty tricks.
When Merck found out that its arthritis drug Vioxx was deadly and caused more
thromboses than another arthritis drug, naproxen, the company invented the hoax
that naproxen was protective rather than Vioxx being harmful.4
ADHD drugs for adults
The benefits are also doubtful when the drugs
are used for adults. As for children, many trials have been carried out by the
same small group of Harvard psychiatrists who have numerous financial ties to
the drug makers. And most trials are flawed by design in the same way, e.g. by
including only patients that have tolerated the drug, and often also only
patients who improved while on the drug. The industry calls this an “enriched
design.” I call it a design that makes them rich.
We are currently doing a Cochrane review on
extended release methylphenidate in adults and have found that every trial has
a flawed design. A medical student we involved with this research was shocked
when he saw this; he had never imagined that clinical trials could be of such
poor quality, also with many missing patient-relevant outcomes. For example, he
wondered why blood pressure was missing when we know that stimulants increase
blood pressure and that many people die from high blood pressure.
A 2014 Cochrane review of immediate-release
methylphenidate showed the expected positive effects for hyperactivity,
impulsivity and inattention, but the trials were of short duration and there
was a risk of bias in many cases.32 The results varied so hugely that I would not have
performed meta-analyses on these data. Most worryingly, the authors could not
determine whether adverse effects were not discussed because none occurred, or
because no data on adverse effects were collected!
Harms from ADHD drugs
Numerous papers have described short-term
harmful effects of the drugs. The increased classroom manageability comes at a
high cost in terms of reductions in curiosity and social interactions. The
children become more isolated, which is hardly a good thing for a developing
brain that builds many new synapses through stimulation.
As noted above, the large NIMH trial showed that
methylphenidate stunts growth33 and stimulants have many other harmful effects,
including sudden cardiac death. Their side effects are similar to the criteria
for bipolar disorder, and in the United States many ADHD children are diagnosed
also with bipolar disorder, which I consider a medical error, as one cannot
diagnose an additional disorder reliably in a drugged person (see above).
Joseph Biederman and his co-workers nonetheless made a diagnosis of bipolar in
23% of 128 children with ADHD and reported this in a paper with a telling
title: “Attention-deficit hyperactivity disorder and juvenile mania: an
overlooked comorbidity?”34 Bipolar is a serious condition often treated with
antipsychotics.
We know far too little about long-term harms
from ADHD drugs, but we know they can cause chronic brain damage (see Chapter
11) and can damage the heart, in the same way as seen in long-term cocaine
addicts, and lead to death, also in children.19 Neurologist Fred Baughman, who has
a website called ADHDfraud.org,35 has explained that Adderall – a mixture of
amphetamine salts – was a weight reduction drug called Obetrol, which was so
addictive that it fell into disrepute and was withdrawn from the market. This
addictive drug is now being sold to little children who are said to have ADHD.
It was withdrawn from the Canadian market in 2005 after 14 children suddenly
died and two had strokes.36 The FDA did nothing, apart from trying to convince
their Canadian colleagues not to withdraw the drug.
FDA trial data show that ADHD drugs cause
psychosis or mania in 2-5% of people treated for one year, whereas no such
cases were reported for patients on placebo.37 These drugs – including atomoxetine – also cause
hallucinations and violence, including homicide, and many children have killed
themselves or suddenly dropped dead while playing with friends.37, 38 One of my friends who is a child psychiatrist told
me that she had been exposed to serious threats from a criminal stuffed with
methylphenidate from a reputable psychiatrist. She also said that
methylphenidate is easily available on the black market, which isn’t
surprising, as it is a narcotic on prescription.
Millions of people are now in treatment with
ADHD drugs based on mainly small, short-term, poor-quality industry trials,
full of bias in the design, analysis and reporting of the data. There are very
few trials of psychosocial interventions. A 2011 Cochrane review of
social-skills training of children found 11 trials, but in eight of them, drugs
were given to both the training group and to the control group, and most trials
had a high risk of bias.39
As far as I can see, ADHD drugs do more harm
than good, which is not surprising, as most of them cause similar harms as
amphetamine and cocaine. People dependent on amphetamine can experience severe
withdrawal symptoms that can last for weeks and which include dysphoria,
irritability, melancholia, anxiety, hypersomnia, marked fatigue, intense
craving for the drug and paranoia.40
It is a paradox that some schools have posted
signs saying “drugfree zones” while its teachers act as more effective drug
pushers than those in the streets. The drugs may solve problems for schools but
not for the children who merely act in ways that bother adults, which are very
much the “symptoms” that define childhood ADHD.
All “education” of teachers, social workers,
kindergarten attendants and others in how to spot symptoms of ADHD and test for
it must stop, as such initiatives are harmful and prevent many of our children
from having a normal childhood.
People with symptoms they think qualify for the
ADHD diagnosis should avoid consulting doctors, as they very likely will
diagnose them and prescribe drugs. It may even be risky to consult
psychologists, as some of them collaborate closely with psychiatrists and think
that drug treatment is what it should all be about. Psychologists in several
countries now fight for the right to prescribe psychotropic drugs, although we prescribe
them far too much already.
As ADHD is not a disease, we should ignore the
criteria for the diagnosis in the DSM and ICD (International Classification of
Diseases) manuals and should stop using this diagnosis. Further, it is not
enough that Adderall has been removed from the market; all ADHD drugs should be
removed, which would ensure that doctors can no longer use them. The idea of
treating behavioural problems with drugs is an utterly sick one, which a very
detailed review from the Oregon Evidence-based Practice Center leaves no doubt
about.41
ADHD is a disaster area, both in terms of
diagnosis, clinical research, and the harms inflicted on millions of healthy
people.
6
Schizophrenia
When I first heard Robert Whitaker explain why
antipsychotics do more harm than good at a meeting in Copenhagen in 2012, I was
reasonably sceptical because it went counter to my training in clinical
pharmacology and psychiatry. However, after having read his two books,1, 2 some of the most important papers quoted in them,
and a lot else, I know that he is right.
Schizophrenia has always been the darkest
chapter in psychiatry’s history book. For centuries, patients were exposed to
the cruelest treatments, often against their will.1 These included
inflicting excruciating pain to distract the lunatic from his raving thoughts;
dropping blindfolded patients in cold water or temporarily drowning them to
create a shock effect; and putting them in a swinging chair, which produced
vomiting and violent convulsions.
Many of these treatments were feared by the
lunatics and the fear was used actively in order to make them behave. The
rantings and ravings that appeared to define the mad – the tearing of clothes,
the smearing of faeces, the screaming – were primarily antics of protest over
inhumane treatment. To understand this is no less important today where many of
the symptoms that seemingly define the disease are caused by the drugs or are
protests over forced treatment. The threat of forced treatment is still being
used to discipline patients in a power game where the patient is always the
weakest (see Chapter 15).
What is particularly tragic about all this is
that the psychiatrists have consistently hailed all their harmful treatments as
being effective. The treatments knocked the disturbing patients down and made
them docile, confused and inactive, which was convenient for the staff. The
patients have rarely agreed with the staff’s success criteria, but their views
are often ignored even today, though the treatments imposed on them are harmful
and cause many deaths.
In the 1800s, patients were sedated with opium
and morphine, which were the chemical “restraints” of the time. But there was
also a very different kind of treatment.1 The Quakers treated the insane with
kindness and respect and organised activities for them. Historians have
concluded that this type of treatment was surprisingly effective. Only about
one third of the patients became chronically ill, and more than half remained
well throughout their lives.
The first half of the 1900s was a particularly
dark era in America. Eugenics was fashionable, and it began with flawed
research that “proved” that insanity is an inherited disease. It progressed
into sterilising and sometimes also castrating the insane, which were seen as
worthless members of society. Leading scientists raised the possibility of
killing the insane, and in 1935 Alexis Carrel, a Nobel Prize winning physician
at the Rockefeller Institute, which supported research in eugenics, wrote in
his book that the insane, or at least those who committed any sort of crime,
“should be humanely and economically disposed of in small euthanisic
institutions supplied with proper gases.”1 Hitler was inspired by the American
view on the insane and Nazi Germany began gassing its mentally ill patients
five years later.
Many treatments introduced in this period killed
large numbers of patients. The idea that insanity could be caused by an
infection led to removal of the patients’ teeth and many other body parts
including the large intestine. Mental patients were deliberately infected with
malaria, as some effect of high fever had been seen in insanity caused by
syphilis.
The barbiturates became a success after German
scientists in 1903 had shown that they were good at putting dogs to sleep, and
they were sometimes used to keep patients asleep for days to “restore their
nervous system,” but this usage ended after it was shown that 6% of the
patients died.
Around the middle of the last century, drastic
treatments were introduced – insulin coma therapy, metrazole, and electroshock,
which caused convulsions and often broken bones – and prefrontal lobotomy, all
of which “worked” by causing brain damage, shutting down the higher functions
first.1
After emerging from insulin coma, patients acted in infantile ways, e.g.
sucking their thumbs and calling out for their mommies, which behaviour was
interpreted by the treating psychiatrists as a return to lucidity. Yet again,
what was valued by the staff was that the patients became friendlier, less
noisy and more “sociable” and spent more time sleeping, and that the nurses
could behave in a more motherly fashion towards these people turned into
children. However, about 5% of the patients died and the long-term outcomes
were devastating.
Metrazole was no less barbaric. It is a
derivative of camphor, which had been used for treatment of the insane already
in the 1700s, as it also caused convulsions. The patients were terrified by the
treatment, which caused spinal fractures in almost half the cases and other
fractures, muscle ruptures, broken teeth and haemorrhages in internal organs.
The injections were typically given two to three times a week, but already
after the first one, patients were forcibly treated, as they begged their
torturers not to kill them.
Electroshock was invented by an Italian
psychiatrist.1
He first put the electrodes in the mouth and anus of dogs, but half of them
died. He then visited a slaughterhouse and saw how the pigs were stunned with
electroshock applied to their heads, which made it easy for the butcher to stab
and bleed the animals.
It was understood right from the beginning that
electroshock works by damaging the brain. Psychiatrists observed that patients
lost their memories, took weeks to recover and often remained fatigued,
intellectually impaired and disoriented, and acted in submissive, helpless
ways. The reason that it “worked” for psychosis was simply that the patients
were stripped of the higher cognitive processes and emotions that give rise to
fantasies, delusions and paranoia.
This “effect” rather quickly dissipated and the
illness returned. The shocks should therefore have been abandoned, but instead,
a perverse idea was introduced: repeating the shocks numerous times, sometimes
on a daily basis, even though the psychiatrists very well knew that the worse
the brain damage, the better the “effect.”
Children weren’t spared. Starting in 1942, 98
children aged four to eleven received shocks twice daily for 20 days. A
ten-year old boy wanted to kill the physicians who had treated him, another
attempted to hang himself. But the psychiatrists considered their treatment a
success and one wrote that she had successfully given a two-year old child the
usual forty shocks.
Some psychiatrists didn’t delude themselves,
however. They found that electroshock produced similar changes in the brain as
physical trauma, with haemorrhages both in animals and people, particularly in
the cortex, which led to permanent impairment of learning capacity, perception
of reality, inventiveness, intuition and imagination. However, this was not
what the psychiatrists told the public, which got the message that
electroshocks are safe and effective. Some patients were scared to death even
after curare was introduced to prevent fractures and tried to escape going
through windows; some were dragged screaming into the shock rooms; and many patients
regarded the shocks as punishment administered by cruel and heartless doctors.
At the same time, the Red Cross determined that prisoners in Nazi concentration
camps who had been electroshocked should be compensated for having suffered
“pseudomedical” experiments against their will!
The frontal lobes are what make us human, but
prefrontal lobotomy was introduced at about the same time, and it earned its
inventor the Nobel Prize. This operation also made the patients childish and
apathetic, and they lost their capacity to make sound judgments. Some died,
others behaved in bizarre ways, and about a quarter never progressed beyond the
surgically induced childhood.
Money clearly played a role. By distorting
completely the results of lobotomy, Rockefeller-funded scientists ensured that
the money kept rolling in, although some patients had descended to the level of
animals, refusing to wear clothes and urinating and defaecating in the corner.
As might be expected, lobotomy was chosen as the “Endlösung” (ultimate
solution) for people who couldn’t be quieted enough with electroshock, and
although it wasn’t the full-blown Nazi euthanasia, a critic aptly called it
“partial euthanasia.”
Also in this case, “troubled” children weren’t
spared, although in one series, which included a four-year old child, two of 11
children died.
Just after the Second World War, the scandal
broke in American psychiatry. Mental hospitals had developed into a sort of
prison where some patients didn’t see a doctor for years and were cuffed, strapped
to chairs, and beaten by the attendants, sometimes with a lethal outcome.1
Human guinea pigs in America
In a most disturbing chapter in Mad in America, Robert Whitaker documents that the Nürnberg
code didn’t apply in America where the psychiatrists abused their patients for
research purposes without their informed consent even as recently as in the
1990s.1
Shortly after the war crime trials in Nürnberg
were over, Paul Hoch and his colleagues in New York experimented with LSD and
mescaline, which they gave to mentally ill patients in order to develop a model
for schizophrenia in humans. Both drugs worked, and Hoch also studied if
electroshock and lobotomy would block the drug-induced psychosis. No one
questioned the ethics of his experiments, and when he presented his results, he
was congratulated for his imaginative work, which was copied by other
psychiatrists.
In 1973, another researcher studied whether
amphetamine and methylphenidate – the most commonly used drug for ADHD – could
stir hallucinations and delusions in the mentally ill, and indeed they could,
methylphenidate being the worst drug. In a New York hospital, 70 people who
came into the emergency room with a first episode of psychosis were put on
methylphenidate, which caused most of them to become so much worse that it took
long to stabilise them on antipsychotics afterwards. Other researchers followed
suit, but generally didn’t describe in medical journals how the patients had
fared. However, in 1987, NIMH scientists admitted that methylphenidate
injections had caused episodes of frightening intensity in patients.
These cruel experiments – which were almost
exclusively an American affair – accelerated and were conducted in relative
obscurity, unnoticed by the general public. In the mid-1990s, however, a
citizens group led by a Holocaust survivor, Vera Sharav, and biology professor
Adil Shamoo alerted the public to the unethical experiments, and Sharav
remarked that such research could only be done on the powerless.
The researchers’ defence was astonishing. They
claimed that patients with schizophrenia volunteered for the experiments to
make a contribution to science, but this was belied when independent
researchers got access to the consent forms, which were unbelievably
misleading. When the human guinea pigs learned about what they had been exposed
to in 1998, they found it appalling and likened the experiments to those done
by Nazi doctors. The researchers’ explanations were pathetic, as illustrated by
this statement from a patient, which is about having the cake and eating it,
too:
“Do you think people really say, ‘Gee, I’ll sign
up for more suffering?’ Many of us suffer enough on our own. And these
[researchers] are the same people who say we don’t have enough insight and so
there have to be involuntary commitment laws because we can’t see that we are
ill.”
Fifty years of such research had led nowhere.
Just like the military torture in Guantanamo led nowhere. There is a good
reason why we have laws, and no good reason why some people are above the law
if they have a high enough position that gives them total power over others.
A different type of crime that I have heard a
good deal about is tampering with the patient’s files, either by adding
something after the event or deleting facts that would look bad in a court
case. In a Danish court case I am involved with, the general practitioner added
false information to the chart after the patient had hanged himself on
sertraline.
The chemical lobotomy
When chlorpromazine came on the market in 1954,
it was first considered a chemical lobotomy, as it produced many of the same
effects as lobotomy. It was also called a chemical straitjacket, as it kept the
patients under control, and later called a neuroleptic.
Psychiatrists noted that chlorpromazine didn’t
have any specific antipsychotic properties; the patients continued to have
delusions and hallucinations but were less disturbed by them.1 However, this
truth was quickly buried, and in 1955, the president of the US Society of
Biological Psychiatry, Harold Himwich, came up with the totally weird idea that
antipsychotics work like insulin for diabetes.3 The hype was extreme. A series of laudatory articles
in New York Times hailed chlorpromazine as being
curative, capable of healing the mind and bringing people back to normal life.
A study in the American Journal of Psychiatry claimed
that only two of 1,090 patients, followed for up to three years, showed faint
signs of Parkinsonism, whereas a more honest psychiatrist had reported two
years earlier that he had seen Parkinsonism in all of
his patients.
According to psychiatric folklore, which we
still hear today, it was the advent of antipsychotics that emptied the asylums,
but this emptying started earlier, both in the United States and in the UK, and
was driven by economic considerations.1, 3, 4
NIMH contributed in a remarkable way to the
organised delusion.1, 5 In 1964, NIMH funded investigators reported on a
six-week study of newly admitted patients with schizophrenia in treatment with
phenotiazines like chlorpromazine. None of the 270 patients became worse and
the drugs reduced apathy, improved motor movement and made patients less
indifferent – exactly the opposite of what these drugs do to patients, and
which the psychiatrists had admitted a decade earlier – and side effects were
said to be “mild and infrequent … more a matter of patient comfort than of
medical safety.” The investigators felt that the phenotiazines were curative
and should no longer be called tranquillisers but anti-schizophrenic drugs. The
study was double-blind and there was a placebo group. What the study tells us
is that,
Investigators who have not been blinded
effectively can see the exact opposite of what is actually true when they
medicate patients. They see what they want to see, which is what is convenient
for them and for their specialty, not what happens.
Isn’t this what psychiatrists have always done?
Convinced themselves that their primitive treatments were effective although
they weren’t? Is it any different to the current misconception that
psychotropic drugs are highly effective? This study contributed to shaping the
erroneous beliefs that schizophrenia can be cured with drugs and that
antipsychotics should be taken indefinitely. I shall say more about the trial
below, as the one-year follow-up data are very telling.
The psychiatrists didn’t ask the patients how
they felt about the drugs but they have suffered the consequences of the fairy
tale ever since, although the scientific facts about what the drugs do to the
brain are sobering.1 The drugs hinder brain function by partially
shutting down vital dopaminergic pathways. This leads to altered behaviour and
thinking, emotional isolation where the patients feel like “zombies,”
development of Parkinson’s disease, and chemical lobotomy because the
dopaminergic pathways to the frontal lobes get partially blocked.
What these drugs produce in the patient is a
disaster, and almost all of the traits people think are caused by schizophrenia
are in fact caused by the drugs: the awkward gait, the jerking arm movements,
the vacant facial expression, the sleepiness, the lack of initiative.1
These symptoms were seen more than a hundred years ago in encephalitis
lethargica, which is caused by a virus, and which predicted the worst outcome
in patients rendered psychotic by an infection. The term schizophrenia was
coined for these patients in 1908.1 This historical background explains
why drug-induced harms are sometimes interpreted as disease symptoms even
today.
The bizarre involuntary and irreversible
muscular symptoms are known as tardive dyskinesia. It is seen in 5% of patients
within the first year of treatment and increases by an additional 5% with each
additional year of exposure,1, 6 which explains why about half the patients in
long-term facilities have it.7 Tardive akathisia is a particular virulent form of
tardive dyskinesia where the patient is driven by a torture-like inner
agitation that compels them into moving their hands and feet nervously or pace
frantically about in an effort to relieve the distress.7
Big pharma and psychiatry kept the public
ignorant about this harm for about 20 years after chlorpromazine came on the
market,7
as such knowledge might have pricked the whole drug balloon, which was such a
cash cow for both parties.1 The American Psychiatric
Association’s astounding silence only stopped when lawsuits were filed with
claims of negligence for failing to warn patients. The risk of developing
malignant neuroleptic syndrome was also largely ignored, but it has been
estimated that 100,000 Americans died from it in a 20-year period and that
80,000 might have lived if the physicians had been warned against it.1
Some patients appreciate being calmed down with
antipsychotics but the more common view is that the drugs are awful. They are
seen as a means of torture and control that may prevent patients from thinking
clearly and reading an entire book for years. The muscle contractions can lead
to physical pain, people are alienated from themselves and emotionally
flattened, and their will may be paralysed. A 1999 survey showed that 90% of
patients on neuroleptics were depressed, 88% felt sedated, and 78% complained
of poor concentration.1
Two physicians have described how a single dose
of haloperidol knocked them down.8 They experienced a marked slowing of thinking and
movement, profound inner restlessness, a paralysis of volition and a lack of
physical and psychic energy, being unable to read or work. David Healy found
the same in 20 staff from his hospital who received droperidol.3 Everyone felt
anxious, restless, disengaged and demotivated to do anything; a psychologist
volunteer found it too complicated just to obtain a sandwich from a sandwich machine.
Some felt irritable and belligerent and many were unable to recognise the
altered mental state they were in and to judge their own behaviour, something
which Peter Breggin calls medication spellbinding.7
It is easy to understand why patients often
report in surveys that the drugs are worse than the disease.3 Yet, there is
very little reference to the terrible drug effects in the psychiatric
literature, which conveys the erroneous idea that these drugs are specific for
psychosis.3
Drug regulators are complicit in this. In its report on risperidone, the UK
drug agency said nothing about how the drug affects mood, attention, clarity of
thought, memory, mental speed, emotional responsiveness, motivation, creativity
or any other intellectual quality.3 It’s unbelievable.
Right from the beginning, patients were hiding
pills in their cheeks and spitting them out into toilets and when they were
discharged, they were unwilling to purchase the drug. About half the patients
avoided taking drugs.1 Such disobedient patients are called non-compliant
in the drug literature, although they do everything they can to comply with
their own view of things. To circumvent this “problem,” Smith, Kline &
French developed liquid chlorpromazine that could be secretly mixed into the
patients’ food. Later, long-acting injectables were developed to control the
rationally acting patients and, although they killed many of them, they were
also hailed as a “major tactical breakthrough.”
We know from telephone help lines that what
medicated persons miss the most are themselves, and even the most deluded
persons are often capable of reporting the harmful effects of the drugs
objectively. They know that the drugs have robbed from them a full sense of
being and that their lives have been rendered meaningless.1 At a Senate
hearing in 1975, a witness said that medicated people suffer a deadlier
confinement than prisoners had ever known, and a senator called neuroleptics
chemical handcuffs that assured solitary confinement of the mind.1
Drug trials in schizophrenia
There is a rather remarkable attitude
prevalent that if a paper is published then its contents become authoritative,
even though before publication the same contents may have been considered
nonsense.
PFLZER PHYSICIAN HASKELL WELNSTEIN1
Drug trials in schizophrenia is a disaster area,
and this is not only because the patients can be more difficult to handle than
other patients in trials, e.g. patients with high blood pressure. When the
Cochrane Schizophrenia Group reviewed 2,000 trials in 1998 it found half a
century of trials of limited quality, duration, and clinical utility.9 Over half the trials had 50 or fewer patients, over
600 different interventions were studied, and 640 different rating scales were
used to measure the outcome, 369 of them only once. The clinical meaning of
these outcomes was obscure, and the quality of reporting was exceptionally poor
and didn’t improve over time. Only 4% of the trials clearly described the
methods of allocation, only 22% described blinding adequately, while some
description of treatment withdrawals was given in 42%.
The authors mentioned that it is difficult to
blind the trials, but this is possible if one puts something in the placebo
that has side effects (see Chapter 3).
So how are we supposed to find out what the
drugs do to patients and whether some are better than others? The Cochrane
Schizophrenia Group has published over one hundred reviews of drugs and some
run over hundreds of pages, but we can take some shortcuts to get to the bottom
of all this. Most importantly, virtually all of the trials are unreliable and
there are five major reasons for this.
1) The placebo controlled trials are highly
flawed in favour of the active drug, as they have been close to 100% unblinded
and as the assessment of the outcome is highly subjective.
2) Almost all trials have included patients
already in drug treatment, and the active drug has often been stopped abruptly,
which can cause terrible harms, including psychosis, akathisia and death, in
those randomised to placebo.
3) The outcomes are not relevant. The trials
don’t tell us whether drug treatment helps the patients get back into society
and lead a normal life.
4) Almost all trials are short-term, although we
know that a beneficial acute effect is replaced by harmful long-term effects
when the drugs are used for more than a few weeks (see below).
5) The head-to-head comparisons of different
drugs are also flawed. The typical trick is to compare newer antipsychotics
with a too-high dose of haloperidol, which makes it possible for the companies
to claim that their drug is better tolerated.1, 10
Using such manoeuvres, it has been possible to
hail the newer, so-called atypical, antipsychotics as breakthrough drugs,
although they are equally bad as, or sometimes worse than, the old drugs.11 The reason that Janssen could claim that its
bestseller risperidone didn’t have more extrapyramidal (muscular) side effects
than placebo was the abrupt withdrawal of the previous antipsychotic drug,
which inflicted such effects on the placebo group to such an extent that one in
six “placebo” patients got them!1 The companies needed to show that
their drugs reduced psychotic symptoms and they made the placebo patients
psychotic by withdrawing their drug cold turkey.
This withdrawal design is lethal. One in every
145 patients who entered the trials for risperidone (Janssen), olanzapine (Eli
Lilly), quetiapine (AstraZeneca) and sertindole (Lundbeck) died, but none of
these deaths were mentioned in the scientific literature, and the FDA didn’t
require them to be mentioned.1 Many of these patients killed
themselves; the suicide rate in the trials was two to five times the usual rate
for patients with schizophrenia, and a major reason was the withdrawal-induced
akathisia.1
An analysis of patient reports on the Internet showed that suicidal thoughts
when taking antipsychotics are strongly associated with akathisia; 13.8% of
respondents reporting akathisia also reported suicidal thoughts, compared with
1.5% of those who didn’t mention akathisia (P < 0.001).12 This harm would be expected to be related to the
dose of the previous drug, and it clearly is.13 It could be argued that those who were most ill got
the highest doses and were therefore more prone to experience these effects,
but the dose effect was so strong that this couldn’t have been the major
factor.
The FDA reviewers repeatedly pointed out that
the companies used a biased design that didn’t contain a true placebo group to
show that their drugs worked, but the drugs were approved.1 This cruel design
has not only been lethal for some patients, it has also produced misleading
results for those who survived, as the patients in the placebo group had been
harmed.1
The FDA forbade Janssen to claim in
advertisements that risperidone was superior to haloperidol with regard to
safety or effectiveness, but this was exactly the message Janssen conveyed in
scientific papers, which the FDA had no control over, although it was wrong. A
meta-analysis of 52 trials (12,649 patients) concluded that there was no basis
for claiming that atypical antipsychotics were any better than old
antipsychotics.4
These industry-sponsored drug trials are
terribly deceptive. Whitaker conducts the thought experiment that if olanzapine
had been the old drug and haloperidol the new one, it would have been easy for
a company to create the impression in its trials that haloperidol was the
superior drug, which it very likely is.1
The most reliable placebo controlled trials are
those of first episode schizophrenia where none of the patients have ever
received drugs before. There is a Cochrane review that approaches this ideal,
but even this review is biased, as the trials are not limited to first episode
patients; it includes studies “with a majority of first and second episode
schizophrenia spectrum disorders.”14
Nonetheless, the review is highly interesting
and the most relevant one. In three trials of chlorpromazine, the participants
were half as likely to leave the study early when they were on drug than when
they were on placebo. Only one of the trials (463 patients), which was
sponsored by NIMH, reported on harms, and there were of course more harms on
chlorpromazine than on placebo.
Another of the trials (127 patients) reported on
rehospitalisations, and double as many patients on chlorpromazine than on
placebo were rehospitalised within three years, relative risk 2.3 (95% CI 1.3
to 4.0). When the patients who dropped out were included in the analysis, the
result was even more striking, relative risk 3.1 (95% CI 1.6 to 5.8). There
were also fewer rehospitalisations in the placebo group at the one-year
follow-up in the NIMH trial, but the difference wasn’t quantified and the
original data appear to have been lost.14
In a fourth randomised trial, Loren Mosher
compared 55 patients in hospital, all of whom received antipsychotics, with 45
patients who were treated in a non-hospital milieu where 67% received no
antipsychotics. The Cochrane review says nothing about the rationale for
Mosher’s trial, although it was unique for its time.1 Mosher was the
chief of the Center for Studies of Schizophrenia at NIMH and he wasn’t against
using antipsychotics. He opened a 12-room Soteria house in 1971, as he wanted
to study whether treating acutely psychotic people in a humanistic way that
emphasised empathy and caring and avoided antipsychotics could be as effective
as drug treatment. There were no locks on the doors, and the idea was to treat
people with respect. His staff were not mental health professionals but people
who had social skills and empathy and who listened to the patients’ crazy
stories (which often revealed traumas with abuse and extreme social failure).15 Thus, Mosher paved the way for what later became
known as Open Dialogue (see Chapter 10).
The results in Mosher’s trial after six weeks
were virtually the same in the two groups for psychopathology. Thus, as
outlined further below, antipsychotics can be avoided in most patients, even in
acute psychosis, where the rationale for their use is otherwise most obvious.
The authors of the Cochrane review were pretty direct about this, as they
pointed out that the available evidence doesn’t support a conclusion that antipsychotic
treatment in an acute early episode of schizophrenia is effective.14
They felt this was worrying given the widespread use of antipsychotics in the
acute treatment of early episode schizophrenia-type psychoses, and also because
the use of antipsychotics for millions of people with an early episode appears
based on the trials for those with multiple previous episodes (which we know
are so flawed that the evidence is useless). What the Cochrane authors didn’t
write about was: What does this mean for use of antipsychotics more generally,
also for multiple episodes of psychoses? Doesn’t it mean that we don’t have the
evidence to support using antipsychotics at all?
The harmful effect of antipsychotics in terms of
an increased risk of relapse (hospital admission) was expected. The drugs block
dopamine transmission, and the brain’s response to this is to produce more
dopamine receptors. This means that the brain becomes supersensitive to
dopamine and at greater risk for a new and more severe episode of psychosis,
whether or not the patients still take drugs.2, 16
In 2014, a huge Cochrane review (55 trials and
5,506 patients) was published of trials comparing chlorpromazine with placebo
for schizophrenia, which was not limited to early episodes.17 I find it astonishing that the authors mention in
the abstract without any reservation that akathisia didn’t occur more often in
the chlorpromazine group than in the placebo group. Worse still, the largest
trial that contributed data to this outcome found significantly
less akathisia in the active group than in the placebo group, relative
risk 0.57, 95% CI 0.37 to 0.88. Since we know that antipsychotics cause akathisia1 and that placebo cannot
cause akathisia, this result speaks volumes about how ridiculously flawed
trials in schizophrenia are. What was seen in the placebo group were cold
turkey symptoms caused by withdrawal of antipsychotics!
There are other problems with Cochrane reviews
in schizophrenia. They routinely include trials in a meta-analysis where half
of the data are missing. I believe this is highly likely to produce misleading
results. Furthermore, it is recommended to use completers-only data, if there
are no data on those who dropped out. As there are often many drop-outs, it can
bias the review in favour of the active drug to analyse the data in this way,
as shown by an analysis of trials of antidepressants performed by the Swedish
drug agency.18, 19
We cannot turn garbage into gold with
statistical alchemy. I therefore believe that the Cochrane schizophrenia
reviews that have allowed so much data to be missing should be redone, with
stricter criteria about which trials to include. But the question is whether it
would be worth the effort when virtually all these trials are biased by design.
Even helped by all these formidable biases, the
outcome of schizophrenia trials has been poor. During the first week of
treatment, clinicians cannot detect any effect of antipsychotics on the
symptoms,20 and even later, the effect may lack clinical
relevance. Based on data from 5,970 patients in trials, Stefan Leucht and
colleagues have shown that minimal improvement on the Clinical Global
Impressions Ratings correspond to about 10 points on the Brief Psychiatric
Rating Scale (BPRS) and 15 points on the Positive and Negative Syndrome Scale
(PANSS).20
What is obtained in recent placebo controlled trials in submissions to the FDA
is far below these minimum improvements, e.g. only 6 points on the PANSS score,3, 21 even though it is easy for scores to improve quite a
bit if someone is knocked down by a tranquilliser and express their abnormal
ideas less frequently.3
A huge NIMH-funded trial, the CATIE trial, of
1,493 patients with schizophrenia randomised to four different antipsychotics,
also showed pretty disappointing results.22 Although it was planned that patients should take
their drug for 18 months, and although patients are constantly coerced to take
their drugs, 74% of patients discontinued it earlier, and olanzapine,
risperidone and quetiapine weren’t any better than an old drug, perphenazine.
This trial, and other large, publicly funded trials,23 undercut completely the legitimacy of psychiatry’s
treatment guidelines for schizophrenia, which recommend the newer, expensive
drugs.
Since the randomised trials are so flawed,
naturalistic studies become interesting. The World Health Organization (WHO)
launched a study in 1969 that lasted eight years.1 It turned out
that patients fared much better in poor countries – India, Nigeria and Colombia
than in the United States and four other developed countries. At five years,
about 64% of the patients in the poor countries were asymptomatic and
functioning well compared to only 18% in the rich countries.
Western psychiatrists dismissed the results with
the argument that patients in poor countries might have milder disease. The WHO
therefore did another study, focusing on first episode schizophrenia diagnosed
with the same criteria in ten countries.1 The results were pretty similar,
about two-thirds were okay after two years in the poor countries versus only
one third in the rich countries.
The WHO investigators tried to explain this huge
difference by various psychosocial and cultural factors but didn’t succeed. The
most obvious explanation, drug use, was so threatening to western medicine that
it went unexplored. Antipsychotics are very expensive and people in poor
countries couldn’t afford them, so only 16% of patients with schizophrenia were
regularly maintained on antipsychotics as compared with 61% in rich countries.1
A 20-year study from Chicago by Martin Harrow showed the same; patients who
were untreated for many years had substantially better outcomes than those on
antipsychotics.16, 24 Confounding by indication was probably an issue, but
Harrow found the same when he compared patients with similar prognoses.25
These results are very convincing and fit all
too well with what we know from the Cochrane review of first episode
schizophrenia14
and about how the drugs destabilise the dopaminergic systems so that patients
become more vulnerable to relapse.1 The WHO studies showed that
recovery is more likely without drugs. A more recent study performed by Eli
Lilly failed to find differences between poor and rich countries, but in this
study all patients were treated with drugs, half of them with olanzapine, the
other half with other antipsychotics.26
Apart from avoiding the damaging effects of
antipsychotics, there are other good reasons why people with schizophrenia
fared so well in poor countries.27 The medical model of schizophrenia – that it is a
brain disease – lowers self-esteem and increases despair, hopelessness,
negative public attitudes and stigmatisation (see further below). In poor
countries, however, the illness is often seen as the result of external forces,
e.g. evil spirits, and people are much more likely to keep the sufferer in the
family and to show kindness, which helps patients recover and participate in
social life again.
Few psychiatrists know about this. They have
asked me whether it would be better than drugs to deprive people of their
liberty by tying them to a tree. This may happen in Africa, but overall, the
communities did a far better job in Africa than we do in the western world
where we have institutionalised deprivation of liberty through legal means and
forced treatment. Over the years, we have killed hundreds of thousands of
patients with antipsychotic drugs (see Chapter 14). Is this really supposed to
be a more “humane” system?
Freedom from neuroleptics should be the desired
therapeutic goal, but psychiatry has again protected its self-made delusions
rather than the patients. In 1998, 92% of patients with schizophrenia in
America were being routinely maintained on antipsychotics.1
What about the benzodiazepines? Since the main
justification for using antipsychotics is to calm the patients down in the
acute phase, one would expect benzodiazepines to be a better alternative.
But big pharma has shied away from comparing
their horrendously expensive and dangerous antipsychotics with offpatent
benzodiazepines that can be acquired almost for free, and psychiatrists have
failed to live up to their professional responsibility by neglecting to perform
such trials themselves. In 1989, 35 years after chlorpromazine came on the
market, only two trials had compared the two types of drugs, and they produced
similar improvements.2 There are now more trials, summarised in a 2011
Cochrane review, and its conclusion is revealing:28
“There is currently no convincing evidence to
confirm or refute the practice of administering benzodiazepines as
monotherapy.”
In actual fact, we should use benzodiazepines
instead of antipsychotics. In 14 trials that had compared them, the desired
sedation occurred significantly more often on benzodiazepines. Benzodiazepines
were compared with placebo in eight trials, and the authors reported that the
proportion of treatment failures wasn’t significantly lower with
benzodiazepines than with placebo (six trials, 382 patients, relative risk
0.67, 95% CI 0.44 to 1.02). My interpretation of these data is entirely
different. Of course benzodiazepines calm patients
down, which a relative risk of 0.67 also implies. Whether or not it is
statistically significant doesn’t matter; it would have become significant with
a few more patients.
So why don’t psychiatrists use benzodiazepines
instead of antipsychotics? And if they find the trials of poor quality,28
then why haven’t they done better trials themselves? The problem is that the
psychiatrists have allowed big pharma to control their specialty to the great
impediment of rational treatment for their patients. We don’t even know whether
antipsychotics or benzodiazepines are any better than morphine in knocking
patients down. Probably not, and they are likely worse, as it is far easier to
withdraw opioids from people than to withdraw antipsychotics or benzodiazepines
(see Chapter 12).
Antipsychotics kill many people
People with schizophrenia have about 20-year
shorter lives than others.29 Suicides play a minor role, and most deaths are
likely caused by antipsychotic drugs. Curiously, about two-thirds of the excess
deaths are called “natural deaths,”29, 30 which they aren’t,
as they are mainly drug deaths.
A meta-analysis of placebo controlled trials
showed that it’s indisputable that antipsychotics kill people (see Chapter 14).31 There are many reasons for this. They can cause QT
interval prolongation on the ECG and life-threatening ventricular arrhythmias,
and large US studies have shown that antipsychotics double the risk of sudden
cardiac deaths in a dose-dependent manner.32, 33 From 2004 to 2012, antipsychotics topped the list
for reports of QT interval prolongation in the FDA’s Adverse Event Database,
and antidepressants came second.34 Antipsychotics also cause falls and hip fracture due
to orthostatic hypotension, sedation and loss of consciousness, and they
increase cerebrovascular adverse events.31 The FDA added warnings of
increased cerebrovascular adverse events to the US prescribing information for
risperidone in 2003, for olanzapine in 2004 and for aripiprazole in 2005.
Other reasons why antipsychotics kill people
include the huge weight gains and diabetes many experience, which shorten life
expectancy substantially. A systematic review of mortality in schizophrenia
showed that mortality had increased in recent decades compared with the general
population; the median standardised mortality ratio for the 1970s, 1980s and
1990s were 1.84, 2.98 and 3.20, respectively.35 As the authors pointed out, an obvious explanation
for this development is the increased use of newer antipsychotics, which are
more likely to cause weight gain and metabolic syndrome than the old drugs.
Antipsychotics can also lead to smoking and
alcohol abuse because the patients may seek relief from these
dopamine-releasing substances to counteract the decrease in dopamine caused by
the drugs.
In agreement with the meta-analysis of the
randomised trials,31 a Finnish study found that the mortality risk for
people with schizophrenia was more than double that for other people; after
adjustment for other risk factors, including smoking, the relative risk was
2.50 (95% CI 1.46 to 4.30) per increment of one neuroleptic.36 This study found a strong inverse relationship
between serum HDL cholesterol and the number of neuroleptics prescribed, i.e.
the more drugs, the greater the risk of dying from heart disease. A large Dutch
study confirmed these results.37 The mortality risk for having a diagnosis of
schizophrenia and using an antipsychotic compared to a control group of
patients who did not have schizophrenia was more than doubled (hazard ratio
2.6, 95% CI 2.0 to 3.2), and it was 8.4 (95% CI 3.1 to 24.1) if a “mood
stabiliser” (anti-epileptic drug) was used. In a cohort of 88 in-patients
followed over 10 years, 39 died, with no instances of suicide. Reduced survival
was predicted by the number of antipsychotics given concurrently (relative risk
2.46, 95% CI 1.10 to 5.47).38 Patients with tardive dyskinesia also have higher
mortality rates, and this harm is directly related to dose.1
But the doubt industry never sleeps.39 One of the worst studies was published in Lancet in 2009 by Finnish researchers.29 It found that
use of antipsychotics for 7-11 years was associated with lower mortality than
no drug use (adjusted hazard ratio 0.81, 95% CI 0.77 to 0.84). This is too good
to be true, and the other main result, that the longer people had used drugs
the lower the mortality, cannot be true either. Other researchers have
addressed the fatal flaws in this study, e.g. 64% of the deaths were not
accounted for and the mortality in patients who were not on drugs was very high
and didn’t concur with other Finnish data.40
In a debate I had with Norwegian psychiatrists
who claimed that antipsychotics reduce mortality in patients with
schizophrenia,41 they referred to the misleading Finnish study29
and also to a Swedish study. The Swedish study found higher mortality with
higher doses than with lower doses,42 entirely as expected, but the psychiatrists didn’t
mention this finding. They also failed to mention that an obvious reason why
untreated patients had a high mortality was that they were different from those
on drugs, which the study authors wrote themselves. They had a higher mortality
of cancer and heart disease than those who received antipsychotics and were
thus at high risk of dying, regardless of whether or not they were treated.
Another “doubt industry study” used FDA data and
was similarly misleading.43 Arif Khan and colleagues reported that
antipsychotics lowered mortality in schizophrenia by more than 50% and that the
drugs also lowered suicides. The authors used person-years instead of persons
and included not only the double-blind phases of the placebo controlled
randomised trials but also the safety extension phases in which the patients
only received active drug (the average duration of placebo exposure was only 33
days, as compared to 132 days on drug). Such analyses are totally unreliable,
as those who continue on active drug are those who tolerate it (I described
this dirty trick in Chapter 3). What Khan’s study really showed – when counting
persons – was that antipsychotics killed people (relative risk 1.65, i.e. a 65%
increase in total mortality), and also caused three times as many suicides
(relative risk 2.83). Khan has been principal investigator of more than 340
clinical trials sponsored by more than 65 pharmaceutical companies and 30
contract research organizations.43 Is this why he published a fatally
flawed meta-analysis in favour of drugs?
A patient history
Bertel Rüdinger is a 40-year old pharmacist who
was admitted to a psychiatric hospital ward for the first time in 2001. The
diagnosis was very severe depression. He was admitted several times, and the
chief of staff resolved that he was in a deep life crisis and needed to get
away from his family and everyday life to recover. While he stayed at a
rehabilitation centre, one of his assigned contact persons became aware that he
heard voices and the diagnosis was changed to schizoaffective disorder.
The following year, he was hospitalised most of
the time and in 2005, he went on life-long disability pension because he was
considered hopelessly ill. From 2003 to 2011, he was exposed to about 40% of
the drugs used in psychiatry and was subjected to extensive polypharmacy, both antipsychotics,
antidepressants and “mood stabilisers.”
He is very grateful that his mother never lost
hope and continued to believe he could have another life. If she hadn’t
softened psychiatry’s violent messages about the hopelessness of his situation,
he would have committed suicide. His other stroke of luck came when his mother
needed a website. The woman who did the programming was pretty hopeless with a
computer, so Bertel thought that if she could do it, he could, too. He learned
how to programme websites, which became his way out of psychiatry.
In 2009, he moved from his protected housing
facility and was fortunate that another such facility sought a webmaster with
user experience. He got the job, and now met patients who had recovered and
also people who had an entirely different approach to mental disorders than he
had been accustomed to. He learned about the Hearing Voices Network and it
dawned on him just how much of his personality the pills had eaten. He
furthermore realised that, being a pharmacist with personal knowledge of mental
disorders and psychiatric drugs, he could help promote other people’s recovery
process. Bertel believes he was the first pharmacist in continental Europe to
start and develop clinical pharmacy in a social psychiatry setting. He stopped
the last psychotropic drug in 2011, but, as for so many others treated with
antipsychotics, it is impossible for him to get rid of the marked obesity his
drugs caused. Therefore, his risk of dying early will forever be considerably
increased because of the drugs he was prescribed.
During Bertel’s ”career” as a psychiatric
patient, he received eight different diagnoses: depression, depression with
psychotic symptoms, borderline, schizoaffective disorder with only depressive
affective symptoms, paranoid schizophrenia, simple schizophrenia,
schizoaffective disorder with bipolarity, and bipolar I with schizoid
personality.
One of the things he learned during his stay in
psychiatry was that in order for the staff to understand people with mental disorders
and their psychological context, trust needs to be established. Many
professionals don’t see a connection between current suffering and life
history. There is rarely time to establish the necessary confidence and all the
forced treatments in psychiatry creates insecurity. Patients don’t open up to
therapists who one day exercise coercion and the next day try to build a
therapeutic alliance.
Bertel says that the psychotropic drugs
prevented him from committing suicide, but only because he was so heavily
drugged that he was totally apathetic and couldn’t do anything. He wouldn’t
recommend such treatment, which had formidable physical, psychological and
social consequences, as prophylaxis against suicide.
Today, Bertel helps people with mental disorders
to use their medication as part of their recovery process and with stopping
drugs that do more harm than good, which some patients have been forced to take
against their will and in excessive dosages. He collaborates with a very good
psychiatrist on this. More commonly, however, his experience is that it can be
difficult or impossible to make psychiatrists understand that psychotropic
drugs are like all other drugs, and that guidelines and recommendations must be
respected.
Pushing antipsychotic drugs
Unfortunately, psychiatrists want the opposite
of what Bertel wants; they want to loosen the guidelines. Danish psychiatrist
Henrik Day Poulsen (see Chapter 2) recently argued that psychiatrists should be
allowed to use three times the maximum dose of antipsychotics recommended by
the drug agency.44 Poulsen claimed that there is no risk in prescribing
these higher doses and referred to safety data from Eli Lilly on olanzapine.
But he forgot to tell the readers that he is on the Lilly payroll, and on many
other companies’ payrolls, too.
Olanzapine is the most used antipsychotic in
Denmark and was at the centre of one of the biggest scandals about
overmedication, which led to dismissal of several leading psychiatrists.
Nonetheless, Poulsen argued that if psychiatrists couldn’t use higher doses, it
would be harmful for patients and increase violent situations in the wards, and
in this he was supported by the Danish Psychiatric Association. However,
several members of parliament and a number of patient organisations felt the
psychiatrists already used too many antipsychotics and in too high doses.
What psychiatrists don’t realise at all is that,
most commonly, patients are violent because of the side effects of the
antipsychotics they take (see Chapter 14); they should therefore come off them
instead of having the dose increased.
Can it really be true that a tripling of the
dose doesn’t cause more harm? Of course not. As noted above, the increased
mortality with antipsychotics is clearly related to dose and number of drugs.
But the silverbacks again displayed their
organised professional denial. They referred to a 2006 report from the Danish
National Board of Health produced by themselves, which claims that the use of
several antipsychotics simultaneously doesn’t increase the risk of death.30 This cannot possibly be correct, and it turned out
that the statistical method used in the report is totally faulty.45 The report showed that those who got four
antipsychotics had a higher mortality than those who got fewer drugs.
The Danish report also showed that half the
patients were in treatment with more than one antipsychotic simultaneously,
although there are no scientific data in support of this and although both
national and international guidelines recommend against it. The record I have
heard about was seven antipsychotics simultaneously. Half the patients were
also in treatment with benzodiazepines and similar drugs although the report mentioned
that this combination increases mortality by 50-65%.30 There were also
more patients than the working group had expected – almost half – that were in
treatment with both antipsychotics and antidepressants, and the report advised
against this massive use of antidepressants.
What was most striking about the report was that
it showed beyond a shadow of doubt that the use of psychiatric drugs was
already out of control, and it was against this background that psychiatrists
wanted to increase overtreatment even more. It’s unbelievable.
A review of medication lists of 214 randomly
selected citizens receiving residential care or home care (median age 84 years)
in Copenhagen was similarly revealing.46 An astounding 65% used one or more psychotropic
drugs (antipsychotics 16%, antidepressants 44%, anxiolytics/hypnotics 27% and
anti-dementia drugs 16%). Many citizens on antipsychotics were also on
antidepressants (53%), anxiolytics/hypnotics (35%) and anti-dementia drugs
(21%). A survey of 500 prescriptions for risperidone in France was also
depressing.47 The prevalence of co-prescription was 43% for
antidepressants, 46% for benzodiazepines, 27% for other neuroleptics, 22% for
“mood stabilisers” and 19% for anticholinergic drugs. The official Danish
recommendations are that patients with dementia should not get antipsychotics,
and that antipsychotics plus anxiolytics/hypnotics should be avoided.
The illegal marketing of antipsychotics is
pervasive,39
as the drugs are so expensive, and this is a main reason why the use of these
drugs is totally out of control. In the UK, half the prescriptions by general
practitioners are issued to people for a variety of non-psychotic problems
including anxiety and sleep problems, and antipsychotics are particularly often
used in people with dementia and in old people.48 In the United States, the use of antipsychotics
doubled in adults and went up eight-fold in children in just 11 years, 49 and in 2005, seven kids per 1,000 were in treatment
with antipsychotics;50 only 14% of prescriptions were for psychoses while
most were for behaviour problems and mood disorders.3
Abilify is currently the most sold of all drugs
in the United States, including statins. When I looked it up, 30 tablets of 15
mg cost $800, which is obscene. Its maker, Bristol-Myers Squibb, agreed in 2007
to pay more than $515 million to settle illegal marketing and fraudulent
pricing practices involving payments to doctors to induce them to use the
company’s drugs, also for off-label use.39 Several other companies also paid
kickbacks to the doctors.39
The history of antipsychotics has many
similarities to that of the SSRIs. The clinical research wasn’t aimed at
clarifying the role of the new drugs for clinicians and patients but was driven
by marketing strategy, and new drugs were much hyped, both in sales pitches and
in industry-sponsored research. When large, independent government-funded
trials became available, it was easy to see that the new drugs aren’t any
better than the old ones.22, 23, 51-53 For example, a
trial in 498 patients with a first episode schizophrenia found no difference in
discontinuation rates between four newer drugs and haloperidol.53 The study was funded by three drug companies but
they were kept at arm’s length.
Such independent trials, also in other areas of
psychiatry and medicine, have taught us that the “best” drugs may simply be
those with the most shamelessly biased data.10
Antipsychotics are standard treatment for
bipolar disorder, which – as explained in earlier chapters – is mainly
iatrogenic, caused by SSRIs and ADHD drugs, and they are also used for
depression. We now see advertisements, e.g. for AstraZeneca, about combination
therapy for depression, and there are preparations that combine the drugs in
the same pill, e.g. Symbyax from Lilly, which contains fluoxetine and
olanzapine, two of the worst psychotropic drugs ever invented.
It’s remarkable that it has been possible to
show in a meta-analysis of published trials that new drugs aren’t better than
old ones, as the research literature is so flawed. A 2009 meta-analysis of 150
trials with 21,533 patients showed that the psychiatrists had been duped for 20
years.54, 55 The drug industry has invented catchy terms such as
“second generation antipsychotics” and “atypical antipsychotics,” but there is
nothing special about the new drugs, and as antipsychotics – new and old – are
widely heterogeneous, it’s plain wrong to divide them into two classes.
Haloperidol was the comparator in most of the trials, and, as noted above, it
was often used in too large doses. Unsurprisingly, the flaws are introduced
deliberately, e.g. an internal Pfizer memorandum explains that by increasing
the dose of the comparator drug quickly, this will result in a high drop-out
rate on that drug due to side effects.56 Given all this, I strongly suspect the old drugs are
better than the new ones.
Eli Lilly’s crimes related to
olanzapine
In 2009, Eli Lilly pleaded guilty to criminal
charges and had to pay more than $1.4 billion for illegal marketing as part of
a settlement with the US Department of Justice.39 The crimes
concerned olanzapine, and as worldwide sales were nearly $40 billion between
1996 and 2009, it’s hard to believe that the fine will have any deterrent
effect.
The crimes were particularly aimed at pushing
olanzapine hard to children and the elderly, and there were many other shady
activities. Posing as physicians, Lilly salespeople asked “planted questions”
during off-label lectures and audio conferences for physicians, and while knowing
the substantial risk for weight gain and diabetes caused by olanzapine, the
company minimised the problem in a widely disseminated videotape called The
Myth of Diabetes. Lilly and their paid prostitutes among doctors also produced
papers describing schizophrenia as a risk factor for diabetes!3 As usual, it’s
never the drug that is the problem, it’s the disease.
Internal Lilly documents were leaked to the New York Times in 2006, which demonstrate the extent to
which the company downplayed the harmful effects of olanzapine.39, 57, 58 However, Lilly instigated legal action against
doctors, lawyers, journalists and activists to stop them from publishing the
incriminating documents on the Internet, and they disappeared.
Even in 2007, Lilly maintained that “numerous
studies … have not found that Zyprexa causes diabetes,” but Lilly’s own studies
showed that 30% of the patients gained at least 10 kg in weight after a year on
the drug, and 16% gained 30 kg. Moreover, both psychiatrists and
endocrinologists said that olanzapine caused diabetes in many more patients
than other drugs,58, 59 and it is likely more harmful than many other
antipsychotics.60
But the company was in a precarious situation,
just like it was before it launched fluoxetine in 1988, as fluoxetine would
soon run out of patent. Lilly fooled people into believing that fluoxetine was
a good drug, and now the company was desperate to fool people again with
olanzapine. In relation to a lawsuit at the superior court of Alaska, details
of the four trials Eli Lilly had submitted to the FDA to get olanzapine
approved were revealed, and a physician wrote a disturbing report about this
for the court.61
The FDA’s cover-up of Lilly’s manipulations were
just as disgraceful as when the FDA protected fluoxetine. The FDA rejected two
of the studies, but the other two were also unacceptable. There was a placebo
lead-in of four to nine days, which means that withdrawal symptoms were
inflicted on the placebo group; a benzodiazepine was allowed – just like in the
fluoxetine trials – but there was no information about how many patients took
it in the placebo and drug groups; more than half the patients dropped out
quickly although the trials lasted only six weeks; there were lots of missing
data; and patients could be switched to open treatment with olanzapine after
only two to three weeks if they had responded poorly. It’s
impossible to get anything reliable out of trials like these. In one
trial, haloperidol was the comparator drug, but it was overdosed up to 20-fold
in comparison with olanzapine.
Despite all this, olanzapine wasn’t better than
placebo in many of the analyses. One of the rejected trials was very large, 431
patients, but olanzapine doses of 5, 10 and 15 mg weren’t any more effective
than 1 mg. The FDA seemed to have panicked over this study, which it buried.
The dose was so low that very few dopamine receptors would be occupied by
olanzapine. Thus, this study not only proved the “chemical imbalance” dopamine
theory wrong, it also demonstrated once again that what we see in trials of
psychiatric drugs are not real effects but mainly biased evaluations because of
poor blinding.
Lilly wanted to make doctors use olanzapine also
for mood disorders and had the audacity to call the drug a mood stabiliser,
although it doesn’t stabilise mood. Like other antipsychotics, it dampens wild
thoughts – in fact, any thoughts. It was a challenge for Lilly that general
practitioners were worried about the harms caused by antipsychotics, but Lilly
was determined to “change their paradigm,” as they euphemistically called it in
an internal document. Lilly also prepared fictitious patient stories for use by
the sales force.60
Lilly’s many tricks of the trade even ensured
that the company got around a threatening patent problem. The patent was
running out but Lilly got a new patent by showing that it produced less
elevation of cholesterol in dogs than a never-marketed drug!62 I have seen many absurdities in relation to the
patenting of drugs, but this one deserves first prize. Olanzapine raises
cholesterol more than most other drugs, and it should therefore have been
marketed as a cholesterol-raising drug, but that wouldn’t have made it a
blockbuster with sales of around $5 billion per year for more than a decade,62
the most widely used antipsychotic drug in the world.
Lilly’s huge commercial success with both
fluoxetine and olanzapine illustrates that in psychiatry it doesn’t really
matter which drugs you have. Corruption, marketing and lies will ensure that
doctors don’t use drugs that are both better and cheaper. As an example of this
information control, a Cochrane review from 2005 reported that the largest
trial with olanzapine had been published 142 times in
papers and conference abstracts!63 This carpet bombing with propaganda contributed to
the fact that, in 2002 sales for olanzapine were 54 times larger than sales for
haloperidol in Denmark. There was no excuse for this waste of money. At the
time, olanzapine cost seven times as much as haloperidol per day, and two years
earlier, a meta-analysis in the BMJ concluded that,
“the new drugs have no unequivocal advantages.”11
Patient organisations contribute to the
corruption. They often receive money from the industry and know only what the
drug firms have told them, or what the psychiatrists have told them, which is
about the same, as they also get their knowledge from the industry. It was
therefore not surprising when the chairman of an organisation for psychiatric
patients in 2001 called it unethical that Danish psychiatrists in her view were
too slow to use the newer antipsychotics such as olanzapine and risperidone.64
Other companies also lied blatantly about their
drugs. AstraZeneca presented data at international meetings indicating that
quetiapine helped psychotic patients lose weight, while silencing a trial
showing significant weight increases and while internal data showed that 18% of
the patients had a weight gain of at least 7%.60, 65 Astra-Zeneca propagated other lies.60 It presented a
meta-analysis of four trials showing that quetiapine had better effect than
haloperidol, but internal documents released through litigation showed it was
exactly the opposite: quetiapine was less effective
than haloperidol.
Stigmatisation
It is often assumed that biological or genetic
explanations of mental illness increase tolerance towards psychiatric patients
by reducing notions of responsibility and blame.66 The core assumption of anti-stigma programmes is
that the public should be taught to recognise the problems as diseases, and to
believe they are caused by biological factors like chemical imbalance, brain
disease and genetic factors. However, studies have consistently found that this
disease model increases stigmatisation and
discrimination, e.g. a systematic review of 33 studies found that biogenetic
causal attributions were generally not associated with more tolerant attitudes;
they were related to stronger rejection in most studies examining
schizophrenia.66
The biological approach increases perceived
dangerousness, fear and desire for distance from patients with schizophrenia
because it makes people believe that the patients are unpredictable,66-69 and it also leads to reductions in clinicians’
empathy and to social exclusion.70
It furthermore generates undue pessimism about
the chances of recovery and reduces efforts to change, compared to a
psychosocial explanation. It is therefore not surprising that participants in a
learning task increased the intensity of electric shocks more quickly if they
understood their partner’s difficulties in disease terms than if they believed
they were a result of childhood events.68
Many patients describe discrimination as more
long-lasting and disabling than the psychosis itself, and it is recognised as a
major barrier to recovery.67, 68 Patients and
their families experience more stigma and discrimination from mental health
professionals than from any other sector of society, and there are good
explanations for this. For example, over 80% of people with the schizophrenia
label think that the diagnosis itself is damaging and dangerous, and therefore
some psychiatrists avoid using the term schizophrenia.68
In contrast to the psychiatric leaders, the
public is firmly convinced that madness is caused more by bad things happening
than by genetics or chemical imbalances.68 This lucidity is remarkable, given
that more than half the websites about schizophrenia are drug-company funded.
The public also sees psychological interventions as highly effective for
psychotic disorders (which is also pretty accurate, see Chapter 10), whereas
psychiatrists opine that if the public’s mental health literacy isn’t improved,
it may hinder acceptance of evidence-based mental healthcare (which means
drugs!).
The spending of millions of dollars (largely by
drug companies) to teach the public to think more like biologically oriented
psychiatrists has had four outcomes: more discrimination, more drugs, more
harms, and more deaths.
Hearing voices
One of the key features in the diagnosis of
schizophrenia is that the patients hear voices. There is another approach to
the voices than the disease-oriented understanding that psychiatry offers,
which does not necessarily involve antipsychotic drugs. Many people begin to
hear voices as a result of extreme stress or trauma, and an association called
the Hearing Voices Network exists in several countries (e.g. http://www.hearing-voices.org/),
which helps people who hear voices to live a normal life. Such networks want to
give these people an opportunity to talk freely about the voices, e.g. in
self-help groups, and support them to understand, learn and grow from them in
their own way.
Hearing voices is called auditory
hallucinations. It is not normal, but on the other hand these voices are real
for the person who hears them. They are therefore not called delusions, which
are thoughts about things that are plain wrong, e.g. when patients think they
are Jesus or Napoleon. But the line is not sharp. What should we say about
people who consider themselves normal but believe they have lived before, or
the many who believe that there is life after death?
Danilo
Terrida.
Toran
Bradshaw.
Jake
McGill Lynch.
Shane
Clancy.
Stewart
Dolin.
Candace
Downing.
Cecily
Bostock.
Woody
Witczak and his wife Kim.
Four
brave American women who fight to get the truth out about how dangerous SSRIs
are. From left to right: Mathy Downing, Wendy Dolin, Sara Bostock and Kim
Witczak. Los Angeles, November 2014.
7
Bipolar disorder
The prevalence of bipolar disorder, previously
called manic depression, has increased dramatically. This epidemic has hit
children particularly, where the prevalence rose 35-fold in just 20 years in
the United States.1 The fact that doctors in America make this diagnosis
in children 100 times more often than in the United Kingdom2 illustrates that it is usually a fake diagnosis in
the United States. True mania in children is extremely rare and the explosion
in bipolar is mainly caused by three things:
1) The diagnostic criteria have become much
broader and any child with temper tantrums runs a risk of becoming diagnosed.
2) The US healthcare system often mandates more
serious diagnoses in order to provide reimbursement, which fosters diagnostic
upcoding.2
3) Increased use of psychiatric drugs and
illegal drugs.
4) Mood swings are common in normal people, and
the drug industry has skilfully used this fact to convince doctors that many
people with depression are bipolar.3
This is a tragedy. Bipolar is often treated with
antipsychotics, and, as noted in the last chapter, the rate of development of
tardive dyskinesia is an alarming 5% per year.4 Even “mild” cases of eye blinking or grimacing can
humiliate, stigmatise and isolate a child, and more severe cases may disable
children with painful spasms in the neck and shoulders, abnormal posture and
gait, or constant agitated body movements and a need to frantically pace.
Studies have found that between one-third and
two-thirds of first episode bipolar patients had become emotionally unstable
after they had used illegal drugs such as cocaine, marijuana and hallucinogens.1
Even the American Psychiatric Association has admitted that all antidepressant
treatments, including electroshock, may provoke manic episodes. A US study of
nearly 90,000 patients aged five to 29 years showed that those treated with
antidepressants converted to bipolar at a rate of 7.7% per year, three times
greater than for those not exposed to drugs, i.e. a drug-induced conversion
rate of about 5% a year.5 This is not only an American phenomenon. A
systematic review of trials in children and adolescents showed that 8% of
people treated with antidepressants developed mania or hypomania on drug and
only 0.2% on placebo.6 A systematic review including all ages also found an
8% rate.7 ADHD drugs can also induce bipolar disorder, as they
are stimulants.
These studies show that there is only one
important reason for the huge increase in the prevalence of bipolar disorder:
doctors. It is an iatrogenic epidemic, and Whitaker has estimated that its
prevalence is 250 times more common now than before the drug era.1 Iatrogenic mania
leads to a lot of misery, including extramarital sexual affairs in people who
would not normally have these impulses.8
Lithium became the magic bullet for mania and
bipolar after a physician had reported his successful treatment of ten manic
patients in 1949.1
But he forgot to mention that he killed one of them and that two others became
severely ill. Lithium is highly toxic and its serum concentration needs to be
monitored. Furthermore, this metal is similar to antipsychotics in its effects,
which include emotional blunting, apathy, a decline in cognitive functioning
and impoverished lives with little social contact.1, 9 Patients who come off lithium may end up worse than
ever before, and one study showed that the time between recurrent episodes
following lithium withdrawal was seven times shorter than it was naturally.1
Withdrawal effects include mania and depression, which mislead people into
believing that lithium has been helpful.
In contrast to other psychotropic drugs, lithium
perhaps reduces suicides. However, this effect is uncertain. In a meta-analysis
of four small trials in patients with unipolar or bipolar mood disorders, there
were unusually many suicides; six on placebo and none on lithium among only 241
and 244 patients, respectively.10 As the authors wrote themselves, the existence of
only one or two moderately sized trials with neutral or negative results could
materially change this finding. Moreover, the placebo group could have an
artificially increased risk of suicide because of withdrawal symptoms (a cold
turkey design).
Just like depression and schizophrenia, bipolar
disorder also appears to have taken a more chronic course because of the drugs.
Earlier, about one-third of manic patients suffered three or more episodes in
their lives, but now it is two-thirds, and antidepressants and ADHD drugs may
cause rapid cycling between ups and downs.1
Another artificial psychiatric epidemic is
bipolar II.11 Unlike bipolar I, it has no mania or psychotic features,
and the diagnostic criteria are very lenient. There only needs to be one
episode of depression, and one episode of hypomania lasting more than four
days. This opens up the floodgates for treating vast numbers of patients with
antipsychotic drugs causing tremendous harm at a huge cost; even the old drug
quetiapine cost a staggering £2,000 a year in the UK in 2011.
The diagnosis of hypomania builds on simplistic
questions like, “I drink more coffee.” Adding insult to injury, bipolar I and
II are mixed together in the industry’s clinical trials so that one cannot see
whether antipsychotics have any effect in bipolar II, which is supposed to be
milder. A really smart marketing trick where some patients pay with their lives
to increase the income for an already copiously wealthy industry.
Abilify (aripiprazole), the currently the most
sold drug in the United States, is not only approved for acute treatment but
also for maintenance treatment of bipolar disorder. However, in 2011,
researchers could find only one trial,12 which suffered from the usual problems – cold
turkey in the placebo group, too short a duration, and low completion rate. The
trial was cited by 80 publications, of which only 24 mentioned adverse events
reported and only four mentioned the study’s evident limitations.
In 2001, GSK published a ghost-written clinical
trial report on the use of paroxetine in bipolar adults.13 It was so manipulated that one of the researchers,
who in addition complained that the data from his study were effectively stolen
from him,14 filed a complaint of scientific misconduct. There
was no effect of the drug over placebo but the published paper led people to
believe there was.13 Furthermore, although it is dangerous to use SSRIs
in such patients because of the high risk of induction of mania, and although
manic symptoms was an outcome in the protocol, the published paper said nothing
about this! The evidence indicated that the GSK-assigned prestigious authors on
the published article never reviewed or even saw preliminary drafts of the
paper, but only saw the final edited manuscript just prior to final acceptance
by the American Journal of Psychiatry.
Like other doctors,15 psychiatrists have great difficulty facing the
damaging results of their actions. They may hail the increase in bipolar as
“better” diagnosis,8 and they will almost always postulate that the drug
unmasked the diagnosis,8 e.g. when 12 of 60 children became
bipolar on antidepressants.1 I have heard professors of
psychiatry say this at public meetings. What a perfect way of burying the problems:
We psychiatrists are good, the drugs we use
are good, and our benefactors, the drug industry, are good, so anything
untoward that happens to our patients are entirely due to themselves or their
disease.
“Mood stabilisers”
I only use this term in inverted commas, as it
is so misleading. “Mood stabilisers” are anti-epileptic drugs that don’t
stabilise the mood; they suppress emotional responsiveness by numbing and
sedating people.9
Psychiatrists have never made the precise meaning of this term clear.3
It is not surprising that doctors think anti-epileptics work for mania, as
everything that knocks people down “works” for mania. Like other psychotropic
drugs, anti-epileptics have many harmful effects, e.g. one in 14 on gabapentin
develops ataxia, which is lack of voluntary coordination of muscle movements.16
These drugs increase the risk of suicidal
thoughts and behaviour. The package insert for gabapentin (Neurontin) states
that the risk of suicidality is doubled, and that, “There were four suicides in
drug-treated patients in the trials and none in placebo-treated patients, but
the number is too small to allow any conclusion about drug effect on suicide.”
I think I can offer Pfizer a more reasonable interpretation of these data.
The trial literature in this area has been
distorted to such a degree that – even with psychiatric measures – it is
extreme. Gabapentin is a notorious example. The drug was only approved for very
few people, those with treatment-resistant epilepsy, but Warner-Lambert, later
bought by Pfizer, promoted it illegally and sold it for virtually everything,
including ADHD and bipolar disorder.15
There was huge corruption and doctors willingly
participated in the company’s illegal activities. Almost 90% of influential
thought leaders were willing to tout gabapentin at meetings after having been
updated on the company’s promotional strategies. They were handsomely rewarded
for harming patients, and Warner-Lambert tracked high-volume prescribers and
also rewarded them. A company executive told a salesperson about “Neurontin for
everything … I don’t want to hear that safety crap.”15
There was also huge corruption of the trial
data, which involved selective reporting of trials, statistical analyses and
outcomes that happened to turn out positive.15, 17, 18 Patients were inappropriately excluded or included
in the analyses, and spin made negative results appear positive. Bias was
already introduced at the design stage, highly likely deliberately, e.g. high
doses were used that led to unblinding, although Pfizer recognised that unblinding
due to adverse events could corrupt the study’s validity. The final layer of
corruption was accomplished by ghostwriters: “We would need to have ‘editorial’
control.”
The company insisted on pressing doctors to use
much higher doses of Neurontin than those approved, which meant a higher income
for more harm. I have often wondered how many people Warner-Lambert and Pfizer
killed with Neurontin.
In 2010, a jury found Pfizer guilty of organised
crime and a racketeering conspiracy. Six years earlier, Pfizer had paid $430
million to settle charges that it fraudulently promoted Neurontin for
unapproved uses, but the size of the fine showed that crime pays. The sales
were $2,700 million in 2003 alone, and about 90% was for off-label use.
We see similar problems with other drugs. For
lamotrigine, for example, seven large, negative trials remained unpublished and
invisible for the public, whereas two positive trials were published.19 Two positive trials are enough for FDA approval, and
the FDA regards the rest as failed trials, though it is actually a failed drug.
In my view, anti-epileptic drugs shouldn’t be
used for mental disorders.
A young man’s experience
Australian child psychiatrist Peter Parry has
described how a young American man was destroyed by biological psychiatry.20 Adam came from a screwed-up family, was physically
abused by a sibling, his parents divorced young, and his mother had a lot of
issues. He was 12 when first diagnosed, and had been branded with depression,
anxiety and severe OCD, which had since disappeared. Unfortunately for Adam,
his psychiatrist apparently worked at one of the two US centres that had gained
fame by inventing and marketing a new diagnosis, childhood bipolar disorder.
The psychiatrist could have asked Adam about a lot, but didn’t, and within
three months, Adam was on many drugs, including several anticonvulsants,
several antipsychotics, a couple of antidepressants and lithium.
The documents expressed concern that Adam was
suffering a degenerative neurological disorder, apparently without any
consideration of the cognitive impairing effects of the heavy pharmacotherapy.
Adam’s parents tended to interpret every
solitary behaviour as part of the “disease” and his mother gained a lot of
collateral from it. Adam began to realise that he only had this “disease” at
home in the presence of two or three people who happened to be a part of his
life, but he also realised that if he questioned his craziness, that was
considered part of the “illness.” So he really felt trapped. Many of his
arguments with his mother that landed him in hospital began several hours
earlier as an argument solely about wanting to stop his medicines. There was
always context.
The “mitochondrial disorder thing” was a
disaster. The testing and consultation dragged out for months and at one point
his mother told him they didn’t know if his brain would keep “degenerating” and
said: “You’re gonna die”.
In only four months, he gained over 25 kg and
felt like a cow, in contrast to having almost qualified for the national
swimming championships a year before his diagnosis. Every SSRI he was put on
completely obliterated his sex drive. Early on, an SSRI caused akathisia and
agitation with insomnia and intense frustration but – although
there were no core symptoms of mania such as euphoria, flight of ideas or
grandiosity – the famous psychiatrist diagnosed this as “mania.”
A thousand articles about the “new disease”
contained very little and generally only in passing about trauma and child
abuse, and rates of physical and sexual abuse in cohorts from the two child
psychiatric centres that pioneered the “disease” were far below rates in
community surveys, and emotional abuse appeared to have not been considered at all.
The sessions with Adam’s psychiatrist involved
his mother and the psychiatrist discussing his symptoms, with little space for
him to talk about the physical and emotional abuse by his brother, or the
background to the conflict with his mother.
The treatment Adam received could trigger a
Medical Board investigation in Australia, yet Adam’s legal inquiries indicated
that his treatment would be deemed “standard practice” in the United States!
Inevitably, Adam’s diagnoses had an impact upon
his sense of identity and familial relationships. Identity development can be
severely damaged by a misdiagnosis of bipolar, where one’s every thought and
feeling can cause doubt as to whether it is a part of the self or some
“disease.”
As noted in Chapter 6, a biomedical explanation
is likely to foster greater rather than less stigma and induce prognostic
pessimism.
8
Dementia
There was a public outcry in England in 2014
when its National Health Service had decided to pay the general practitioners
£55 for each case of dementia they diagnosed. The official aim was to “increase
the identification of patients with dementia and to ensure that they and their
families and carers get the support that they need.”1 No one really promised too much with this political
mumbo jumbo.
Dementia is not an emergency, however, so there
is time to find out what care these people need. This can be done discreetly,
without stigmatising people with a diagnosis many fear so much that they
consider severe dementia worse than death. Sometimes, however, a diagnosis can
be useful, as it may help the families understand what is going on; may relieve
the demented persons from being held responsible for their actions and
behaviours; and gives them an opportunity to put their legal affairs in order
before they have lost their capability to think clearly or are declared
mentally incapable.
One doctor talked about crossing an ethical line
that has never been crossed before – cash for diagnoses – and argued that if he
saw someone with memory impairment and called it dementia, he would be
rewarded, but if he called it mild cognitive impairment or depression, he
wouldn’t get paid. He added that the diagnostic process depended on trusting
that the doctor was acting in the patient’s best interests, which must not be
contaminated by such financial incentives.
So, is this blowing for a diagnosis hunt among
the unsuspecting elderly who come to see their doctor for other reasons based
on good evidence? Absolutely not! Hunting for diagnoses and rewarding people
for saddling their horses and lassoing whatever they come across that looks
like a demented person is screening. But no trials that could tell us whether
screening for dementia does more good than harm have ever been performed.2
The UK National Screening Committee issued an
exemplary report six months before the reward for each demented head was
introduced. The report contains everything we need to know to make an informed
decision.2
After having gone through the available tests for dementia and Cochrane and
other systematic reviews about types of support we might consider offering, the
report concludes, as did also the US Preventive Services Task Force, that we
should not screen for dementia or mild cognitive impairment.2
I cannot recall ever having seen an official
report that kills a public health initiative as completely as this one. I am sure
this reflects that it wasn’t written by geriatricians, but by two public health
people not on industry payroll, as geriatricians recommend and use drugs that
don’t work for dementia.
The report leaves no doubt about how foolish the
whole thing is. It dutifully mentions the possibility that “Early diagnosis of
dementia could potentially allow people with dementia and their carers to plan
for the future whilst the patient still retains the capacity to participate in
decision making, and to start any potential treatment earlier.” But what
treatment? This looks like a carefully crafted pharma friendly statement, but
“treatment” can be so much else than drugs, and indeed it should be.
The report says by the end that screening may
harm more people by falsely alarming them than it might help. The facts are
these:2
·
it is only in people aged 85 and
above that a positive test is likely to indicate that a person has dementia;
·
drugs do not reduce the risk of
progression to Alzheimer’s disease;
·
the effects of
acetylcholinesterase inhibitors and memantine are so small that they may not be
clinically meaningful;
·
other types of drugs do not
provide any benefits either;
·
there is no evidence that any
pharmacological intervention results in improvements in quality of life or
well-being;
·
cognitive stimulation leads to
improvements in global cognitive function, self-reported quality of life and
well-being, and in staff ratings of communication and social interaction;
·
physical exercise, massage/touch therapies
and music therapy could perhaps be helpful.
What this tells us is that we should care for
our elderly, give them something meaningful and stimulating to do, and
encourage them to be physically active. We have always known that.
The small effects registered in drug trials are
likely spurious, as they can easily have been caused by unblinding bias because
of the drugs’ conspicuous side effects.
A Cochrane review of three acetylcholine
esterase inhibitors, donepezil (Aricept), galantamine and rivastigmine, didn’t
pay attention to this problem and concluded that, “The three cholinesterase
inhibitors are efficacious for mild to moderate Alzheimer’s disease.”3
Even without considering the unblinding problem,
I would dispute this conclusion. The improvement in cognitive function was 2.7
points, in the midrange of a 70-point scale. This is less than the 4 points the
FDA considers the minimally relevant clinical change.4 We can also compare with the smallest effect that
can be perceived on the Hamilton scale for depression, which is 5-6, although
the maximum on this is scale is only 52 (Chapter 3).
Perhaps it plays a role that the Cochrane review
was written by a statistician who might not know much about drugs, e.g. she
wrote that “donepezil appears to have no serious or common side effects.” This
looks like a sentence in a glossy advertisement for the drug or a trial report
written by Pfizer, the vendor of Aricept, and it is highly misleading. The
harms are both common and serious, and 29% of the patients left the drug group
on account of adverse events, as compared to only 18% in the placebo groups.3
The most common side effects of donepezil are nausea, diarrhoea, not sleeping
well, vomiting, muscle cramps, feeling tired, and not wanting to eat. This is
not what we would want for an old person who might already have problems with
not sleeping well, feeling tired, and not wanting to eat.
The list of frequent side effects in Pfizer’s
product information for Aricept is very long.5 Hypotension and syncope occurs in more than 1% and
when old people fall, there is a considerable risk that they break their hip
and die. A large Canadian cohort study showed that people who took
anti-dementia drugs had almost a doubled risk of hospitalisation for syncope
compared to demented people who didn’t take these drugs, and they had more
pacemakers inserted and more hip fractures.6 Most astonishingly, more than half the patients who
were admitted to hospital for bradycardia were retreated with the same type of
drug after discharge!6 This is yet another illustration that doctors cannot
handle psychotropic drugs safely. Another study, of 5,406 nursing home
residents in the United States with advanced dementia,
found that one third received cholinesterase inhibitors and one fourth
memantine, also a drug used for dementia.7 None of these patients
should have received these drugs.
It is particularly interesting that no benefits
for society could be found for any intervention,2 as we often hear
about the economic burden of dementia and how important it is to intervene.
These political sales pitches – which tend to coincide with general elections –
are vacuous.
A long-term trial of 565 patients with mild to
moderate Alzheimer’s disease that compared donepezil with placebo found no
meaningful effects whatsoever, and the authors concluded that donepezil isn’t
cost-effective, with benefits below minimally relevant thresholds.8 In contrast to other trials, it was publicly funded.
This trial was excluded from the Cochrane review,3 for no good
reason, as far as I can see. The outcomes after three years were similar on
drug and placebo with respect to institutionalisation, progression of
disability, and behavioural and psychological symptoms.8 The trial was published
in 2004, but six years later, Eisai Medical Research’s TV commercials for
Aricept implied that the patients’ cognitive and daily functioning, including
attention, focus, orientation, communication, social interaction and
engagement, will be restored to normal.9 “Don’t wait. Talk to your doctor about Aricept,” as
the ads said. The FDA told the company that it had broken the law.
The English initiative is unethical, costly and
harmful. It impacts negatively on their quality of life to give people a
diagnosis of dementia several years before they or their loved ones would have
detected anything themselves. If left alone, many of them would have died
peacefully without ever having thought about the possible terror of their brain
slowly becoming dissolved. They might also have preserved their dignity and
independence if left undiagnosed. Above all, few of us would want to get pitied
and seen upon as someone who “needs help.”
We should not disrupt the lives of our elderly
with useless diagnoses of dementia. Our prescription drugs are the third
leading cause of death,10 and those who have been lucky enough to have
survived till old age shouldn’t be lured into taking drugs for dementia. We
should remove the drugs from the market to ensure doctors cannot use them.
A 2007 report described what it called the gap
between the number of people diagnosed with dementia and the estimated
prevalence. It found for the 65-69 age group that five people per 1,000 were diagnosed,
against an expected 13.2 I wonder why the Goodness Industry
always sees such gaps as a problem? It’s not necessarily a problem. It’s a gift
to people that so many of them don’t “need help.” But of course there will
always be some who could be helped by their families, but aren’t, as they and
their families have not yet realised that they are demented.
The criteria for the diagnosis have been
broadened, and DSM-5 doesn’t even use the term dementia, but speaks about mild
neurocognitive disorder, which means “Evidence of cognitive decline from
previous higher level of functioning in one or more cognitive domains.”11 I think everyone above 50 would qualify for these
criteria.
Guess where the foolish idea of rewarding
doctors for head-hunting demented brains came from? Yes, it was pushed by the
UK’s Alzheimer’s Society, which is funded by Eli Lilly,12 one of the big pharmaceutical companies committed
to the field.13 The society says that, “Over 800,000 people in the
UK are living with dementia but only 43% of these people currently receive a
diagnosis … This prevents people from accessing the medicine and support that
they not only so desperately need but deserve.” The Society also calls Lilly a
“fantastic partner, and their contribution to the Alzheimer’s Society Early
Diagnosis campaign is highly valued.” I am sure Lilly values the symbiotic
relationship even more.
The Financial Times has
also enlightened us:14 “The high risks involved in Alzheimer’s drug
development have deterred investment, prompting David Cameron, UK prime
minister, to launch a push last year through the G8 group of leading economies
to find ways of incentivising research.”
Okay, I got it. A sure way of incentivising
research is to give us all a diagnosis of dementia or mild cognitive impairment
the first time we forget something. We might even invent childhood mild
cognitive impairment. The political tactics also involved calling the
initiative “case finding,” to avoid it from being shut down by the National
Screening Committee. However, there is no difference between case finding and
screening. Case finding is screening.15
The Alzheimer Society of Canada also receives
industry money and it launched an awareness month campaign in 2012 with the
central message, “The need for an early diagnosis.”16 According to the society’s head, “The earlier you have
access to the drugs that are available … the more likely these drugs are to
help manage your symptoms and potentially even slow down the progression of the
disease.” Industry speak, and utterly wrong. In Quebec they say: Cod always
begins to rot from the head down. But perhaps we should invent a greyish ribbon
and arrange runs for the cure, hoping we won’t get lost on the way because we
have forgotten not only who we are but where we are.
The industry-sponsored trials are extremely
hyped. A rhetorical analysis of 13 such trials of donepezil showed that 7
encouraged off-label use and that phrases such as ‘‘well tolerated and
efficacious’’ were common.17 The authors also found that the average reported
benefit was equivalent to a few months’ change in the progression of
Alzheimer’s. And then we have not even factored in the unblinding bias in the
trials.
The sales of these totally useless drugs bring
in billions of dollars annually, and useless diagnostic tests can likely do the
same. The FDA has approved a first drug/tracer to light up amyloid, for use
with positron emission tomographic (PET) scans, which have a price tag of
$3000-$4000.18 Eli Lilly, the manufacturer, specifies on the label
that the scan does not establish a diagnosis of Alzheimer’s disease or other
cognitive disorders.
So what is the scan for? It is a gross failure
in this area of research that drug development is based on the hypothesis that
Alzheimer’s disease is caused by the formation of amyloid plaques in the brain.
At least four companies, including Eli Lilly, have developed antibodies, and
they substantially reduced beta-amyloid in phase 2 trials.19 However, the phase 3 trials have shown uniformly
negative results for patients, but instead of giving up on a wrong hypothesis
cherished for more than two decades, its acolytes have questioned everything
but the hypothesis. This looks like professional hara-kiri to me, but in mental
health, people can make fools of themselves and have excellent careers at the
same time. It is really odd.
I have spoken to Peter Whitehouse, whose
original neuroscience research led to the development of the major
anti-dementia drugs. He has written a book about the myth of Alzheimer’s
disease where he explains that it’s not a brain disease or a mental illness.20 He now fights for the de-medicalisation of memory
dysfunction and to make people understand that, contrary to what we have
learned, the symptoms we associate with Alzheimer’s are not simply a brain’s
molecular breakdown occurring in old age, and the much touted plaques in the
brain are not related in any simple way to declining memory. Many people with
plaques do not develop Alzheimer’s. I thought we were on safer ground here than
with the myth about the chemical imbalance for mental disorders, but alas,
there is also a heavy mythology around Alzheimer’s that benefits clinicians,
researchers and the drug industry while harming patients. No different from
psychiatry, really.
Pfizer has provided a most bizarre example of a
me-again drug with donepezil.10 It was the biggest player in the
lucrative market for Alzheimer’s disease with over $2 billion in annual sales
in the United States alone.21 Four months before the patent expired, the FDA
approved a new dose, donepezil 23 mg, which would be patent-protected for three
more years, whereas the old doses of 5 and 10 mg were not.
The advertising was directed towards patients
and contained untrue statements, but the scam worked. One would have thought
that doctors, patients and relatives would have been smart enough to use either
20 or 25 mg of the drug to save money, but no. And the FDA failed us again of
course. Its own medical reviewers and statisticians recommended against
approval, as the 23 mg dose didn’t produce a clinically meaningful benefit,
whereas it caused significantly more adverse events, particularly protracted
vomiting. The reviewers even added that the adverse events could lead to
pneumonia, massive gastrointestinal bleeding, oesophageal rupture and death,22 bit this didn’t impress the director of the FDA’s
neurology division, Russel Katz, who overruled his scientists.
What should we then do for demented people? Take
care of them! A systematic review of 33 trials of agitated demented people
showed pretty large effects of care,23 which could be communication skills training,
activities, music, touch, massage and talking to people.
We make people demented with
psychotropic drugs
It’s likely that all psychotropic drugs can
cause chronic brain damage, which is often permanent, and the hallmark of which
is impaired cognitive function (see Chapter 11). Since psychotropic drugs are
so commonly used, a great deal of the dementia we see today is iatrogenic, i.e.
caused by doctors. A 17-year follow up of the Framingham Heart Study found that
use of antidepressants increased the risk of developing dementia by about 50%.24
Benzodiazepines seem to double the risk of
dementia.25 At the peak of their use, 10% of the entire Danish
population could be in treatment.26 In 2007, it was estimated in a National Audit Report
that 560,000 people in England have dementia,27 which suggests that around 50,000 people in England
suffer from iatrogenic dementia. I think it is safe to say that the magnitude
of the problem is about this big, as the other psychotropic drugs also cause
dementia, and as the usage of psychotropic drugs increases with age. The report
also said that the main risk factor for dementia is age, and that
cardiovascular factors are also important.27 Not a single word about drugs
causing dementia, of course.
I have problems accepting that age is a risk
factor for anything. We cannot lower our risk by changing our birth
certificate, so it’s not a modifiable risk factor but an inevitable consequence
of continuing to survive. If anybody insists on calling age a risk factor, I
shall insist that birth is a risk factor, which with 100% certainty leads to
death at some point.
Imagine if we didn’t have drugs and didn’t
even know what they were, and a novelist wrote about a planet where people took
so many drugs that every citizen could be in treatment with 1.5 drugs every
day, from when they were born till they died (which is the drug consumption in
Denmark). Further, that the doctors on this planet made many people demented
with drugs they said would make them happy by correcting a chemical imbalance
in their brain, but which harmed the citizens in many other ways than just
taking away their memories. And that these doctors were then praised and
received a premium for bringing in every patient they had harmed in this way
with their brain-active chemicals. Would you then not say that this plot was
just too fanciful, too unrealistic and too much science fiction, and that you
wouldn’t be interested in reading the novel? I bet you would. But this is what
we have today on planet Earth.
9
Electroshock
Electroconvulsive therapy (ECT) has a long
history.1 Like its predecessors, insulin coma therapy and
metrazole, which also cause convulsions, it could have a short-term effect on
some psychiatric disorders, but the more I read, the more uncertain I become.
The Cochrane review on schizophrenia is from
2005.2 More people improved with ECT than with placebo or
sham ECT, relative risk 0.76 (95% CI 0.59 to 0.98), but this finding is
uncertain. It is barely statistically significant, the trials were small (only
392 patients in 10 trials), and the authors noted that the larger the trial,
the smaller the effect, which suggests that negative trials exist that haven’t
been published.
The review authors tried to reduce bias, e.g.
they only used scores if provided by patients or independent raters or
relatives, not the therapist. But there were many problems with the trials, and
the authors were too generous in my view, as they only excluded trials if more
than 50% of people were lost to follow-up. The authors reported that ECT was
better than sham ECT for the Brief Psychiatric Rating Scale, but there were
only 52 patients in the analysis, and we have no idea for how many patients
data were missing or why. Further, the difference was only 6 on a scale that
goes to 126, which is a good deal below what is a clinically relevant
difference (see Chapter 6).
ECT was considerably less effective than
antipsychotics, e.g. twice as many patients weren’t improved in the ECT group,
relative risk 2.18 (CI 1.31 to 3.63).
The authors didn’t draw firm conclusions about
any short-term benefit, and there was no evidence for any long-term benefit.
Other systematic reviews have also failed to find benefits beyond the treatment
period, for either schizophrenia or depression.3, 4 In my view, it cannot be justified to use ECT for
schizophrenia.
As for depression, a 2003 review found that ECT
was more effective than simulated ECT (6 trials, 256 patients, effect size
-0·91, 95% CI-1·27 to -0·54), corresponding to a Hamilton score difference of
10, and ECT was also better than drugs (18 trials, 1,144 participants, effect
size -0·80, 95% CI -1·29 to -0·29).4 However, the quality of the trials
was poor; most trials were small; the results would likely change materially if
a few neutral studies were identified; the trials rarely used primary outcomes
that were relevant for clinical practice; and the data suggested that ECT
caused cortical atrophy in the brain.4 The authors advised that the
trade-off between making ECT optimally effective in terms of amelioration of
depressive symptoms and limiting the cognitive impairment should be considered.
Researchers often have difficulty using plain language that readers understand.
I think that what they meant was that it’s uncertain whether ECT for depression
does more good than harm.
Psychiatrists believe ECT can be life-saving for
some people, but there are no convincing data in support of this belief,3, 4
whereas we know that ECT can be deadly. The UK review included four
observational studies of total mortality but the results were unclear.4
Another, more comprehensive systematic review found a death rate of about 1 per
1000,3
which is 10 times higher than what the American Psychiatric Association says.3
As it may seem surprising that ECT can kill people, I shall tell you what a
mother conveyed to me before a lecture I gave in Brisbane. The psychiatrists
killed her son with ECT but the doctors succeeded in resuscitating him. When he
woke up, he had severe burns after the procedure and during the next two to
three months he couldn’t say anything people could understand. He is
permanently brain damaged and his social skills are very poor; he cannot live
on his own.
Patients do not share the psychiatrists’ views
on ECT, particularly not in relation to its long-term harms. In 2003, the UK
Royal College of psychiatrists’ fact sheet stated that more than eight out of
10 depressed patients who receive ECT respond well and that memory loss is not
clinically important.5 However, in a systematic review, the patients gave
an affirmative response to the statement “electroconvulsive therapy is helpful”
in only between 29% and 83% of the various studies,5 and the lowest
satisfaction levels were obtained in studies led by patients rather than by
psychiatrists.
Studies of ECT using routine neuropsychological
tests have concluded that there is no evidence of persistent memory loss, but
what is measured is typically the ability to form new memories after treatment
(anterograde memory). Reports by patients of memory loss are about the erasing
of autobiographical memories, or retrograde amnesia, and they are pretty
damning.5
With a strict definition of memory loss, between 29% and 55% of the patients
are affected, and with looser criteria, the range goes from 51% to 79%. Other
studies also suggest that ECT may cause permanent brain damage.3 In the 1940s, it
was acknowledged that ECT works because it causes brain damage and memory
deficits, and autopsy studies consistently found brain damage, including
necrosis.3
To say, as the psychiatrists who authored a
Cochrane review of depressed elderly did,6 that, “Currently there is no evidence to suggest
that ECT causes any kind of brain damage, although temporary cognitive
impairment is frequently reported” and that “ECT seems to be a safe procedure”
is plainly wrong. The official guidance for general practitioners in Denmark on
depression is even worse. It states that, “Many have an unfounded fear of ECT
treatment, although there is no evidence that the treatment causes brain
damage; in fact, there is strong evidence that new nerve cells are formed in
response to treatment.”7 What the guidance really says is that ECT causes
brain damage, as new nerve cells form in response to brain damage!
Some leading psychiatrists admit that ECT is one
of the most controversial treatments in medicine,8 and the UK National Institute for Health and Care
Excellence (NICE) recommends that ECT only be used to achieve rapid and short-term
improvement of severe symptoms, after an adequate trial of other treatments has
proven ineffective, or when the condition is considered to be potentially life
threatening, in individuals with severe depressive disorders, catatonia, and a
prolonged or severe manic episode. The Royal College of Psychiatrists appealed
this decision, as the college found it would prevent patients from receiving
ECT who might benefit, but the appeal was rejected.5
ECT doesn’t seem to have long-lasting beneficial
effects, whereas it causes permanent and serious harm. It “works” by making
people confused and it destroys people’s memories, which are what define us as
humans.
Repeated audits by the Royal College of
Psychiatrists showed that many hospital trusts failed to adhere to the
college’s standards,5 e.g. one audit found that only a third of ECT
clinics met the standards.4 There are also wide variations in
clinical practice and in rates of usage.3-5 In Denmark, forced
treatment with ECT quadrupled in just seven years in the 1990s, but forced
treatment is immensely unpleasant, the patients are very scared, it often
elicits colossal bitterness and anger, and it is perceived by the patients as a
breach of trust.9
In my view, ECT should be forbidden, as it
destroys people and is widely abused as forced treatment. As long as this
hasn’t happened, we must ensure at the very least that no one can be forced to
get it (see Chapter 15).
I saw a very moving documentary in the Danish
Parliament about Mette, a nurse who had heard voices since she was eight years
old and had been a psychiatric patient for 15 years.10 The film won the best foreign film award at Mad in
America’s International Film Festival in 2014. Mette had been diagnosed with
paranoid schizophrenia and had received vast amounts of medicine, 150
electroshock treatments and a disability living allowance. Mette was
stigmatised and surrounded by prejudice but after she decided to reclaim her
own life and leave psychiatry, she achieved some of her greatest goals. Mette
and the filmmaker, and many current and previous patients, psychologists and
psychiatrists were in the audience and I asked why on earth her psychiatrists
had continued exposing her to all these electroshocks when they so obviously
didn’t help her. No one was able to give me a satisfactory reply.
Mette’s story illustrates what I mean by
psychiatrists’ abuse of forced treatments. Even when they so clearly don’t
work, psychiatrists continue out of despair to try them in an endless
progression, which is harmful for the patients’ brains and personalities.
Some psychiatrists have never used electroshock.
One is Ivor Browne from Ireland who reserved the therapy for patients in
lifethreatening situations, which he never encountered in his long career.11 The fact that ECT is never used in Trieste in Italy
also demonstrates that ECT can be dispensed with.
ECT is about as primitive and unspecific a
“therapy” as one can think of. No one who experiences computer problems would
dare send electricity into the computer that changes what is stored there and
how the programmes function. Our brain is the most extraordinary “computer” we
can imagine and ECT surely induces changes, which is the very rationale for its
use. I therefore wonder why anyone would dare to use ECT.
You many think it’s too easy for me to dismiss
both ECT and drugs as treatments for depression, as I am not a psychiatrist and
not depressed. So let me tell you this. I have known many people with
depression, including some very close to me, and have seen how damaging the
treatments have been. I have also studied the scientific literature. Therefore,
should I one day suffer from serious depression, the only treatment I would
accept is psychotherapy.
10
Psychotherapy and exercise
Do as much as possible for the patient, and
as little as possible to the patient
BERNARD
LOWN, NOBLE PEACE PRIZE WINNEF
Psychotherapy is a very broad concept. It comes
in many varieties, there are many schools of thought, and there are thousands
of trials. To start with, I shall point out some key issues.
The underlying theories and the applied methods
are rarely crucial. It is more important that the therapist is intelligent and
empathic and is able to establish a good relationship with the patient, which
makes it possible to arrive at a mutual understanding of what the problems are,
what caused them, and what the best way forward would be. When we respect the
patients and treat them as reasonable beings, they will respect themselves,
which is the first important step towards healing.
Psychiatric drugs keep patients locked in the
patient role and change their personality in ways that are often highly
undesirable for the healing process and also disliked by the patients.1-5 Many patients describe how the drugs take their
feelings away and that they care less about others, which makes it more
difficult for them to learn to cope with life’s challenges. Psychotherapy is
the opposite of this. It is about teaching people to overcome the challenges
they face rather than numbing them with drugs.
Psychiatrists often assume that they should be
the leaders of multidisciplinary teams, as they are the only ones who can
prescribe drugs. However, considering the harms they create with their many
diagnoses and drugs, they should generally not lead such teams. The focus
should be on avoiding psychiatric diagnoses and drugs as much as possible and
on understanding the patients. Psychologists have this expertise, whereas few
psychiatrists get trained in psychotherapy today.
In the long term, the harmful effects of
psychiatric drugs exceed their benefits. This is not so for psychotherapy. A
good psychotherapist can sometimes achieve remarkable results that may last for
a lifetime with no side effects, and although there are bad therapists and it
can go wrong, it is clear to me that the benefits of psychotherapy outweigh any
harms. Furthermore, therapy can often be given in groups, and it therefore need
not be expensive, either for the individual or for society, in contrast to
drugs.
Politicians traditionally argue that there are
so many people with mental disorders that they cannot afford to provide
psychotherapy to the extent they would like, but why don’t we hear the same
politicians criticise the waste of so much money on far too expensive drugs
that are no better than other, off-patent drugs? Psychiatry’s current tunnel
vision with its sole focus on drugs is immensely expensive for our national
economies, as this strategy has dramatically increased the number of
chronically ill people and the number of people on disability pensions.4 It would be far cheaper and lead to considerable
improvements in mental health, if we used drugs very little and provided people
with the psychotherapy they need.
We should remove all reimbursements for
psychiatric drugs and use the vast amounts of money saved to offer
psychotherapy for a small fee, at no additional cost to society.
There is a shortage of professionals who can
provide psychotherapy. However, many people are helped by paraprofessionals who
can be experienced patients (recovery mentors), residents in the area, or
students.6 They ground their therapeutic relationship not so
much in established theory or empirical research but in day-to-day experience
and common sense. They have usually had some degree of training, and are
connected to and supervised by professionals.6 Self-help programmes (see below)
and the help of relatives and friends can also have beneficial effects on
mental disorders and they don’t cost anything.
Since psychiatrists who prescribe pills earn
much more money than those who practise psychotherapy, we will need to remove
this incentive by paying handsomely for psychotherapy.
Some interventions are so simple that we don’t
need to prove in randomised trials that they work. Much of what we can do to
help people with mental problems is in this category, at least when we deal
with relatively mild cases. In more serious cases, we need trials to guide us.
Psychotherapy for anxiety and
depression
Anxiety is a psychological problem and all
parents have experienced that they can lessen their children’s anxiety quite
easily. It doesn’t require a psychotherapeutic education or any knowledge of
receptors and transmitters in the brain to do this, it only requires that you
take an interest in other people.
Shyness is a good example. People have always
drunk alcohol to lessen their shyness in social situations, particularly before
attempting to make successful contact with the opposite sex. In psychiatry,
this common human condition is called social phobia. It was a rare disease
until the drug companies dubbed it social anxiety disorder, which sounded
better for marketing purposes, and invented a market for it. They boosted sales
tremendously, aided by PR firms and their paid allies among psychiatrists and
patient organisations.7 The pool of patients went up from about 2% to 13% –
one in every eight people – handsomely helped by the ridiculous criteria in DSM
that broadened over time.
In this way, shyness became a disease to be
treated with a drug every day. I don’t deny that some people are disabled by
their shyness, but when industry marketing and corruption take over, it becomes
the many that are treated and not the few.
Exposure therapy can be highly effective for
people with anxiety, including those with obsessive compulsive disorder. It
puts participants in direct and prolonged contact with the feared situations
and I shall give an astounding example, which I experienced as a young student
at the University of Uppsala in Sweden. I lived in a hostel and the student
across the corridor, Bengt, was very shy. I couldn’t recall I had ever seen him
with a woman. But one day Bengt started to attend a course with a fine name I
have forgotten. He explained that they went through various exercises, one of
which involved taking off their shirts while sitting on the floor and moving
close together so that their bare backs touched each other. When we heard about
these bodily exercises, the corridor’s most witty guy invented the name “the
hugging course.”
We found it quite amusing and a bit laughable,
but that was before we saw the remarkable result of this group-based psychotherapy.
Sometimes, when I met Bengt in the kitchen in the morning at weekends, he
prepared breakfast for two and smiled in a subtle way as he walked back to that
night’s trophy. Now and then, I caught a glimpse of the woman and noted that it
was a new one each time. When I asked him why he didn’t stick to the one he
already had, he just smiled again. Our shy friend had developed into a
formidable Don Juan, which I appropriately nicknamed him.
There is no doubt that shyness should be treated
with psychotherapy and not drugs. A 24-week trial randomised 375 patients with
social phobia to sertraline or to gradual exposure to the feared symptoms.8 It found a similar effect of exposure and
sertraline, but during an additional six-month follow-up the exposure group
continued to improve, whereas the patients from the sertraline group did not.
This is what we would expect. Put people on drugs and they don’t learn anything
about how to cope with their anxiety. In contrast, psychotherapy usually has
lasting effects.
A Cochrane review of 41 trials in children and
adolescents with mild to moderate anxiety showed very large effects from
cognitive behavioural therapy.9 The odds ratio for remission, compared with waiting-list
controls, was 0.13 (95% CI 0.09 to 0.19), and the reduction in anxiety symptoms
had an effect size of -0.98 (95% CI -1.21 to -0.74). There was no difference
between individual, group and family/parental formats, and cognitive
behavioural therapy wasn’t better than other psychological therapies or
treatment as usual. The outcome was assessed blindly in 32 of the 41 trials.
The effect was smaller in large trials but the largest trials also showed large
effects.
A Cochrane review of psychological therapies for
generalised anxiety disorder in adults also found positive effects.10
A systematic review found a substantial effect
on depression from psychotherapy, effect size 0.67, but the effect decreased
with an increasing number of patients and after adjustment for this it was
0.42.11 A 2013 trial of 469 patients with depression in
general practice that had not responded to drugs found that the addition of
cognitive behavioural therapy had a reasonable benefit, effect size 0.53.12
A Cochrane review of anxiety and depressive
disorders did not find a difference between the results obtained by
paraprofessionals and professionals (psychiatrists or psychotherapists), effect
size 0.09, 95% CI -0.23 to 0.40.6 The paraprofessionals performed far
better than a control condition, odds ratio 0.34, 95% CI 0.13 to 0.88. These
results agree with those from numerous other studies.6, 13
Even people without any professional education or supervision can be very
helpful for patients with mental disorders,13 which begs the question: Can patients also help
themselves? Indeed they can.
An intervention with the funny name
bibliotherapy relies on written texts, computer programs, or
audio/video-recorded material.6 Meta-analyses have found effect
sizes ranging from 0.53 to 0.96 for various problems, including difficulties
with sleep, sexual problems, depression, anxiety, and other mood disturbances.
Psychoeducation is part of many treatment strategies, and it might also be
considered a kind of bibliotherapy.6 A Cochrane review of self-help where
printed materials, audio or video recordings, computers or the Internet were
used to teach adult patients behavioural or cognitive behavioural therapy for
anxiety found a clear effect compared with no intervention, effect size 0.67,
95% CI 0.55 to 0.80 (72 studies and 4,537 participants), but it seemed to be
somewhat less effective than face-to-face therapy.14
A systematic review that compared sleeping pills
of the benzodiazepine type with behavioural therapy found only one randomised
trial where people had used a sleeping diary.15 The authors therefore included 20 before-and-after
studies in their review and the results were pretty convincing despite the weak
design. Both types of treatment had large effects, with mean effect sizes
greater than 0.80, and the only difference was that people fell asleep faster
on behavioural therapy than on drugs.
Simply being kind and empathic may also help
people fall asleep. I once knew a nurse who – when she had time – didn’t give
old people at the hospital ward sleeping pills but caressed them gently on the
neck, whereupon they relaxed and fell asleep. When I was young, I attended a
course where we learned how to relax and fall asleep while resting our head on
our arms across the table. I was convinced it would fail, but I fell asleep
very quickly. Later, I demonstrated the technique to a friend who had trouble
falling asleep. My demonstration of how to relax in all muscles and breathe
slowly and deeply while listening to your own, calm hypnotic voice was so
effective that I fell asleep while I was still talking!
Psychotherapy for obsessive
compulsive disorder
Obsessions are often related to thoughts about
microbial contamination, and typical compulsions are cleaning, washing,
praying, counting or checking the same things many times in a pathological way.16 The quality of life is often severely affected,
also for the family that can suffer immensely from the person’s neurotic
behaviour, as it was called not so long ago. It is therefore fortunate that
behavioural and cognitive behavioural therapy are highly effective.
A Cochrane review of trials in adults found that
psychotherapy resulted in far fewer symptoms than if the patients had received
treatment as usual (waiting list controls), effect size -1.24, 95% CI -1.61 to
-0.87 (seven trials and 241 patients).16 This effect was obtained despite
the fact that, in all but one trial, some participants in both groups were
concurrently receiving drugs.
Another Cochrane review, also in adults, found
an even larger effect compared with a waiting list condition, effect size
-1.65, 95% CI -2.62 to -0.67 (calculated by me), but this result was based on
only three small trials with 87 patients in total.17 The review furthermore showed that psychotherapy
was better than antidepressants (clomipramine or sertraline), effect size
-0.36, 95% CI -0.72 to 0.00 (calculated by me) (three trials with 118 patients).
In contrast to psychotherapy, the effect of
SSRIs is substantially smaller for obsessive compulsive disorder. A Cochrane
review of 17 trials and 3,087 adults found an effect size of -0.46, 95% CI
-0.55 to -0.37 (calculated by me).18
Thus, there is no doubt that obsessive
compulsive disorder should be treated with psychotherapy and not with drugs.
However, in 2014 the chairwoman for the Danish OCD association argued that
patients with OCD, including children, should take antidepressants and should
ignore the tragic stories about people who had committed suicide while on
SSRIs.19 She claimed that SSRIs protect against suicide,
also when used in children, and argued that to ask a patient with OCD not to
take the drug would be the same as asking a diabetes patient not to take
insulin. She said that therapy and follow-up by the doctor was needed to
“support the drug effect the pills have.”
Her article might as well have been written by
Lundbeck. I therefore asked her whether her association accepted industry
money, which wasn’t the case. The association allowed me to publish an article
in their journal where I explained why antidepressant drugs should be avoided
in children and young people.20
My reply caused a former patient to write her
story, which is all too typical.21 Aged 16, with severe OCD, her psychiatrist had
given her a pill saying it stabilised serotonin in the brain. Six months later,
she got suicidal thoughts for the first time. Six years later, she was still on
drugs but her psychiatrists were only interested in renewing her prescriptions.
She persuaded her fourth psychiatrist to taper off the drug, and then one
evening she suddenly noticed the beautiful and joyful song of the birds, for
the first time in years. The happiness she felt was indescribable. She hadn’t
felt any progress before she dropped the pills and declared war on OCD, helped
by her psychologist. Another psychologist told me that his name had been
deleted from the list of therapists at the OCD association and that he
suspected it was because he was against drugs. He also suspected that industry
money was involved, but it seems that the harmful myths the industry and psychiatrists
have created together are so powerful that it is not always necessary to
corrupt patient organisations with money. Words are enough.
The former patient ended her story with a
brilliant idea. She asked if it was fair that pills were subsidised when
psychotherapy wasn’t and suggested:
Couldn’t we introduce an arrangement where we
got money by saying no to happy pills, which we could then use to pay the
psychologist?
Psychotherapy for schizophrenia
The good results obtained by psychiatrist Loren
Mosher by avoiding using antipsychotics (see Chapter 6) were threatening to
other psychiatrists.22 His staff treated people with empathy and respect,
with as little medicine as possible, and they had fewer relapses and functioned
better in society in terms of holding a job and attending school than those
receiving antipsychotics. None of his staff were psychiatrists and it was
offensive to these professionals to suggest that ordinary people could help
crazy people more than psychiatrists with their “wonder” drugs. But Mosher was
the chief of the Center for Studies of Schizophrenia at the US National
Institute of Mental Health, so it wasn’t obvious how he could be stopped. The
NIMH clinical project committee therefore raised doubts about the scientific
rigour of his research team and reduced the funding for Mosher’s project to
such a low level that is was a financial kiss of death.22
This is the standard method used in healthcare
by the silverbacks when the results of a project threatens the status quo and
their carefully pruned self-image. Mosher tried to get around the obstacle by
applying for funding from the NIMH division that dealt with social services,
and the peer review committee was very enthusiastic. However, the clinical
projects committee killed his project right off, as it threatened the very
credibility of academic psychiatry with its medical model of drug therapy. This
was done with derogatory remarks about the study’s postulated “serious flaws” and
with the fatal blow that further funding would only come forward if Mosher
stepped down so that the committee could redesign the project with another
investigator!
This is one of the ugliest manoeuvres I have
ever seen being used against a high-ranked investigator, and a bitter Mosher
said 25 year later that, “If we were getting outcomes this good, then I must
not be an honest scientist.”22 When the committee had killed the
project for good, and it was no longer risky to be a little honest, it came
with a remarkable admission:
“This project has probably demonstrated that a
flexible, community based, non-drug residential psychosocial program manned by
non-professional staff can do as well as a more conventional community mental health
program.”22
They made Mosher an outcast and threw him out of
the NIMH three years later. Others in America who dared question the merits of
neuroleptics learned quickly that this would not advance their career, and NIMH
did not allot any more funds to this type of project.4
However, Mosher’s approach was adopted in
several European countries, and the physicians reported similarly good outcomes
as Mosher’s, with minimal use of drugs.22 Many years later, psychiatrist
John Bola analysed the follow-up data from Mosher’s study that had gathered
dust in the archives and discovered that they were even more positive than what
Mosher had published.22
Mosher’s results have been confirmed in Finland.4
It began in 1969, when psychiatrist Yrjö Alanen instructed his staff to listen
to patients, who despite paranoid utterances told meaningful stories, often
about their difficult past. The core treatment was group family therapy where
the focus was not on psychotic symptoms but on preserving hope by talking about
the patient’s past successes to help strengthen the patient’s grip on life.
Unfortunately, today the Finnish guidelines are rather mainstream in the sense
that they call for the patients to be kept on drugs for at least five years
after a first episode, which is a prescription for disaster.
In Lappland, Jaakko Seikkula continued and the
method became known as Open Dialogue therapy. A study of 75 patients, 30 of
whom had schizophrenia and 45 other psychoses, showed that two-thirds were
never exposed to antipsychotics, and after five years, 80% were working, in
school, or looking for work.4 Seikkula has explained to Whitaker
that if people are put on medication, they lose their grip on life and can no
longer take care of themselves. The idea is therefore to limit the use of
psychotropic drugs by having open meetings where participants share their thoughts
freely with each other. The language used at these meetings is very different
from the language therapists usually use, and they listen more to the patients’
experiences and ideas and also to the family.4 As Danish philosopher Søren
Kierkegaard wrote in the 1800s, we should meet our fellow human beings where
they are, and this also applies to psychiatry.
An important part of the method is that the team
organises a meeting within 24 hours if a psychosis is on its way. Only two to
three new cases of schizophrenia appear each year in western Lappland, a 90%
drop since the early 1980s, which is because the duration of the psychotic
episodes rarely exceeds the six months required for the diagnosis. Spending on
psychiatric services also dropped.
Psychotherapy for schizophrenia seems to be
cost-effective. According to a NICE guideline from 2012, a systematic review of
the economic evidence showed that cognitive behavioural therapy improved
clinical outcomes at no additional cost, and economic modelling suggested that
it might result in cost savings because of fewer hospital admissions.23
There have also been remarkable results in the
United States.4
The most severely disturbed children in California, with histories of sexual
and physical abuse and horrible neglect, which all other institutions had given
up on, were assigned a mentor in a shelter who gave the kids their
personalities back by withdrawing the often multiple drugs they were on and by
establishing emotional relationships with them, which isn’t possible to do with
a heavily drugged person. When a child arrived, the staff didn’t ask what was
wrong with it but what had happened to it. Their behaviour had often worsened
after they were put on drugs.
In randomised trials of getting people back to
life, the Individual Placement and Support model, which is a highly defined
form of supported employment, has had dramatic effects.24 A small trial of a novel seven-month psychosocial
treatment designed to prevent a second episode of psychosis in first episode
remitted patients is also interesting.25 After 12 months, there were fewer relapses,
compared to usual care. This effect was not sustained long-term, perhaps
because the patients in the psychosocial group adhered more to their medication
than those in the usual care group.
It wasn’t until 2014 that the first trial of
psychotherapy in people with schizophrenia who were not on antipsychotic drugs
was published.26 The authors had chosen patients who had all
declined to be treated with drugs. The effect size was 0.46 compared to
treatment as usual, which is about the same of that seen in trials comparing antipsychotics
with placebo, which is a median of 0.44.26’ 27 This drug effect is much exaggerated, however,
because of unblinding bias and because serious harms were inflicted on patients
in the placebo groups who got exposed to a cold turkey (see Chapter 6). This
means:
The effect of psychotherapy is likely better
than the effect of antipsychotics.
Peter Breggin has described what a remarkable
effect empathy, caring and understanding can have in patients with severe
schizophrenia.28 As an 18-year old college freshman without any
mental health training, he volunteered at a state mental hospital and
approached the patients as he would want himself to be approached, with care and
concern, and with a desire to get to know the patients and finding out what
they needed and wanted. He was immediately appalled by how abused and
humiliated the patients were by the authoritarian and sometimes violent staff,
and by the brain-damaging treatments they used, including insulin coma therapy,
electroshock and lobotomy, all the while he was told that these treatments
“killed bad brain cells,” which he found unlikely of course.
Breggin developed an aide programme in which 15
students were assigned their own patient among those who were chronic inmates
considered beyond help – burnt out schizophrenics – who had not yet been
subdued by chlorpromazine. He and his colleagues were able to help 11 of the 15
patients to return home or to find improved placements in the community. During
the next one to two years only three returned to the hospital. The programme
drew national headlines and was praised as an important innovation by the Joint
Commission on Mental Illness and Health in 1961. This was the last
psychosocially oriented document to be issued by NIMH. Ever since, the focus
has been on co-operative efforts with the drug industry to promote biochemical
explanations and drugs.
By taking an interest in the patients in his
private practice, instead of destroying them with drugs and electroshock and
pigeonholing them with diagnostic labels, Breggin never burnt out but has
continued to enjoy his work long after normal retirement age. In my opinion,
this is the recipe for becoming a successful psychiatrist. Since 1968, when
Breggin started his practice, he has never put a patient on a psychiatric drug
except for occasional sleeping pills during a crisis or withdrawal.
In the study from the early 1970s, where
Rosenhan and seven other normal people were admitted to a psychiatric hospital
because they said they heard voices (see Chapter 2), interesting observations
were made about contacts between staff and patients.29 The staff generally avoided continuing conversations
patients had initiated, and by far their most common response consisted either
of a brief reply to the question, offered while they were “on the move” and
with the head averted, or no reply at all. The encounter frequently took the
following bizarre form:
Pseudopatient: “Pardon me, Dr X, could you
tell me when I am eligible for grounds privileges?”
Physician: “Good morning, Dave. How are you
today?” (moves off without waiting for a response).
Physicians, especially psychiatrists, were even
less available than the rest of the staff. They were rarely seen on the wards.
Quite commonly, they would be seen only when they arrived and departed, with
the remaining time being spent in their offices or in the cage.
This happened a long time ago and it might not
be representative of today’s psychiatry, but the problem Rosenhan described is
still with us. Psychiatrists have found out recently that if they talk more
with their patients with schizophrenia, there is less need of forced treatment.
Professor Merete Nordentoft conveyed this positive experience in a TV debate
with me. I wonder, however, why this is something that psychiatrists should
rediscover. Shouldn’t they have known this all along? I also wonder why it is
extremely rare that anyone uses the principle of Open Dialogue.
Exercise
Exercise is good for many things, including
self-esteem, so it could be viewed as a type of psychotherapy. Whatever its
effects on mental disorders it is better to encourage people to exercise than
to take psychiatric drugs. Exercise is recommended in the United Kingdom for
mild depression, and GPs may write a prescription for it, typically for half a
year.4
The patients have found that exercise helps them focus on their health rather
than on their sadness and to stop thinking of themselves as “victims.”
Schoolteachers have good experiences with
exercise, e.g. sending the kids for exercise with music between classes, which
they say can have dramatic effects on those who are at risk of getting an ADHD
diagnosis. It makes them calmer and more attentive in class afterwards, which
is an experience many of us have had.
Exercise also has an effect on depression. There
are few longterm comparisons between SSRIs and exercise, but those that exist
are interesting. In a four-month trial of 156 patients with major depression,
the effect was similar for exercise and sertraline, but six months later only
30% of the patients in the exercise group were depressed, as compared with 52%
in the sertraline group and 55% in a group that was randomised to both exercise
and sertraline.30 The poor result in the combined group was expected,
as it is difficult to perform psychotherapy in drugged people. The differences
were seen despite a low treatment contrast: 64% of patients in the exercise
group and 66% in the combination group reported that they continued to
exercise, but 48% of the sertraline patients also initiated an exercise
programme.
A Cochrane review of exercise found an effect on
depression that was very similar to that reported for SSRIs and for
psychological therapy.31 A systematic review of exercise in old people with
depression found a similar effect (effect size of 0.34).32
There are also trials of exercise as prophylaxis
in general populations of children. In a Cochrane review of trials that
compared vigorous exercise with no intervention, six studies reporting anxiety
scores showed an effect of exercise (effect size -0.48, 95% CI -0.97 to 0.01).33 Five studies reporting depression scores were also
positive (effect size -0.66, 95% CI -1.25 to -0.08). However, the trials were
generally of low methodological quality and highly heterogeneous with regard to
the population, intervention and measurement instruments used.
11
What happens in the brain?
Calling psychiatric drugs
“anti”-something is a misnomer
The deceptions in psychiatry also extend to drug
names. It makes sense to talk about antibiotics, as these drugs cure infections
by killing or inhibiting the growth of microorganisms. In contrast, a chemical
cure for mental diseases doesn’t exist. Antipsychotics don’t cure psychosis,
antidepressants don’t cure depression, and anti-anxiety drugs don’t cure
anxiety; in fact, these drugs can cause psychosis,
depression and anxiety, particularly if used longterm and if people try to get
off them.
These drugs are not “anti” some disease. They
don’t cure us, they simply change us by causing a wide array of effects in
people,1 just like street drugs do. And they are not in any
way targeted, although the drug names suggest they are, for example, there is
nothing selective about selective serotonin reuptake inhibitors (SSRIs). This
term was invented by SmithKline Beecham to give paroxetine an advantage over
other SSRIs, but it was adopted by all companies.2 There are serotonin receptors throughout the body,
and the drugs have many other effects than increasing serotonin, e.g. they can
affect dopamine and noradrenaline transmission and can have anticholinergic
effects.3 The drugs don’t even target depression; they have
similar effects to many other brain-active substances, including alcohol and
benzodiazepines. It is therefore not surprising that a Cochrane review found
that alprazolam, an old benzodiazepine, performed better than placebo for
depression and similarly to tricyclic antidepressants.4 Whether any of these drugs have a true effect on
depression is another matter, and they likely haven’t (see Chapter 3).
Some of the many unspecific effects are called
beneficial by the drug companies, although it can be disputed whether the
patients really benefit, and the rest they call side effects. “Side effect” is
a marketing term used to imply that a problem is minor, although these effects
are often the main ones, seen in most patients, e.g. sexual disturbances with
SSRIs and excessive sedation with antipsychotics. The distinction is wholly
arbitrary, e.g. delayed ejaculation caused by SSRIs can be beneficial for those
bothered by premature ejaculation but detrimental for others, as SSRIs can
prevent ejaculation from occurring altogether.
We know a good deal about how the drugs interact
with receptors in the brain and influence neurotransmitters, but despite quite
different biochemical effects at the molecular level, they work more or less in
the same way, either by suppressing emotional reactions so that people get
numbed and pay less attention to significant disruptions in their lives or by
stimulating them.2, 5-7 It is noteworthy that psychotropic drugs are
developed based on rat experiments and selected if they disrupt the rat’s
normally functioning brain.6
Since psychiatric drugs – just like alcohol,
marijuana, heroin and other addictive substances – alter people’s personality
in significant ways and make it substantially more difficult for them to live a
normal social life and learn how to cope with life’s difficulties, it would be
more adequate, if we insist on using the prefix “anti,” to call them
antipersonality pills or antisocial pills, as many patients get socially
isolated and care less about themselves and others. SSRIs, for example, reduce
the identification of negative facial expressions of anger and fear in human
volunteers,8 and some patients say they feel like living inside a
cheese-dish cover.
My preferred “anti”-term for antidepressants
would be antisexuals, as their main effect is to ruin people’s sex lives. As
other psychiatric drugs, e.g. ADHD drugs and antipsychotics, may also impair
people’s sex lives, we might call the whole lot antisexuals, or anti-life
pills, as they prevent people from living a full life.
Antipsychotics I would call antihumans, as they
impede the ability to live a normal enriching life and the ability to read,
think, concentrate, be creative, feel and have sex. There isn’t much life left
for people on antipsychotics, and some describe it as being a vegetable or a
zombie. It’s no surprise that some patients commit suicide on antipsychotics
and cannot see any hope. We often hear that schizophrenia carries a considerable
risk of suicide but never hear about what this risk is for people who
deliberately avoid taking antipsychotics. We cannot use the randomised trials
to assess by how much antipsychotics increase suicides, as they are flawed by
the cold-turkey design, which artificially increases suicides in the placebo
group (see Chapter 6).
What I have just described illustrates how
powerful drug marketing is. Merely by the language used, it fools us into
believing in all sorts of things that just aren’t true.
The way psychiatric drugs came into widespread
use is also telling. None of the early drugs were developed in a rational
fashion, based on a profound knowledge of biochemistry and receptors, but were
discovered in a haphazard way and came into psychiatry because of their adverse
effects, not because of some specific effect.
As noted earlier, the barbiturates came into
human use after it was discovered that barbital was very effective in putting
dogs to sleep.
The first antipsychotic drug, chlorpromazine, is
a phenotiazine, which are compounds developed in the late 1800s for use as
synthetic dyes. In the 1930s, they were used as insecticides and for swine
parasites.9 In the 1940s, they were found to limit locomotion to
such an extent that rats could no longer avoid electric shocks in escape
experiments. Next, they were used in surgery for their numbing effect to
enhance the effect of anaesthetics. Chlorpromazine was first used as an
antihistamine for allergies but doctors observed that it made patients
emotionally detached and disinterested in anything, which they described as a
chemical lobotomy. When it was tried in patients with mania, the psychiatrists
observed that it induced a profound numbness, an indifference where the
patients didn’t express their preoccupations, desires or preferences and rarely
asked questions, like being separated from the world “as if by an invisible
wall.”
This is also what the patients feel. The
predominant subjective effects reported by patients on the Internet when they
take antipsychotics are sedation, cognitive impairment and emotional flattening
or indifference.10
Chlorpromazine wasn’t called an antipsychotic in
the beginning, but a major tranquilliser or a neuroleptic, and it was acknowledged
that its effects were highly unspecific. Right from the start, Smith, Kline
& French promoted the idea of lifelong treatment with chlorpromazine.11 It was hailed as a great advance, as it kept the
patients docile and quiet, which was very popular with the staff in psychiatric
wards. It was a formidable conflict of interest that the same staff evaluated
whether patients had improved or not, and this conflict of interest clouds
psychiatric research even today. People seem to have forgotten that the US
Joint Commission on Mental Illness and Health stated in 1961 that the principal
purpose of antipsychotics is to make highly disturbing persons more appealing
to those who must work with them.12
The first benzodiazepine was chlordiazepoxide
(Librium), which was synthesised in the mid-1950s based on work on chemical
dyes, just like for chlorpromazine. It was discovered by accident in 1957 that
the compound has hypnotic, anxiolytic and muscle relaxant effects.13
The first tricyclic antidepressant was
imipramine, which is an analogue of chlorpromazine.14 It was developed in an attempt to improve on the
effectiveness of chlorpromazine and wasn’t originally thought to be a treatment
for depression. However, although the drug’s tendency to induce manic effects
was described as being quite disastrous in some patients, this paradoxical
reaction to a sedative led to its testing in depressed patients.11
SSRIs are said to have been developed in a
rational fashion based on knowledge of receptors, but I have my doubts. The
serotonin hypothesis is stone dead (see Chapter 3) and I don’t see these drugs
as any more rational than the others. What we have learned is that a detailed
knowledge of receptors won’t help us when we see patients because very
different drugs may exhibit the same effects.
During my medical studies, I took great interest
in clinical pharmacology and learned a lot about receptors, chemistry, and mode
of action. But one thing really puzzled me, which I just couldn’t figure out.
Why was it that antihistamines, which were used against allergies, also worked
for psychosis? Why was it that so many drugs, developed to fit with a certain
receptor, also worked for completely different diseases that had nothing to do
with that receptor? It took me many years to fully realise how deceptive the
double-blind placebo controlled drug trial is when the outcome is subjective
(see Chapter 3). Today, I have little interest in receptors and drug chemistry,
as the drugs’ side effects often explain why they seem to work for the most
diverse diseases. Unfortunately, no one cares that what we measure in our
trials is mostly bias. The drug regulators don’t care the slightest bit, and
the drug industry and their paid allies among doctors cash in. It is really
foolish that new drugs can be approved if they happened to show an effect in
two placebo controlled trials, no matter how bad they fared in many other
trials, with no demands about avoiding unblinding bias, no demands about how
large the effect should be to make any difference, and no demands about using
clinically meaningful outcomes.
In the old days, antipsychotics were called
major tranquillisers and benzodiazepines minor tranquillisers, which was more
honest than current-day “anti”-disease nonsense, as it was the tranquillising
effect that led to their human use. However, not even this terminology was
okay, as it is a matter of dose how sedated people become.
Despite their humble history, antipsychotics are
nonetheless at the heart of the fairy tale about progress in psychiatry.9
Antipsychotics decrease dopamine levels, and the number of dopamine receptors
goes up to compensate for this. If the drugs are suddenly stopped, the response
can very well be a psychosis, a phenomenon known as oppositional tolerance or
supersensitivity psychosis. A psychosis can even develop during continued
treatment because of this, and may not respond to increased dosages.15
A similar phenomenon is seen with
antidepressants. They increase serotonin levels, which results in a decrease in
serotonin receptors, and sudden drug withdrawal can therefore cause depression.
This rebound effect is also seen for benzodiazepines and lithium.6, 11 After a short while, people can experience worse symptoms than ever
before, even while they are still on the drugs. And if
they try to taper them off, it may become worse still.
Obviously, our brains tolerate poorly being
forced into a new equilibrium with chemicals, and if the new homoeostasis has
lasted for more than a few weeks, people become dependent on them, just like
they do on street drugs.
Genetic studies and transmitter research
Billions of dollars have been spent on finding
genes predisposing to psychiatric diseases and on finding their biological
causes, and this has resulted in thousands of studies of receptors and brain
transmitters. In 2010 alone, NIMH spent $400 million on brain and basic
behavioural research,16 but the output of this enormity of research
investment has been close to none.1
The hype created by the researchers has given
the public a totally wrong impression of what we know about genetics,
transmitters and receptors in relation to mental illnesses. As an example,
genetic association studies in ADHD have not found anything of interest. What
has been reported has been weak associations,17 but the published literature isn’t honest about
this. A review of all articles asserting that polymorphisms of the gene coding
for the D4 dopaminergic receptor are associated with ADHD found that only 25
summaries out of 159 mentioned that this association confers a small risk.18 I had heard several professors of psychiatry say in
interviews that genetic factors were the most important causes for the
development of ADHD, but I didn’t believe it, among other things because ADHD
is not a disease. It took some years before one of the ADHD professors revealed
what the evidence was for this claim. She said there was 80% agreement between
identical twins.19 So, people who are identical are pretty much
identical also when it comes to branding them with the social construct we call
ADHD. Surprise, surprise. This doesn’t tell us anything about ADHD, it tells us
more about that there is observer variation when labelling people with ADHD, as
there wasn’t 100% agreement.
The idea that ADHD is caused by a deficit of the
dopaminergic system, the origin of which is mainly genetic, is also unfounded.17
There are no reliable neurochemical, genetic, neuropharmacological or imaging
data in support of the dopamine-deficit hypothesis of ADHD.17 Further, drugs
that selectively inhibit the noradrenaline transporter and that do not affect
the dopamine transporter are as efficient psychostimulants as those that affect
the dopamine transporter, and L-dopa, which enhances dopamine release and
effectively alleviates parkinsonian symptoms by correcting an overt dopamine
deficit, is not effective in ADHD.17
I cannot go through the vast literature here,
but everything I have looked at, also that which proponents of the theories
wanted me to read because they found it convincing, has been a disappointment
in terms of a genetic or biochemical explanation for the major psychiatric
diseases. For example, a positron emission tomography study in Science that claimed that people with schizophrenia had more
dopamine receptors than controls was later refuted, and also in this area,
investigators have ignored inconvenient findings, e.g. when they found that
receptor density was related to exposure to antipsychotics.11
The believers have modified their dopamine
hypotheses for ADHD and schizophrenia so much along the way to make them fit
with the many contradictory data, that it looks like what science philosopher
Karl Popper called pseudoscience. When a hypothesis is made immune towards
rejection experiments, science ceases to exist.
It is similarly absurd to attribute a complex
phenomenon like depression to one neurotransmitter when there are more than 200
such transmitters in the brain that interact in a very complex system we don’t
understand.17
But biological psychiatrists cannot afford to face the reality, as it would
mean that their house of cards and their attractive funding opportunities would
collapse. I would be thrilled if one day a true defect in the brain was found
in people with a mental disorder that could be fixed with a drug, but it’s not
likely to happen.
Chronic brain damage
Brain imaging studies are central to the many
attempts to make psychiatry look more scientific than it is. Clearly, if it
could be shown that a diseases leads to brain damage, this would be a strong
argument for drug treatment, particularly if similar studies showed that drugs
reduced the damage.
For rheumatoid arthritis, we have drugs that
work, as judged by imaging studies. Disease-modifying agents slow down
progressive joint destruction, but the drugs that accomplish this are dangerous
and sometimes kill patients. In psychiatry, we only have the harmful effects of
the drugs, which not only kill some patients but also damage their brains.
Furthermore, it hasn’t been documented that psychiatric diseases can cause
brain damage. It is absurd that psychiatrists treat millions of patients with
psychiatric drugs for decades or for life under the pretence that they prevent
brain damage.
It wouldn’t be surprising if there were many
brain imaging studies in the psychiatric literature, and if many of these were
flawed, and this is indeed the case. One such study, which a psychiatrist
professor sent me because he found it convincing, couldn’t separate spontaneous
remission of the depression from drug effects, which the authors themselves
acknowledged;20 a randomised trial is needed for this. A large
study of 630 people found that use of antidepressant drugs, and not the
depression, was related to smaller brain volumes and more white matter, but the
differences were small and the study was cross-sectional.21
Brain imaging studies in patients with ADHD have
not been revealing either.17
A 2012 systematic review surveyed the
methodological state of the art in 241 functional magnetic resonance imaging
(fMRI) studies.22 The review found that many of the studies didn’t
report on critical methodological details with regard to experimental design,
data acquisition, and analysis, and many studies were underpowered. Data
collection and analysis methods were highly flexible, with nearly as many
unique analysis pipelines as there were studies. The review concluded that
because the rate of false positive results increases with the flexibility of
the design, the field of functional neuroimaging may be particularly vulnerable
to false positives. Fewer than half the studies reported the number of people
rejected from analysis and the reasons for rejection. Another review used
meta-analysis and found that the false positive rate of neuroimaging studies
lies between 10% and 40%.23
A 38-page report from 2012 written for the
American Psychiatric Association about neuroimaging biomarkers was totally
negative, as it concluded that “no studies have been published in journals
indexed by the National Library of Medicine examining the predictive ability of
neuroimaging for psychiatric disorders for either adults or children.”24
This means that researchers can get the result
they want by manipulating their research. However, despite this huge potential
for bias, studies and meta-analyses – performed by people who, judging from
their papers, clearly didn’t like what they found – have convincingly shown
that antipsychotics shrink the brain.25, 26 They do this in a dose-dependent manner,9, 25
and they also shrink the brain in primates.27 In contrast, the severity of illness had minimal or
no effects.25
There is no reliable evidence that the psychosis per se can damage the brain,28 and although a large 2013 study claimed this,29 it couldn’t separate the effects of treatment from
any possible effect of the disease, which the authors acknowledged. A study
that included patients with first episode psychosis found that short exposure
to antipsychotics could lead to brain shrinkage of the gray matter, again with
no relation to the severity of the illness.30
It is wrong to tell patients they need to
take antipsychotics to prevent brain damage; the fact is that antipsychotics
cause brain damage, not the disease.
Schizophrenia is not a
progressive brain disease, which many psychiatrists think it is.27 They believe the
disease leads to chronicity and social incapacity, but this perception is
influenced by selection bias. The patients they see at their hospitals are the
worst cases, not those that recover, and the truth is that about 40% achieve
functional recovery.28
I have not seen any convincing research showing
that it is the disease that causes brain damage, whereas I have seen convincing
research showing that the medication causes brain damage.25, 28, 31
In paper after paper I have read, the authors didn’t even consider the obvious
idea that it could be the medication and not the disease that caused the brain
damage. This is inexcusable, given what we have known about these drugs for
decades and given that virtually all patients have received medical treatment
for their disease.
Chronic brain damage with persistent personality
changes, e.g. with cognitive decline and emotional flatness long after the
patients have come off the drugs, has been documented for virtually all
psychiatric drugs.5, 31 Chronic brain
damage is related to the length of drug exposure and often worsens when the
dose is increased, whereas it will usually improve considerably when drugs are
tapered off. If it had been the disease that caused the problems, patients
should have become worse when the drugging was reduced.31 In addition to increasing memory problems, common
symptoms for all the drugs include emotional instability with irritability and
angry outbursts, which can be mistaken for Alzheimer’s, terrifying the patient
and the family.31
Antipsychotics kill nerve cells so effectively
that their possible use against brain tumours has been explored.11 The brain damage
affects neurotransmission, including the number of receptors, and there is
nothing strange about this. Hashish, LSD, alcohol and other brain-active
substances may also lead to chronic brain damage and personality changes.
Although the science is convincing, psychiatrists
rarely tell patients that their drugs can cause brain damage. Leading
psychiatrists often say the opposite, that it is important to take
antipsychotics and antidepressants since untreated schizophrenia32 and depression33, 34 can cause brain damage, and that the sooner a person
gets diagnosed and treated, the better the outcome.11 I consider this
lie to be similarly detrimental for patients as the lie about the chemical
imbalance.
Recently, an influential depression researcher
mentioned that depression doubles the risk of dementia and that antidepressants
can help the brain regenerate.34 He referred to a meta-analysis,35 which is typical of the pseudoscience in psychiatry.
It didn’t mention anything about previous treatment, and there wasn’t the
slightest hint that the increased risk of dementia could be due to the
medication, although this is far more likely (see Chapter 8).
Clinical observations confirm that
antidepressants can cause chronic brain damage.36-38 Withdrawal symptoms and other SSRI-related harms can
persist for years after patients have come off the drugs.1, 39 Further, there are many credible reports about
persistent sexual dysfunction in humans,37, 40 which among other things involve genital anaesthesia
and pleasureless orgasms.41 Rats can become permanently sexually impaired after
having been exposed to SSRIs early in life,42 which we have confirmed in our systematic review of
animal studies.43 It is very likely that these effects are caused by
an SSRI-induced inhibition of dopamine transmission. This can also explain why
SSRIs can cause tardive dyskinesia and tardive dystonia, just like
antipsychotics can.40, 44-47 Dechallenge and rechallenge experiments have
confirmed that SSRIs cause these movement disorders.45, 47
Benzodiazepines can also cause chronic brain
damage,6, 31
and a carefully conducted study suggests that they double the risk of dementia.48
ADHD drugs used early in life can also cause
chronic brain damage. Animal studies have shown that this impairment includes
anxiety, depression, less tolerance to stress, less response to natural
rewards, less response to a novel environment and loss of sexual interest and capability.49-52 Children treated with stimulants often develop
atrophy of the brain,53 but, as always, some researchers have argued that it
is the disease that causes the atrophy, which is a pretty bizarre idea, as ADHD
is not a disease but just confirmation that some kids are more active and
irritating than others.
Psychiatrists have often used imaging studies to
justify medicating children with ADHD,54 but these studies are just as flawed as all the
other studies that purport to show that the disease is the problem, not the
drug. The researchers have failed to report whether the patients had received
ADHD drugs, but other researchers have found out that this was indeed the case.17
The few recent studies that studied unmedicated ADHD children have carefully
avoided making straightforward comparisons of these patients with normal
children, in contrast to all the studies where the researchers failed to report
that the children were on drugs. This looks like large-scale scientific
misconduct.
Addiction to psychiatric drugs
One of the best-kept secrets in psychiatry is
that drug treatment leads to dependence, which makes it difficult for people to
get off the drugs again because of abstinence symptoms.31 It is
extraordinary that leading psychiatrists have denied this throughout so many
decades55 and that most of them even today fiercely deny that
SRRIs can lead to dependence. Patients are not as easy to fool as the
psychiatrists, however, and they know all too well that they become dependent
on the drugs, including the SSRIs.56, 57
There are several facts that should make it
obvious to dispassionate observers that treatment with psychiatric drugs can
lead to dependence.
As far as I know, all brain-active substances
are addictive, including alcohol, opioids, barbiturates, benzodiazepines and
street drugs, some of which are the same or very similar to prescription drugs.
And withdrawal symptoms have been demonstrated empirically for all psychotropic
drugs.
Furthermore, given the mechanism of action, we
can predict that dependence must occur. Brain-active substances up- or
down-regulate receptors and create a new homoeostasis (equilibrium), which
means that the brain no longer functions normally. Therefore, if the disturbing
agent is suddenly removed, withdrawal symptoms occur in some people. We know
about this also from other areas of clinical pharmacology, and we often call it
a rebound effect. If a proton pump inhibitor prescribed because of heartburn is
suddenly stopped, the dyspeptic symptoms may become even worse than before the
drug was started. These mechanisms get many patients hooked on a drug for life,
as the withdrawal symptoms make them believe that they still need the drug.
The deception about the dependence problem
wouldn’t have been possible if it wasn’t for a massive cover-up to which the
drug industry, drug regulators and doctors have all contributed. This unholy
alliance has a long history. In the 1930s, addiction to barbiturates wasn’t
recognised and doctors pointing this out were ignored.58 It took 40 years before the addiction problem was
finally accepted by the UK Department of Health and it was realised that the
reason people continued with barbiturates indefinitely wasn’t that they were
ill but because they couldn’t stop them without great suffering. In 1955, the
United States produced so many barbiturate pills that 7% of the population
could eat a pill every day. It looked like the ultimate realisation of the
dream of a quick fix for life’s pains, which Aldous Huxley described in 1932 in
Brave New World where the citizens could take Soma
pills every day to give them control over their lives and keep troubling
thoughts away. In his time Soma pills were the barbiturates. Today TV
commercials in the United States urge the public to do exactly the same. They
depict unhappy characters that regain control and look happy as soon as they
have taken a pill.59
In the 1960s the benzodiazepines got their turn.
Doctors believed they were harmless and prescribed them for almost anything,
and Hoffman-La Roche pushed diazepam (Valium) to become the top-selling drug in
the world.58
Sales of benzodiazepines were so high that 10% of the Danish population could
be on them,60 which is extraordinary since the effect disappears
after a few weeks because of development of tolerance. The companies denied for
decades that benzodiazepines cause dependence, and although serious dependence
was documented already in 1961, it wasn’t generally accepted until more than 20
years later.61 The collective denial was huge. Even in 1980, the UK
drug regulator concluded, based on submitted reports of adverse events, that
only 28 people became dependent on benzodiazepines from 1960 to 1977. The true
number is more likely to have been around half a million.
After the authorities, in the 1980s, at long
last admitted that the huge consumption of benzodiazepines was a public health
disaster and had started to warn against them, usage went down.60 At the same
time, the American Psychiatric Association tightened the criteria for substance
dependence, very conveniently just before SSRIs appeared on the market.61
I have often wondered how much corruption was involved, as this change in
criteria must have been worth billions for the companies.
The change was really major. Before 1987
dependence meant development of tolerance to a substance or withdrawal
symptoms, which is how most people would define it. But from 1987 at least
three criteria out of nine were needed and a time criterion was also added.61
It was now totally obscure whether a person was
dependent or not and, as usual in the DSM manual, no one can remember all this
or apply the criteria consistently from case to case. There is a lot of
arbitrariness, and judgments and grades are involved. For example: “A great
deal of time” (how much?); “substance often taken” (how often?); “Important
social, occupational, or recreational activities given up” (what is important
and who decides on this?); “Frequent intoxication or withdrawal symptoms” (how
frequent?); “Substance often taken to relieve or avoid withdrawal symptoms”
(this criterion is meaningless; if a patient misses just one dose of
paroxetine, it can elicit withdrawal symptoms – does “often” mean taking three
paroxetine pills a day?).
The new criteria took the power of decision away
from patients, as some of them require judgments by others, e.g. whether the
patients “fulfil major role obligations at work, school or home.” I don’t
dispute that judgments by others can be needed, e.g. if a heroin addict denies
his dependence, but I firmly believe that patients in drug treatment should
speak for themselves.
The time criterion is awfully foolish. Symptoms
should have persisted for at least one month or should have occurred repeatedly
over a longer time period. Very many patients who are dependent on drugs don’t
fulfil the time criterion. They might have tried to stop a few times but
quickly resumed treatment and decided never to try again because of the
terrible abstinence symptoms they experienced. Such patients are not dependent
according to the time criterion, although they are the ones who are the most dependent!
The new criteria are a smokescreen that serve to
deflect attention away from the fact that SSRIs cause dependence. We found in
our research that withdrawal symptoms were described with similar terms for
benzodiazepines and SSRIs and were very similar for 37 of 42 identified
symptoms,61
but when Lundbeck was interviewed about our findings, the company denied that
people could become dependent on SSRIs.62
The worst argument I have heard – also from
professors of psychiatry – is that patients are not dependent because they
don’t crave higher doses. If that were true, then smokers are not dependent on
nicotine because they don’t increase their consumption of cigarettes!
To describe similar problems as dependence for
benzodiazepines and withdrawal reactions for SSRIs is irrational, and for the
patients it’s just the same. It can be very hard for them to stop either type
of drug. In a survey, 57% of 500 Danish patients agreed to the sentence: “When you
have taken antidepressants over a long period of time it is difficult to stop
taking them,”56
and in another survey, 55% of 1,829 patients in New Zealand taking
antidepressants mentioned withdrawal effects, which 25% described as severe.5
Drug regulators, the extended arm of
industry
It is difficult to see much difference between
the regulators and the regulated. It took more than a decade after drug
agencies had the information about dependency before they warned about it, both
for benzodiazepines and SSRIs, and the process was characterised by denial,
downplaying of harms and even misrepresenting them.58, 61, 63 The UK regulator described withdrawal reactions
after SSRIs as generally rare and mild, but independent researchers showed that
the regulator had classified 60% of the “mild” reactions as moderate and 20% as
severe!63
The trick with the new DSM criteria for
dependence was uncritically accepted by the authorities, which relied on them
when they denied the dependence potential of SSRIs. For example, the UK
regulator stated in 1998 that use of SSRIs doesn’t lead to dose escalation and
drug-seeking behaviour,61 as if this would prove they
weren’t addictive. Drugs can be addictive without having these properties, and
it wasn’t even correct that SSRIs don’t lead to drug seeking behaviour. They
do, as the same regulator acknowledged in 2004 when it even admitted that the
SSRIs met the new, narrow criteria for dependence.
Studies conducted by Beecham on paroxetine in
the mid-1980s before the drug came on the market showed that it could produce
dependence in healthy volunteers but, despite being warned by senior figures in
the field, the company did nothing and the studies weren’t published.2
A few years after the introduction of SSRIs,
concern was raised again about dependence. However, the drug companies and
their paid allies among psychiatrists confused the issues and tended to
interpret any withdrawal reactions as relapse.61 Paroxetine was
even marketed directly to consumers as “non-habit forming” in the United States,61
and on the back of British packets of fluoxetine, this message appeared: “Don’t
worry about taking Prozac over a long period of time – Prozac is not
addictive.”2
As recently as 2000, the European Medicines
Agency firmly stated that, “SSRIs do not cause dependence.”58, 61
However, the agency also noted that SSRIs “have been shown to reduce intake of
addictive substances like cocaine and ethanol. The interpretation of this
aspect is difficult.”58 The interpretation is only difficult for those who will not see. In 2003 the World Health Organization
published a report noting that three SSRIs (fluoxetine, paroxetine and sertraline)
were among the top 30 highest-ranking drugs for which drug dependence had ever
been reported!58
The drug companies also did what they could to
obscure the issues,61 and the psychiatrist silverbacks on drug company
payrolls have been immensely useful for the drug companies, as they have helped
them hook more than one hundred million patients on drugs most of them didn’t
need. First the barbiturates, next the benzodiazepines, and now the SSRIs. And when
problems arise, psychiatrists and companies use the same tactic: Always blame
the disease, never the pills,2, 5, 64 which the next section is about.
Drug dependence is often
misinterpreted as relapse of the disease
As stated earlier, all psychotropic drugs can
cause dependence.31 It can be useful to divide withdrawal symptoms into
two phases: the immediate withdrawal phase consisting of new and rebound
symptoms, occurring up to six weeks after drug withdrawal, depending on the
drug elimination half-life, and the post-withdrawal phase, occurring after six
weeks,6, 31, 39
and which may sometimes last for years.1, 39, 65
Many people cannot get off SSRIs even when slow
tapering is attempted. Out of 20 patients with panic disorder and agoraphobia
who had been treated successfully with behavioural therapy, nine had withdrawal
symptoms, which subsided within a month in six of them.66 In the three other patients, who had all received
paroxetine, the symptoms persisted and all three developed cyclic changes in
mood that are characteristic for bipolar disorder but which they had not had
before. Other studies have confirmed that about half the patients experience
withdrawal symptoms.56, 67, 68
It is pretty clear in this case that when
patients treated successfully with behavioural therapy get symptoms when a drug
dose is gradually reduced, it is likely to be withdrawal symptoms and not a
return of their panic disorder. Unfortunately, psychiatrists and other doctors
have a pronounced tendency to interpret withdrawal symptoms as disease
symptoms, and the rating scales they use for grading the severity of the
disease mislead them, as they often contain items that are withdrawal symptoms.11
Doctors therefore put pressure on patients who try to stop taking drugs to
continue with them.
I once explained at a large meeting for
psychiatrists that many patients have difficulty stopping antidepressants, but
to my big surprise a professor said he had no trouble withdrawing patients
successfully. This might be because it is so common to interpret abstinence
symptoms as relapse of the disease. If you always do that, you won’t have any
problems, as you simply put those patients back on full dose who cannot
tolerate the withdrawal symptoms. But it’s a tautology. Somewhat like: “This
drug works for all patients with hysteria, and if it doesn’t work for some
patients, it’s because they don’t have hysteria.”
Stuart Montgomery from the UK, who has numerous
financial ties to drug makers, seems to interpret all
withdrawal symptoms as relapse.69 He studied 135 patients with depression who had
responded to eight weeks of treatment with paroxetine and whom he randomised to
drug or placebo for one year. Although paroxetine was
withdrawn abruptly – cold turkey – in the 67 patients randomised to placebo, he
didn’t mention a single withdrawal symptom in his paper! After having
inflicted tremendous harms on the placebo group patients, the authors concluded
that they had confirmed “the reports from acute studies that the side-effects
on paroxetine diminish with time until they become indistinguishable from
placebo.” It’s unbelievable. One of the patients committed suicide by hanging
while on paroxetine during the first eight weeks.
Internal Pfizer documents show that Montgomery
deliberately avoided to inform the drug regulator for which he worked that he
also worked for Pfizer at the same time.58 He informed Pfizer about how the
regulator had reasoned in relation to its application for sertraline and
advised the company about what it should do in order to get the drug approved.
Others are more thoughtful but may still lead
their readers astray. A 2003 systematic review in the Lancet
reported on 4,410 patients in 31 trials who had been randomised to continue on
active drug or placebo after having responded to an antidepressant drug.70 The relapse rate was 18% for patients who continued
on active drug and 41% for those who continued on placebo. This seemingly
impressive effect made the authors conclude in their abstract that “continued
treatment with antidepressants would benefit many patients with recurrent
depressive disorder.”
Most people only read the abstract so they won’t
know that the authors were more cautious in the main text. They explained that
the increased risk of relapse in the placebo group might be due to a withdrawal
reaction rather than a relapse. They also noted that this problem has been
identified for lithium, for which acute withdrawal leads to manic relapse, and
that trials with a withdrawal design (often called maintenance studies or
relapse prevention studies) quite clearly inflated the apparent efficacy of
lithium. In their own meta-analysis, they found that even after one to three
years, there was a clear difference between the active group and the placebo
group. However, some patients suffer from withdrawal symptoms for years, which
would be expected to increase the risk of a new bout of depression, but it
would then not be a true depression but a druginduced withdrawal depression.
Furthermore, there were rather few relapses in this time period and pure chance
could therefore also have influenced the findings. What might be most
important, a follow-up of one to three years is too short (see the
schizophrenia withdrawal study below).
It’s tricky that withdrawal symptoms and disease
symptoms can be the same. If a patient reduces the dose of an antidepressant
and becomes depressed, it doesn’t necessarily mean that the disease has come
back. Two hallmarks of withdrawal-induced, depression-like symptoms are that
they usually come rather quickly and usually disappear within hours when the
full dose is resumed, whereas it takes weeks before the patients get any better
if they have a true depression.
A trial of 242 patients with remitted depression
illustrates these diagnostic difficulties.71 The patients had received open maintenance therapy
with fluoxetine, sertraline, or paroxetine for four to 24 months, after they
had become well. They then suddenly had their therapy changed to a double-blind
placebo for five to eight days, but the timing of the treatment interruption
was unknown to the patients and clinicians. The investigators had developed a
43-item list based on withdrawal symptoms reported in the literature, and after
the placebo period patients were asked if they had experienced any of these.
This checklist approach will tend to exaggerate withdrawal symptoms, and the
study was funded by Eli Lilly, the maker of fluoxetine, which had an obvious
interest in showing that fluoxetine causes fewer withdrawal symptoms than the
two other drugs because of the very long half-life of its active metabolite,
about one to two weeks.
But the results are nevertheless interesting.
The three most common withdrawal symptoms were worsened mood, irritability and
agitation (Table 11.1), which have nothing to do with relapse of the depression
and, as expected, relatively few people had symptoms on fluoxetine. Out of 122
patients on sertraline or paroxetine, 40 had an increase in their Hamilton
depression score of at least eight, which is a clinically relevant increase.
There would have been many more withdrawal
symptoms if the drugs had been withdrawn for two to three weeks, but in fact 25
of the 122 patients fulfilled the authors’ criteria for depression. Thus, this
study shows why most doctors get it wrong when they think the disease has come
back. Think about it. How many are likely to get a new depression in a random
week in a group of 122 patients whose depression has been in remission for four
to 24 months? Not 25 patients but perhaps one patient!
Table
11.1. Withdrawal symptoms in patients with remitted depression during a 5-8-day
placebo period 4 to 24 months after remission.
In six short-term treatment trials, in which
treatment was stopped abruptly and replaced by placebo at a time unknown to the
investigators and patients, Eli Lilly reported withdrawal symptoms in 44% on
duloxetine and 23% on placebo.68
People may get terrible symptoms when they try
to stop, both symptoms that resemble the disease and many others including some
they have never experienced before and which can frighten them, e.g. electric
shock sensations in the head after SSRIs.72
Leading psychiatrists don’t understand any of
this, or they pretend they don’t. Virtually all the silverbacks have
interpreted the maintenance studies of antidepressants and antipsychotics as
meaning that these drugs are very effective in preventing new depressions and
psychoses,9, 73, 74 and that patients should therefore continue taking
the drugs for years or even for life. In Denmark, it is a national goal that
over 90% of patients with schizophrenia should be in drug treatment. This is a
national tragedy.
Psychiatrists also say that depression has a
more chronic course today than in the past. For example, the American
Psychiatric Association’s Textbook of Psychiatry from 1999 stated that not long
ago most patients would recover from a major depressive episode, whereas now “depression
is a highly recurrent and pernicious disorder.”5
Psychiatrists overlook the fact that it is
themselves that have created this epidemic by their systematic denial of the
substantial role abstinence symptoms play and their reluctance to get patients
off their drugs. Since there is no evidence that mental illness is chronic and
lifelong, there is no scientific justification for the lifelong use of
psychiatric medications. The apparent “chronicity” in mental disorders is an artefact
of the medications themselves.1 This was shown in a study of 172
patients with recurrent depression who had been in remission for at least 10
weeks since their last episode.75 Of those who continued to take drugs, which they
were supposed to do according to international guidelines, 60% relapsed in two
years. The relapse rate was similar for intermittent users (64%) whereas it was
46% in those who did not take drugs and only 8% in those who did not take drugs
and received psychotherapy. Differences in disease severity could not explain
these results, so they were not due to confounding by indication.
A careful analysis of 66 withdrawal studies of
antipsychotics showed what the main problem is with such studies.9, 76 The relapse rate was three times higher in the
groups with abrupt withdrawal than in the gradual-withdrawal groups!
As I have explained throughout this book,
psychiatric drugs, if taken for more than a few weeks, create the diseases some
of them have a short-term effect on, or other or even worse diseases, and acute
conditions become chronic.2, 5, 6 36, 77, 78 This has been brought up time and again over the
last 30-40 years, but no matter how strong the new evidence, leading
psychiatrists every time swept it under the rug as quickly as possible.5, 9
It is too painful for them that, after they left the unscientific
psychoanalysis behind, they must now accept that biological psychiatry, which
on the surface made their speciality look as scientific as internal medicine,
has not kept its promises.
Maintenance (withdrawal) studies were done for a
good reason, to find out for how long patients need to be on drug. However,
they are highly misleading if they are short-term. There are very few long-term
studies, but one such study in 128 patients with schizophrenia is illuminating.79 Remitted first episode patients were randomised to
dose reduction or discontinuation, or to maintenance therapy, for two years,
after which the clinicians were free to choose the treatments they felt the
patients needed.
Seven years after the randomisation, 103
patients could be located. The short-term results showed that two years after
randomisation, more patients had relapsed in the dose reduction/discontinuation
group than in the maintenance group (43% versus 21%). However, after seven
years, there was no difference (62% versus 69%). Furthermore, relapse was not
the study’s primary outcome. It is much more important that patients recover
from their schizophrenia, and more patients had recovered in the dose
reduction/discontinuation group than in the maintenance group after seven years
(40% versus 18%). This happened despite the fact that the dose in last two
years before the seven-year cut-off was 64% higher in the maintenance group,
and that fewer patients had stopped taking their drug completely at seven years
in this group (six versus 11 patients). Thus, the patients who had their dose
decreased or discontinued fared much better in the long term than those who
continued taking their antipsychotic drug.
A large meta-analysis of the placebo controlled
trials showed that the apparent effect of continued treatment with
antipsychotics on relapse prevention decreases over time and is close to zero
after three years.80 Moreover, most of these trials are flawed, as
patients on placebo were exposed to cold turkey withdrawal of their drug.
There is a Cochrane review of intermittent drug
treatment for schizophrenia, but it isn’t relevant, as the results from all
included trials are short term.81
It is really bad medicine to keep patients on
their drugs for years based on the false belief that this improves their
prognosis.
The chemical imbalance nonsense
When I lecture for psychiatric patients and ask
them whether they have been told that they need a drug to fix a “chemical
imbalance” in the brain, roughly half of them confirm this. Quite often, they
have also been told that this corresponds to being a patient with diabetes
needing insulin. The fairy tale comparing antipsychotics and antidepressants
with insulin was invented by psychiatrists in the 1950s,5, 11
and at the same time, the psychic energizers changed name to antidepressants.5
The “drug revolution” in psychiatry has even been likened to the introduction
of penicillin but, as David Healy has dryly noted, in contrast to penicillin,
there are more dead bodies in the drug groups than in the placebo groups of the
trials.5
The chemical imbalance story is being told about
all psychotropic drugs, also for benzodiazepines, but it is a blatant lie.1, 5, 9
It has never been documented that any of the large psychiatric diseases is
caused by a biochemical defect and there is no biological test that can tell us
whether someone has a particular mental disorder.
As an example, the idea that depressed patients
lack serotonin has been convincingly rejected.2, 82, 83 Some drugs that decrease
serotonin also seem to work for depression,2, 5 e.g. tianeptine,
and the Irish drug regulator banned GSK from claiming that paroxetine corrects
a chemical imbalance. Furthermore, mice genetically depleted of brain serotonin
weren’t depressed but behaved like wild-type mice in the wild.84 There is much else that speaks against the chemical
imbalance story, e.g. it takes weeks before antidepressants seem to work,85 and the effect – if any – comes slowly and
gradually, whereas monoamine levels in the brain increase in one to two days
after the start of treatment.83 Further, why should these drugs
“work” in social phobia, which is not considered a lack-of-serotonin disease?83
Nonetheless, until 2003, the UK drug regulator
gave the industry a helping hand by propagating in patient information leaflets64
the false and totally undocumented idea about lack of serotonin as the cause of
depression.
Dopamine metabolites are normal in patients with
schizophrenia, but when they are medicated, their dopamine receptors increase
by about 50% in response to the drugs’ lowering of dopamine.9
In the beginning, when I explained to doctors
that many patients had been told they had a chemical imbalance, I was often met
with angry responses demanding that I documented my so-called allegations. They
obviously didn’t like to admit that they lied to their patients. I referred to
what patients, caregivers and others had told me, and to websites where
patients share their experiences, but this was taken to mean that I didn’t know
what I was talking about, as if it didn’t have any value to listen to patients.
When I argued that the documentation on the Internet is very convincing because
patients rather consistently have had the same experiences, I was told that
these were just anecdotes which, moreover, had not been published in a peer
reviewed journal. As if that would make any difference!
The organised denial is deeply disturbing. In
the Danish study of 500 depressed or bipolar patients I have quoted earlier,
80% agreed with the sentence: “Antidepressants correct the changes that
occurred in my brain due to stress or problems.”56
When – pretty rarely, I must say – psychiatrists
admitted that it has never been demonstrated that any psychiatric disease is
caused by a chemical imbalance, they added that it’s just a metaphor, as if it
doesn’t matter to use metaphors. It certainly does. Doctors use this metaphor
to persuade patients, who feel badly about their medication and want to quit,
to continue their suffering in the hope of obtaining some effect later. A
Danish silverback, Professor Poul Videbech, illustrated this recently at a
meeting where I argued that far too many people are in antidepressant
treatment. He said in front of 600 people, “Who would take insulin from a
diabetic?” and used the same allegory in an interview. So I suppose he means
it.
People have told me about medical students who
were put on an antidepressant the first time they consulted a doctor because
they had difficulty with their studies, with the false messages about
correcting a chemical imbalance like with insulin. When the students tried to
stop and got abstinence symptoms, they were told it was their depression that
had come back. In one case, the psychiatrist said bluntly at the very first
visit that the student should take the pills for life! When we deal with cancer,
we know it’s important that patients don’t lose hope, but in psychiatry, where
hope is much more essential, as it’s so important for recovery, some doctors
take the hope away by saying the pills are for life.6 But there are no
“rest-of-your-life” drug trials, so it’s pure speculation, and wrong, too. An
important reason why most studies only last a few weeks is that many patients
drop out of them early, as they don’t like the drugs.
It is difficult not to get angry when confronted
with such stories. In 2003, six US psychiatric survivors were also angry. They
announced a “fast for freedom” and sent a letter to the American Psychiatric
Association and other organisations stating that they would begin a hunger
strike unless scientifically valid evidence was provided that the various
stories the public had been told about mental disorders were true.5
They asked for evidence that major mental illnesses are biologically-based
brain diseases and that any psychiatric drug can correct a chemical imbalance.
They also required the organisations to publicly admit if they were unable to
provide such evidence.
The medical director of the American Psychiatric
Association tried to get off the hook by saying that, “The answers to your
questions are widely available in the scientific literature.” The hunger strike
ended when people started getting health problems, but it was clear that the
Association bluffed when it stated in a press release that it would not “be
distracted by those who would deny that serious mental disorders are real
medical conditions that can be diagnosed accurately and treated effectively.”
The Catholic Church couldn’t have invented a better bluff, if people had
required proof that God exists: “We priests and cardinals will not be
distracted by those who would deny that God exists and knows about people’s
problems and can treat them effectively.”
To a considerable extent, psychiatry is a
pseudoscience, and the hoax about the chemical imbalance should be dealt with
in the courts, as it looks like consumer fraud.
12
Withdrawing psychiatric drugs
It is not only dangerous to start taking
psychiatric drugs, it can also be dangerous to stop them. Withdrawal from
psychiatric drugs should be done carefully under experienced clinical
supervision.
PETER BREGGIN1
The worst drug epidemic ever
As explained in the last chapter, psychotropic
drugs don’t fix a chemical imbalance, they create one, which is why it is so
difficult for many patients to come off the drugs again.
It is scary how many patients continue for years
on end with SSRIs, particularly when considering that naturalistic studies have
not found any benefit from long-term use.2 In 2014 Finnish TV interviewed me for a documentary
about depression, and the journalist had usage data from the Social Insurance
Institution. Of 260,322 people who were on SSRIs in 2008, many were also on
them the following years (some might have been temporarily off them). Even five
years later, 45% still took them (Figure 12.1). What is most worrying is that
the curve flattens out, which suggests that many patients are hooked on the
drugs for life.
In New Zealand, 52% of patients reported having
taken their antidepressants for more than three years,3 and in the United States, 60% were still taking
their antidepressant after two years, just as in Finland, and 14% had taken the
drug for at least 10 years.4 Overall usage for women aged 40-59 was a staggering
23%, and only 29% had seen a mental health professional within the last year.
Such data indicate that the usage is out of control. If we conservatively
assume that 30% of the patients take the drugs because they cannot get off
them, it means that we have over 100,000 drug addicts in Denmark on SSRIs,
which is about the same number of drug addicts we have on benzodiazepines.
Figure
12.1. Number of people out of 100 in Finland who were still taking an SSRI up
to five years after starting a prescription.
General practitioners contribute the most to the
misery. They deliver more than 90% of mental healthcare.5 In Australia, they prescribe about 90% of the
antidepressants, most often for mild depression,6-8 despite the fact that there is international
consensus that they don’t work and shouldn’t be used for mild depression, and
71% of the antipsychotics are also prescribed by them.7 I have heard an influential Danish general practitioner
explain at a meeting that antidepressants are helpful as bridge therapy in mild
depression before the patients can get an appointment for psychotherapy. This
is very bad medicine.
To be on drugs year in and year out has little
to do with having a disease and a lot to do with having a drug dependence.
People with uncomplicated episodes of major depressive disorder (lasting no
longer than two months and not including suicidal ideation, psychotic ideation,
psychomotor retardation, or feelings of worthlessness) are hardly more likely
to have a further episode within 12 months than people with no history of major
depressive disorder, and the relapse rates are very low (3.7% versus 3.0%).9 Historical data are also revealing.10 Of Emil Kraepelin’s 450 “depressed-only” patients
from about a hundred years ago, 60% experienced only a single episode of
depression, and only 13% had three or more episodes; similarly, more than half
of 2,700 depressed patients admitted for a first episode from 1909 to 1920 in
New York had only a single episode and only 17% had three or more episodes; and
when 216 patients in Sweden were followed for 18 years, 49% never experienced a
second episode, and an additional 21% had only one other episode.
Ages ago, before the huge abuse of psychotropic
drugs started, depression was a self-limiting disease that in most cases was
over in a few months, and even today the median duration of an untreated
depression is only three months.11
This is not what Figure 12.1 tells us. And it
doesn’t make it any better that the other major indication for SSRIs is
anxiety, as it is similarly wrong to treat anxiety with addictive drugs for
years. Treatment with antidepressants doesn’t even seem to lower the risk of
further bouts of depression; it seems to increase this
risk.12 The studies that show this suffer from various
weaknesses, e.g. confounding by indication when treated and untreated patients
are being compared, but even so, it’s interesting that the median time to
recovery in patients who suffered from a second episode of depression was 23
weeks when they received drugs and only 13 weeks when they didn’t.11
As explained in other chapters, it’s clear that
long-term treatment with psychotropic drugs is harmful. If it were true that
psychiatric patients are comparable to patients with diabetes, the number of
disabled mentally ill would have gone down after we introduced antipsychotics
and antidepressants, but the number of people with psychiatric diagnoses forced
into early retirement has exploded in all countries where the trend has been
examined.10
I agree with Whitaker and Breggin that many, or likely even most, people on
disability suffer from drug-induced harm, not from a mental illness. We have
never seen such a gigantic catastrophe of iatrogenic disease production before.
The catastrophe has also hit our children hard.
In 1987, just before the best-selling SSRIs came on the market and before the
use of ADHD drugs skyrocketed, very few children were disabled by mental
illness in the United States; 20 years later it was more than 500,000, a
35-fold increase.10 A 2002 survey of US child and adolescent
psychiatrists showed that 91% of their patients were treated with psychiatric
drugs.13 In only the remaining 9% was psychotherapy used
without drugs. Overmedication is far worse in the United States than elsewhere,
undoubtedly because of this country’s ultraliberal traditions, also in
healthcare. In 2000 psychotropic drugs were used in 6.6% of US children
compared to 2.0% of German children.14 For stimulants, the rates were 4.3% vs. 0.7%, a
six-time difference.
As Whitaker says, the huge overmedication would
be impossible if psychiatry were honest,10 and The Guardian
suggested what honest information might look like:15
Imagine that, after feeling unwell for a while,
you visit your GP. “Ah,” says the doctor decisively, “what you need is
medication X. It’s often pretty effective, though there can be side-effects.
You may gain weight. Or feel drowsy. And you may develop tremors reminiscent of
Parkinson’s disease.” Warily, you glance at the prescription on the doctor’s
desk, but she hasn’t finished. “Some patients find that sex becomes a problem.
Diabetes and heart problems are a risk. And in the long term the drug may
actually shrink your brain.” Next comes a story that illustrates just how mad
our societies have become with respect to biological psychiatry.
Imagine that a virus suddenly appears that makes
people sleep 12-14 hours a day and move around slowly and become emotionally
disengaged. Some gain 10, 20 or 40 kg of weight, their blood sugar and
cholesterol go up, and they develop diabetes. People infected die substantially
earlier than other people, some kill themselves, and parents panic over the
thought that their children might also contract this horrible disease. Hundreds
of millions of dollars are awarded to scientists to decipher the workings of
the virus and they find out that it blocks a multitude of receptors in the
brain – dopaminergic, serotoninergic, muscarinic, adrenergic, and histaminergic
– which lead to compromised brain function. MRI studies find that the virus
shrinks the cerebral cortex, which is tied to cognitive decline. A terrified
public clamours for a cure.
Such an illness has in fact hit millions of
children and adults. What was just described are the effects of Eli Lilly’s
bestselling antipsychotic, olanzapine (Zyprexa).
I modified slightly a thought experiment
invented by Whitaker.10 It is the same type of madness that keeps our
societies totally indifferent to the fact that our prescription drugs are the
third leading cause of death after heart disease and cancer.16
How can it be done?
My guess is that physicians do not stop the
SSRIs because they have already had a few difficult experiences with what can
happen. I suspect they want to think that the problems are not
withdrawal-related, but a reappearance of the mythical chemical imbalance or a
new onset of bipolar disorder. When you stop to think of how many patients the
average family physician or psychiatrist puts on SSRIs, including themselves,
family and friends, and the long-term results of these prescriptions, the
cumulative misery effect is so large that if the physicians really became
educated, they would be unable to live with themselves.
STUART SHIPKO, PSYCHIATRIST FROM CAUFORNIA17
Shipko describes his profession’s organised
denial. He is undoubtedly correct that many doctors shy away from taking their
patients off their drugs because of bad experiences. It is also true that
doctors know shockingly little about abstinence symptoms and about how to taper
off drugs safely.1
No one taught them how to stop drugs, whereas they have learned all too well
from their silverbacks and the pharmaceutical industry how to start them and
always to blame the disease for untoward symptoms, which helps them get out of
their conundrum. It is much easier to renew a prescription than to stop an
addictive drug, and it generates a much greater income, as more patients can be
seen per hour.
People who want to stop drugs are mostly left to
fend for themselves, sharing information on the Internet and through social
media. A patient sent me her story about how she escaped the tyranny of
life-long treatment and an incompetent psychiatrist:16
After a traumatic event, I was prescribed happy
pills without adequate information about possible side effects. A year later, I
asked the psychiatrist to help me stopping the drug, as I didn’t feel it was
helpful. She convinced me that I was undertreated and should have a higher dose
and warned me against stopping the drug, as it could lead to chronic
depression. During a time when the psychiatrist had long-term sick leave, I had
the courage, supported by a psychologist, to taper off the drug. I had been on
it for 3.5 years and had become more and more lethargic and indifferent to
everything. It was like escaping from a cheese-dish cover. Tapering off the
drug is not unproblematic, it gives you a lot of abstinence symptoms. When the
psychiatrist returned after her illness, she was “insulted” about my decision
to stop the drug. However, I was much better, and in reply to my question that
I was no longer depressed, she said, “I don’t know.” “But if I don’t want happy
pills?” “Well, then I cannot help you!” was the answer. This psychiatrist had a
close relationship to a manufacturer of happy pills.
Unfortunately, this story is pretty typical. I
have received thousands of emails from patients and their relatives and they
have inspired me to read more about patient experiences on websites. Scientific
progress can be obtained in many ways and it is vitally important that we
listen to patients’ experiences with drugs. This is often far more reliable
than what we can read in carefully manipulated reports of industry-sponsored
research.
In a better world, psychiatrists would be eager
to teach patients how to live without toxic substances in their brain, but in
the real world many psychiatrists try to keep their patients on medications
indefinitely.18
Doctors feel disrespected when patients ask to come off the drugs they have
instituted, and a very common discharge notice in hospital patients’ charts is:
“The patient doesn’t want drugs. Discharged.”
It is therefore often psychologists, other
therapists, pharmacists, friends and relatives that help patients come off
their drugs. Some psychologists are worried about the possible legal
implications, but given the disaster doctors have created and their
unwillingness to help, I believe others must. When a system is harmful to
people, we have a moral duty to fight it, and as long as the psychologists only
help a patient psychologically who has decided herself to get off a drug, there
shouldn’t be any legal problems. I suspect the reluctance of some professionals
is due to fear of being exposed in the media if something goes wrong (see
below). For example, withdrawal psychosis is seen in 30-40% of long-term users
of antipsychotics, and if a patient stops the drug and commits a horrendous
act, everyone howls that patients must never stop taking their drugs.18
Few clinical challenges are more difficult and hazardous than removing
antipsychotic drugs from a patient after years of exposure. Stopping lithium
also involves a high risk of rebound mania.18
In 2012, the UK Royal College of Psychiatrists
asked 817 patients what it was like for them to come off antidepressants, and
63% reported withdrawal symptoms.19 The most common symptom was anxiety (70%); other
interesting symptoms were electric shocks/head zaps (48%), stomach upsets
(33%), flu-like symptoms (32%), depression (7%) and suicidal thoughts (2%).
But the report ended with a false statement of
course: “We would also like to reassure readers that despite some people having
symptoms of withdrawal when stopping antidepressants, antidepressants are not
addictive.”
Patients may get horrible symptoms when they try
to stop the medication. A patient trying to get off olanzapine described it as
pure hell, with terrible anxiety, severe panic attacks, paranoia, and horrible
tremors.10
In contrast, it is usually easy to stop drugs in children, which is fortunate,
as children should not receive psychotropic drugs.1
Most patients are unable to judge themselves
because the drugs have changed their brains. When the brain is deranged, it
cannot detect that it is deranged; an outside observer is needed for this. The
drugs reduce or cloud the highest human functions, including love, creativity
and spirituality, and many people have no idea what they have been missing
until they have come off their drugs.18 This is what Peter Breggin calls medication
spellbinding.1
While patients are on drugs, they often feel they have improved even when they
have clearly become worse. It is important to know this. Doctors tend to
believe when patients say they are well and will therefore be inclined to
increase the dose to obtain further “improvement,” but the statement “I’ve
never felt better in my entire life” may simply mean that the patient is
heading for a manic episode.1 Antidepressants change people’s
lives for the worse while they think they are getting better.18
When patients are in the midst of painful
psychiatric drug withdrawal, their brain is in a state of drug-induced crisis
and it is truer than ever that they cannot believe what their mind tells them.
Patients will usually feel they are themselves and will try to explain away
their odd behaviour if confronted with it and during a tapering attempt they
will often totally deny that they have become irritable, agitated, hostile or
difficult in other ways and will react with anger over such “accusations.”
This is one of the reasons it is so essential
that patients are not alone, but that close relatives or friends observe them
carefully. It can be downright dangerous if the family accepts the patient’s
false explanations. It is therefore preferable that the patient permits that
friends and family can contact the therapist if they become concerned.1
When patients have left suicide notes, only
very rarely is there any indication that the drug was the problem; patients
simply don’t know this and think it is themselves that are the problem.1
Abrupt withdrawal is particularly dangerous.
With several classes of drugs, people may be struck by the extreme degree of
restlessness known as akathisia, which predisposes to out-of-character
violence, including suicide and homicide. A slow taper is necessary, which is
best done with firm support from the family and close friends and in
collaboration with a professional with considerable psychopharmacological
knowledge. Unfortunately, few doctors have such knowledge and ever fewer are aware
of the spellbinding phenomenon.
Spellbinding also works the other way round.
When reducing drug dosage, patients may not notice any improvement or change in
their condition, although everybody else can. Also in this case support is
needed from significant others to prevent the patient from giving up the
withdrawal attempt.
It is not surprising that many patients who have
failed every time they tried have ultimately accepted their fate. It often
requires strong determination, a lot of time, patience, and a long tapering
period to get patients off the drugs while making the abstinence symptoms
bearable. If patients have been on drugs for years, the tapering period may go
up to more than a year. Danish psychiatrist Jens Frydenlund has told me that
his record is eight years for an SSRI! He has worked with drug addicts for
decades, and like other psychiatrists who have experience with both legal and
illegal drugs,1
he says that it is generally much easier to stop heroin than to stop a
benzodiazepine or an SSRI because the abstinence symptoms with heroin disappear
rather quickly.
Frydenlund once listened to a new patient’s
story for two hours, which, according to her father, was the first time anyone
had listened to her, and concluded by telling the patient that she didn’t have
schizophrenia but was a pill addict. He slowly took her off the monstrous
amounts of drugs she was on, one by one, and she got well.
Half the patients with schizophrenia are in
co-treatment with benzodiazepines, although this increases mortality (see
Chapter 6), but Frydenlund has succeeded in getting almost all the patients off
their benzodiazepines at two hospitals where he worked. The National Board of
Health inspected him three times in 2014, as they are worried that he uses so
few drugs! Another Dane, child psychiatrist Lisbeth Kortegaard, has stopped
ADHD drugs in virtually all children that her colleagues had medicated and her
experience is the same as Breggin’s,1 that the kids improve considerably
and become normal kids again when she takes them off their drugs. Her
colleagues became so hostile towards her going against the grain that I
encouraged her to leave her post as chief physician and open her own practice,
focusing on detoxifying children, which she has now done.
What we need more than anything else in
psychiatry are detox clinics all over the country, in all countries, with easy
and quick access free of charge, and education about the harmful effects of
psychotropic drugs and how to stop them. Millions of people worldwide need
help, and public investment in detox clinics would be highly profitable and
beneficial in terms of fewer disability pensions, fewer drug deaths (see
Chapter 14), much healthier citizens, and fewer serious crimes (see earlier
chapters).18
It is of utmost importance to tell people how
they can come off the drugs without consulting the doctor who started them on
drugs, as he will often be against it. It is a sad testimony to this fact that
most attempts to reduce or stop drugs are initiated by patients or their
families.1
Families often react to the chronic brain damage they have observed, with the
patient becoming lethargic, apathetic, indifferent, caring less, suffering from
memory lapses or doesn’t seem like himself anymore.
Peter Breggin has written a most instructive
book about drug withdrawal symptoms and how tapering should be carried out.1
It should be obligatory reading for all doctors who use psychotropic drugs, as
it will change forever the way they use them. The book is also very useful for
patients and their relatives and friends, as it can help patients get safely
off their drugs against their doctor’s wishes. There are also useful websites,
created by non-profit organisations or psychiatrists.20-23 One should only taper off one drug at a time.
People who have succeeded in coming off
psychiatric drugs and returning to a normal life often call themselves
psychiatric survivors, which is a very apt term. One such person, lawyer Jim
Gottstein, has given this advice:24
You have to take responsibility for your own
mental health and behaviour.
You have to learn to recognise your symptoms.
You have to learn what works for you.
Breggin also advises that the patient should be
in charge of the pace of the taper and warns that, without the patient’s own
motivation and determination, withdrawal attempts are likely to fail.1
Many patients report that the very last step, where they go from a very small
dose to nothing, is the worst, so this is when strong determination and support
is most needed.
It is important to reverse the medical
disempowerment that is usually at play, and Breggin explains why:1
Nurses, psychologists, social workers, teachers
and other non-prescribing people have often been taught that their task is to
push patients to comply with the prescribed medication. In this authoritarian
model, the physician stands atop the professional hierarchy and prescribes
pills much as one would expect an all-knowing judge to dispense justice. Like
the patient, those lower down the hierarchy are supposed not to make any
independent judgments or comments about the drugs. This model is not feasible.
Patients and their families can look up information about drugs on the
Internet, and so can non-prescribing professionals, and they can quickly learn more
about a drug’s harms than their doctor, who talks to salespeople, listens to
industry-sponsored lectures, and relies on data from industry-run trials.
Furthermore, psychotherapy requires an honest and open dialogue with the
patient that cannot exclude discussing the patient’s medication, particularly
as the drugs are often the cause of the patient’s problems.
A more egalitarian and respectful model of
treatment is the norm in other areas of medicine, e.g. in diabetes, which the
patients often control themselves. In the mental health field, however, where
the patient’s self-determination is much more important than in other areas of
medicine, the authoritarian model is still alive and well. This must stop.
13
Organised crime, corruption of
people and science, and other evils
We have allowed psychiatry’s medico-industrial
complex to grow like a malignant tumour, sending metastases in all directions
in our societies, and we have allowed the psychiatric oligarchs to medicalise
normality – even in our schools and in preschool children – and turning what
were previously acute conditions into chronic ones. Another similarity to
malignant tumours is that psychiatric drugs kill huge numbers of people (see
next chapter).
Bribery and illegal marketing have to a
substantial degree contributed to the drug epidemic. Although both practices
are illegal, 52% of Danish general practitioners have experienced a salesperson
saying the drug could be used outside the approved indication, and 34% have
been exposed to information about drugs based on unpublished results.1
We have allowed drug companies to commit
habitual crime that involves pervasive corruption of leaders among doctors and
other decision-makers and to lie to us routinely, both in their research and
marketing and in their interactions with drug regulators.2
According to the definitions in US law, big
pharma commits organised crime,2 and the crimes have been
particularly evil in psychiatry. A disproportionate number of the criminal
activities have involved psychiatric drugs and have included illegal marketing,
Medicare and Medicaid fraud, bribery of doctors, civil servants and politicians
right up to the ministerial level, and disposal of evidence.
In 2012, I combined the names of the ten largest
drug firms with “fraud” on Google and much of what I found on the first search
page involved psychiatry.2 The cases I described were often
about illegal promotion to our most vulnerable citizens, children and the
elderly, often accompanied by kickbacks to doctors to induce them to use
particular drugs:
·
ziprasidone, an antipsychotic,
Pfizer
·
pregabalin, an epilepsy drug,
Pfizer
·
oxacarbazepine, an epilepsy drug,
Novartis
·
buproprion, an antidepressant, GSK
·
paroxetine, an antidepressant, GSK
·
lamotrigine, an epilepsy drug, GSK
·
quetiapine, an antipsychotic,
AstraZeneca
·
risperidone, an antipsychotic,
Johnson & Johnson
·
olanzapine, an antipsychotic, Eli
Lilly
·
valproate, an epilepsy drug,
Abbott
Psychiatry is a goldmine for big pharma.2
The diagnoses are vague and easy to manipulate, and many drugs are hilariously
expensive, although they are not any better than off-patent drugs, but that’s
no hindrance for their widespread use.
Leading psychiatrists are at high risk of
corruption, both financially and of their academic integrity and objectivity,
and in fact psychiatrists collect more money from drug makers than doctors in
any other specialty; they are also “educated” with industry’s hospitality more
often than any other specialty.3 Leading psychiatrists are highly effective drug
pushers, also for uses that are illegal for the companies to advertise, and
they are often very well paid for their “assistance,” even when they publish
textbooks and papers that ghostwriters have written for them,2 which is
considered scientific dishonesty.
Until 2015, it was little known that Allen
Frances, chairman of DSM-IV, which has earned the American Psychiatric
Association more than $100 million, and two other psychiatrists, John P.
Docherty and David A. Kahn, had been very active in promoting risperidone in
return for cash.4 They received about one million dollars for helping
Johnson & Johnson market risperidone partly illegally, for non-approved
indications. It started in 1995, one year after publication of the DSM-IV, and
involved what an ethics specialist has called serious deception, corruption and
distortion of the scientific evidence. Frances and his colleagues wrote
guidelines designed specifically to persuade physicians to prescribe
risperidone as first-line treatment for schizophrenia. These guidelines were
not independent, and they were developed in close collaboration with the
company. When they were done, the three psychiatrists established Expert
Knowledge Systems for the purpose of creating and helping implement a
risperidone marketing plan, which included to “influence state governments and
providers” and to identify key opinion leaders who could tout risperidone at
meetings advertised as Continuing Medical Education lectures. Johnson &
Johnson later had to pay more than $1.5 billion for its unlawful and deceptive
marketing that included lies about the life-threatening harms of risperidone.2
In 2006, the drug industry accounted for about
30% of the American Psychiatric Association’s $62.5 million in financing.5 Psychiatrists who received at least $5,000 from
makers of antipsychotics wrote three times as many prescriptions to children as
other psychiatrists although the drugs were not approved for most uses in
children. Joseph Biederman and other Harvard psychiatrists, who more than
anybody else have pushed drugs heavily to children, had underreported their
earnings to university officials; each of them had made more than a million
dollars from drugs makers during eight years. As is well known, studies have
shown that researchers who are paid by a company are more likely to report
positive findings when evaluating that company’s drugs.2
It is very lucrative for doctors to participate
in industry-sponsored trials, as they get publications, fame and other
benefits.2
Above all, they get money, which can be used for other research at the clinic
or to supplement the doctor’s private economy. Specialists may receive as much
as $42,000 for enrolment of one patient in a trial, and patients may therefore
be coerced into participating, or coerced into continuing taking a drug that gives
them unpleasant side effects or even increases their risk of dying, as payment
is sometimes only provided for patients that stay in the trial to its planned
finish date.
Top psychiatrists can earn millions of dollars
for themselves and may attract much larger sums for their institutions, which
explains why they cover up for the psychiatrists’ misdeeds. As an example, the
corruption at Emory University where Charles Nemeroff worked was kept secret
for more than a decade.2 One reason why the scam could
continue for so long was that at least 15 whistleblowers were ordered
psychiatric evaluations by Emory’s psychiatrists who reportedly wrote up such
exams without even examining the targeted doctors or gathering factual
evidence, where after several of them were fired. Some of these “evaluations”
were done by Nemeroff himself.
Doctors who take money from many companies
usually argue that they are not in the pocket of industry because they are not
dependent on any particular company. But company people don’t see it that way;
they call them drug whores.6 What the doctors really say it that it’s okay to be
a prostitute as long as you make sure you have many customers every day so that
you aren’t dependent on any particular one.
Our academic institutions have also allowed
themselves to become corrupted. They grant ownership to the collected data to
the sponsor and often accept that the doctors will have little influence on any
publications.7 The competition for research funds means that
companies can shop among the various academic centres and choose those who are
least willing to raise uncomfortable questions.
Patients know perfectly well they cannot trust
the pharmaceutical industry. In large surveys, it ended up at the bottom, along
with automobile repair shops and tobacco companies, in terms of the confidence
people had in the industries.2 The reason patients trust their
medicines is that they extrapolate the trust they have in their doctors into
the medicines they prescribe. Patients don’t realise that virtually all of
their doctors’ knowledge about drugs comes from the industry they don’t trust.
Furthermore, they don’t know that their doctors may have self-serving motives
for choosing certain drugs for them, such as a well-paid second job in a
company, which many doctors have,2 and that many of the drug
industry’s crimes are only possible because corrupt doctors contribute to them.
The health professionals’ main task is to find
out whether the treatments they might consider using have beneficial effects
that exceed the harmful ones. When it comes to drugs, we have completely failed
in this task. We have left it to the industry to carry out the pivotal placebo
controlled trials, although we know that companies often cheat with their
studies,2
which they can do behind closed doors because they don’t allow others to get
access to the raw data for re-analysis.
Not even the doctors who provided the data are
allowed access to the full data set, but it is the patients who suffer the
consequences of this corruption of the evidence base.2 When the FDA in
2003 was reviewing unpublished data from trials of SSRIs in children and
adolescents to see if the drugs increased suicide risk, the academics who had
published positive results of these drugs were worried and issued a report
disputing evidence that their use increased suicidal behaviour. They had
contacted the companies to get access to the data they had themselves
generated, but some drug companies refused to provide them.8
It is really scary and totally unacceptable
that the only people in the world who have seen the entire dataset in industry
trials are company employees.
If independent investigators want to do their
own trials and ask a company for matching placebos, this request will often be
refused, or the company will demand a ludicrous sum for the placebos knowing
that this will stop the trial.2
Industry-sponsored randomised trials aren’t
science. Medical science aims at finding the truth and at improving the
treatment of patients, but when trial data are secret, it cannot be considered
science. It is marketing dressed up as science, and the trials are often
flawed.2
Rigorous science should put itself at risk of being falsified but the industry
protects its hypotheses by ad hoc modifications, or by
designing trials that make them immune to refutation.2 Thereby, the
industry puts its hypotheses in the same category as pseudoscience.9
The industry also often changes the analysis
plan once the sponsor has seen the data.2, 10, 11 Until recently, it was difficult to detect such
cheating, as trial protocols were regarded as confidential. About 15 years ago,
however, our research group succeeded in getting access to a cohort of
protocols submitted to a research ethics committee in Copenhagen.10 We included 102 trial protocols and their
corresponding publications; three-quarters of these trials were industry
funded. To our great surprise, at least one protocol-defined primary outcome
had been changed in 63% of the trials. And in 33% of the trials, a new primary
outcome was introduced in the published report that didn’t exist in the
protocol. Not a single publication acknowledged that primary
outcomes had been changed!
The reason this is so devastating for the
trustworthiness of trials is that there are often many outcomes, which may be
further divided or combined, creating even more chances of hitting the bull’s
eye. Roughly just half of all trials are ever published, and in those that see
the light of day only half of the outcomes are included.2, 10
What we are left with is therefore only a quarter of the studied outcomes, and
this quarter may have been subjected to data torture until they confessed.
Psychiatry provides many examples of the fact
that we cannot trust industry-sponsored research at all.2 For example, what
predicted the effect of fluoxetine in head-to-head trials against other
antidepressants was who the sponsor was.12 When fluoxetine was the experimental drug,
fluoxetine was best, and when it was the control drug, it was worst. As another
example, a study of 142 trials of six antipsychotics or antidepressants showed
that most deaths (62%) and suicides (53%) were not reported in articles when
compared with summaries of the same trials on websites.13
Randomised trials were introduced to protect us
from the many useless treatments on the market, but oddly enough, they have
given the ultimate power of knowledge production to big pharma that now uses
them for getting approval for treatments of little or no value, and which are
often harmful.2
It’s very strange that we have accepted a system where the industry is both
judge and defendant, as one of the most firm rules in laws of public
administration is that no one is allowed to be in a position where they
evaluate themselves.
Drummond Rennie, deputy editor at JAMA, has
explained how corrupt industry-supported drug trials are by comparing them with
court trials.16 In a court trial, the various parties, judge, jury,
opposing counsels, witnesses and police, are independent of one another. In a
clinical trial, it is very much in the interest of the drug’s sponsor to make
everyone in the process its dependent, fostering as many conflicts of interest
as possible. The sponsor designs the trial so that it will likely have an
outcome that pleases the sponsor; the sponsor pays those who collect the
evidence, often doctors or nurses, and pays those who analyse the evidence,
drops what is inconvenient, and keeps it all secret – even from the trial
physicians. The sponsor deals out to the FDA bits of evidence and pays the FDA
(the judge) to keep it secret. Panels (the jury), usually paid consultant fees
by the sponsors, decide on FDA approval, often lobbied for by paid grass-roots
patient organisations who pack the court. If the trial is positive for the
sponsor, the sponsor pays subcontractors to write up the research and impart
whatever spin they may; they pay “distinguished” academics to add their names
as “authors” to give the enterprise credibility, and often publish in journals
dependent on the sponsors for their existence. If the drug seems no good or
harmful, the trial is buried and everyone reminded of their confidentiality
agreements. Unless the trial is set up in this way, the sponsor will refuse to
back the trial, but even if it is set up as they wish, those same sponsors may
suddenly walk away from it, leaving patients and their physicians high and dry.
In short, we have a system where defendant, developers of evidence, police,
judge, jury, and even court reporters are all induced to arrive at one
conclusion in favour of the new drug.
Our drug regulators should be impartial judges,
but they are part of the problem. They are firmly against providing independent
researchers access to unpublished study reports, trial protocols and other data
in their possession, constantly arguing that they need to protect the
commercial interests of the drug industry.15 They seem to have forgotten that their job is to
protect the patients. They are keen to protect themselves and keep their work
away from public scrutiny. Corruption at the FDA is common, and when the
higherups overrule the agency’s own scientists and make obviously harmful
decisions, it smells of corruption.2 I don’t think patients are aware
that the drug regulatory authorities expose them to many ineffective and
harmful drugs that kill them in huge numbers.2
In matters of health, there should be no
tolerance for deception,16 and yet, that is exactly what we
often see in industry-sponsored research and marketing. Lundbeck has
illustrated this with escitalopram, and I have previously described in detail
how Lundbeck convinced the world that a molecule can be better than itself.2
Lundbeck’s evergreening of
citalopram
Lundbeck’s drug citalopram (Cipramil or Celexa)
was one of the most widely used SSRIs, and when the patent ran out, Lundbeck
had a new patent ready for the same substance. Citalopram consists of two
halves, which are mirror images of each other, but only one of them is active.
Lundbeck threw out the inactive half, patented the active half, and called the
rejuvenated me-again drug escitalopram (Cipralex or Lexapro).
Lundbeck delayed market entry of cheap, generic
citalopram by paying the manufacturers to stay away and was fined €94 million
by the European Commission for this violation of EU antitrust rules.17 Lundbeck produced some trials comparing the two
versions of the molecule and claimed that me-again was better than old me,18 but even if we take the results at face value, they
showed that there was no meaningful difference between the two versions of the
drug; after eight weeks the difference was 1 on a scale that goes up to 60,
which is irrelevant (see Chapter 3).
Interestingly, this happened in the country
where Hans Christian Andersen wrote The Emperor’s New
Clothes. Independent researchers found that the efficacy appeared to be
better for escitalopram than citalopram (odds ratio 1.60; 95% confidence
interval 1.05 to 2.46) in head-to-head trials, but when they did an indirect
comparison of the two drugs based on 10 citalopram and 12 escitalopram placebo
controlled trials, the efficacy was similar (odds ratio 1.03; 0.82 to 1.30).19 Usually, direct comparisons are more reliable than
indirect comparisons, but the drug industry distorts its research to such an
extent that the indirect comparisons are sometimes the most reliable ones.
Lundbeck’s partner in America, Forest, was fined
more than $313 million and faced numerous lawsuits from parents of children who
had either committed or attempted suicide, and Forest pleaded guilty to charges
relating to obstruction of justice and illegal promotion of citalopram and
escitalopram for use in children and adolescents.2, 20 Six years earlier, a Forest executive lied before
Congress saying that Forest followed the law and had not promoted any of the
drugs to children.
Forest engaged in widespread corruption of
doctors to promote Lundbeck’s drugs,2 and in 2009 the US Senate released
some really nauseating documents it had requested from Forest.21 Forest would communicate that escitalopram offers
superior efficacy and tolerability over all SSRIs, which is totally surreal. I
have never heard of any drug that is both more effective and safer than all
other similar drugs. We are told that sales mirror the promotional effort,
which is true. Sales of SSRIs are closely related to the number of drugs on the
market (r=0.97),22 and in the Unites States each new agent added to
the aggregate use without a concomitant decrease in previously introduced
agents,23 which shows that the use of these drugs doesn’t
reflect a genuine need; it’s about marketing.
Furthermore, the Forest documents speak about
producing ghostwritten articles for “thought leaders,” and the company
recruited about 2,000 doctors as drug pushers to tout Lexapro at meetings,
using the slide kit prepared by Forest.
There was also a huge programme of “trials,”
where the results seemed to have been determined beforehand, before the trials
had even started, and of course there were “unrestricted grants” to help the
American Psychiatric Association and others to develop “reasonable practice”
guidelines, which was about improving “the percent of patients who adhere to
the full duration of therapy.” Total corruption of academic medicine resulting
in immense harms to the many patients who cannot get off the drug once they
have adhered to “the full duration of therapy.”
So what was Lundbeck’s reaction to the partner’s
crimes? “We know Forest is a decent and ethically responsible firm and we are
therefore certain that this is an isolated error,” said the sales director of
Lundbeck.24 Perhaps this confidence in Forest’s business ethics
is related to the fact that Lexapro had sales of $2.3 billion in 2008.2
At any rate, it’s perverse that anyone calls a company like Forest decent and
ethically responsible.
Lundbeck’s CEO Ulf Wiinberg also had an
interesting sense for business ethics. In 2014 he had to leave his job because
he had received shares as a “gift” from a company in which Lundbeck bought
shares one month later.25 The value of the shares was about $1 million, and
in addition to this, Wiinberg received about $3 million from Lundbeck when he
left.26 He likely won’t need social benefits. He has
already taken them himself.
Psychiatry’s fantasy world
The leading psychiatrists have created a
pseudo-world of their own, full of erroneous ideas based on poor science and
pseudoscience, particularly in relation to the validity of diagnoses, the
effects of diseases on the brain, and the effects of drugs on patients. In this
pseudo-universe, they have been heavily supported and seduced by a criminal
drug industry that has earned billions on the lies while killing millions of
patients, many of whom should not have received the drug that killed them.
Psychiatrists are supposed to be experts on
psychiatric drugs, but they aren’t – they are surprisingly ignorant. In 2014,
the American Psychiatric Association wrote on its homepage about depression
that:27
“Antidepressants may be prescribed to correct
imbalances in the levels of chemicals in the brain. These medications are not
sedatives, ‘uppers’ or tranquilizers. Neither are they habit-forming. Generally
antidepressant medications have no stimulating effect on those not experiencing
depression.”
All of this is wrong, and even healthy people can develop numbness or
mania on an antidepressant. The association furthermore noted that, “If a
patient feels little or no improvement after several weeks, his or her
psychiatrist will alter the dose of the medication or will add or substitute
another antidepressant.” There is no good evidence that it’s helpful to
increase the dose or switch between drugs, and if it seems that a drug is
better than another it’s very likely just because the patient would have improved
anyway at this point in time, even without treatment.
In 2008, John Ioannidis from Stanford remarked
that the assumed effectiveness of antidepressants perhaps was a myth
constructed from small randomised trials with non-relevant outcomes, improper interpretation
of statistical significance, manipulated study design, biased selection of
study populations, short follow-up, and selective and distorted reporting of
the results.28 He also asked for very large long-term trials.
Three years later, a group of prominent
psychiatrists responded:29
“Persistent, untreated depression produces a
type of neurodegenerative disorder, associated with synaptic changes … Similar
to poor control of blood sugar in diabetics, poor control of symptoms in Major
Depression is associated with worse long-term outcome and greater overall
disability … antidepressants prevent relapses … 53% of the placebo patients
relapsed, whereas only 27% of drugtreated patients relapsed … After the FDA
issued a black warning [sic] against antidepressants, antidepressant
prescriptions for this population diminished and there has been a concomitant
increase in actual suicide … There have been concerns regarding whether certain
antidepressants may cause suicides. We now know this is a myth largely fuelled
by the media … Newer studies of children do not confirm an increase in suicidal
ideation … Naturalistic studies show that the incidence of suicide rate tends
to go down as the incidence of antidepressant treatment goes up.”
All of this is seriously wrong or misleading.
These authors quoted Robert Gibbons three times and Göran Isacsson once (see
Chapter 3 about their research) to “prove” their point that antidepressants
protect children against suicide, although the truth is that they double the
suicide risk. Their paper is from 2011. I fail to understand how Stefan Leucht,
who has published much good research and is an editor in the Cochrane
Schizophrenia Group, could coauthor all this harmful nonsense, but it says
something about how deep the collective delusions and denial in psychiatry go.
They hit even the best of psychiatrists. It is very, very tragic.
A 2012 newspaper article called “Behind the
myths about antipsychotics” was similarly tragic and also deeply ironic because
its authors, four leading Danish psychiatrists, propagated what they warned
about, myths about antipsychotics.30 They wrote that:
Most patients suffering from schizophrenia have
disturbances in the dopamine system; the genes are by far most important (about
70-80%); large international registry studies show that patients with
schizophrenia who are not treated with antipsychotics are at higher risk of
dying prematurely than patients who are in treatment; numerous studies have
documented that the risk of new psychotic episodes and a more severe course of
the disease is increased if patients stop taking the antipsychotic medicine; in
our large study, we found no indications that polypharmacy with antipsychotics
increases mortality; and large register-based studies in Denmark and Finland
show that concomitant treatment with several antipsychotics is not associated
with increased mortality.
All of this is totally wrong or seriously
misleading (see Chapter 6). I shall describe why these myths are so harmful for
patients based on a patient story that comes from one of the four authors’
university hospital in Copenhagen. The patient had been admitted with mania,
and although he had asked not to be treated with drugs, he received forced
treatment with olanzapine, and in his own words: At discharge, when I had been
declared cured after my first episode diagnosis, I tried to behave well,
fearing that I might not be released after all. The psychiatrist forcefully
urged me to continue with olanzapine. I didn’t dare tell her that I had spat
out most of the pills in the washbasin and therefore asked, for the sake of
appearances, for how long she thought I should take the drug? For the rest of
my life, she replied, because I had a chronic disease, with a great risk of
relapse, and I need not be afraid of the side effects.
The patient didn’t take the drug because he had
read a newspaper article I published in January 2014 about ten myths in
psychiatry,31 which also exists in English,32 and he has been well ever since without drugs.
Is there any hope for a specialty like this? I
have heard critical psychiatrists say that leading psychiatrists seem to suffer
from cognitive dissonance, as what they see and hear doesn’t influence them.
Many patients who have managed to get out of the medicine hell by their own
efforts say that the drugs have stolen many years of their lives.
A Danish witch hunt
The same day my article about the ten myths
appeared, the chairman of the Danish Psychiatric Association declared in the
same newspaper, on its website: “Antidepressant drugs protect against suicide.”
A month later, 16 Danish professors in psychiatry responded to my article, but without
mentioning my name, just like one was not supposed to mention the evil
Voldemort’s name in Harry Potter.33 They wrote that a number of studies show that
treatment with antipsychotics increase longevity, compared with no treatment.
This isn’t true; antipsychotics shorten life (see Chapter 6).
My first article was “Psychiatry gone astray.”31
I responded to the professors in a new article, which I called “Leading
psychiatrists have still gone astray.”34
Two months later, the Danish Psychiatric
Association attempted character assassination of me and they almost succeeded.
They wrote a one-page letter to the Cochrane Schizophrenia Group and to the
Cochrane Depression, Anxiety and Neurosis Group in which they complained about
my first article.31 They focused on a sentence, which they quoted out
of context: “the citizens of Denmark would be better off, if all psychotropic
drugs were withdrawn from the market.” In actual fact, my article ended thus:31
“Psychotropic drugs can be useful sometimes
for some patients, particularly in short-term use, in the acute situations. But
after my studies in this area, I have arrived at a very uncomfortable
conclusion: Our citizens would be far better off if we removed all the
psychotropic drugs from the market, as doctors are unable to handle them. It is
inescapable that their availability causes more harm than good. The doctors
cannot handle the paradox that drugs that can be useful in short-term treatment
are very harmful when used for years and create those diseases they were meant
to alleviate and even worse diseases. In the coming years, psychiatry should
therefore do everything it can to treat as little as possible, in as short time
as possible, or not at all, with psychotropic drugs.”
The psychiatrists mentioned in their letter that
I had been criticised by the Minister of Health, the director of the National
Board of Health, the director of the Danish Patients Association, the president
of the Cancer Society, the president of the Danish Psychiatric Association and
the president of the Organisation of Danish Medical Societies. The criticism by
the last-mentioned president actually came six months earlier, when my book
about the drug industry’s crimes was published.2 His criticism was
erroneous and he appeared not to have read my book, but that didn’t affect the
psychiatrists the slightest bit, as they were now on a witch hunt. They
enclosed a translation of his criticism in their letter, but not my published
rebuttal of his criticism. They ended their letter by asking: “How do you, with
the specific knowledge you have on antipsychotics and antidepressants, respectively,
evaluate Peter Gøtzsche’s statements as presented in his article. We would be
very pleased if you would take up the task of making such an evaluation.”
It wasn’t the editors in the two review groups
who responded to the letter, but Cochrane’s CEO, deputy CEO and two other
people in Cochrane’s leadership. I wasn’t consulted on the Cochrane
leadership’s response to the psychiatrists. I knew that Cochrane had received
various complaints from people and organisations about whether Cochrane
supported my views on the matter as expressed in my book,2 but not that the
Danish Psychiatric Association had contacted Cochrane.
While I was on holiday in a jungle in Panama,
surrounded by birds, tarantulas, monkeys, butterflies and sloths, with little
contact to the outside world, and therefore with no chance of defending myself,
the news that my own organisation had denounced me ran amok in the Danish
media, and the psychiatrists celebrated their kill by reading aloud Cochrane’s
letter at the Danish Psychiatric Association’s annual meeting.
The letter from Cochrane’s leadership, which was
only one page, said that, “Cochrane is treating very seriously the points you
raise concerning comments made by Professor Gøtzsche on the use of psychotropic
medication. I want to state explicitly that these are not the views of The
Cochrane Collaboration on this issue and we do not endorse them.” The letter
furthermore noted that I was speaking on my own behalf, which was correct, and
as “part of the promotional work” I conducted surrounding publication of my
book, which wasn’t correct. I wrote my newspaper article in order to draw
attention to some major problems in psychiatry and it started thus:
“I have researched antidepressants for several
years and I have long wondered why leading Danish psychiatrists, including
several professors, base their practice on a number of erroneous myths, which
are unfounded. These myths are harmful to the patients, particularly since
Danish psychiatry is extremely top-down controlled. Many psychiatrists are well
aware that the myths don’t hold and have told me so, but they don’t dare
deviate from the official positions because of career concerns. Being a
specialist in internal medicine, I don’t risk ruining my career by incurring
the professors’ wrath and I shall try here to come to the rescue of the many
conscientious but oppressed psychiatrists and patients by listing the worst
myths and explain why they are harmful.
There was only one reference to my book in the
article, and it was necessary, as I wrote that I had estimated in my book that
just one of the many antipsychotics, olanzapine (Zyprexa), has killed 200,000
patients worldwide.
The Cochrane letter also stated that, “The views
contained in this book are also not the views of Cochrane.” This comment was
unnecessary, as it is evident that what people write in their books are their
own views, not those of any organisation, and as the psychiatrists had not
referred to my book. Furthermore, my book is not about my personal views. It’s
about facts, and with its more than 900 references, it’s unusually well
documented.
There was a sentence in the Cochrane letter,
which was not a response to an issue the psychiatrists had raised but stood on
its own and was misunderstood: “We will be asking Professor Gøtzsche to share
with Cochrane colleagues any unpublished data that is not yet publicly
available, so that it can be incorporated objectively into new or existing
Cochrane Systematic Reviews as appropriate; and then be seen and evaluated by
you [the Danish psychiatrists] and other specialists in the field.”
It came as no surprise to me that Danish
journalists interpreted this as meaning that I had now come under Cochrane
censorship and wouldn’t be allowed to publish anything unless it had been
approved by Cochrane. This was of course not the intention of the letter. We do
research on unpublished data we have obtained from the European Medicines
Agency about antidepressants, but we are evidently under no obligation to share
these data with anyone before we have finished our own research and decide to
do so of our own free will. Our first papers have come out and they show that
the clinical study reports contain extensive data on major harms that don’t
exist in published journal articles or in trial registry reports.35, 36
The letter from Cochrane’s leadership proved to
be a threat to what I had built up over 30 years, including my centre, which is
on government funding. The Minister of Health declared publicly that my person
and the centre wasn’t the same thing, which I and my senior researchers
interpreted as meaning that I could be fired. Very weird indeed, as I had done
nothing wrong. I simply pointed out what I have detailed in this book and what
many others have pointed out before me.
Cochrane’s leadership sent a letter to the
newspaper that broke the story explaining that there had been
misunderstandings. But it was too late. The damage had been done and not a
single journalist admitted they had misrepresented the first letter, even
though some of what they had written was demonstrably untrue. I published
various rebuttals, including an article with a similar title as one of H. C.
Andersen’s famous novels, “The Cochrane feather that became five hens,” which
is about how rumours become established truths when they are repeated often
enough.
The newspaper that broke the story seriously
misrepresented the first Cochrane letter,37 which the second letter pointed out. For example,
the subheading stated that I did not have support “for a number of
controversial statements about the drug industry and the use of psychiatric
medicine.” Some people interpreted this as an acquittal of the drugs industry’s
dirty methods and a verdict about my book, but Cochrane now clarified that it
neither supported nor refuted my interpretation of the evidence. The newspaper
wrote that, “the organisation doesn’t agree either with the views Peter
Gøtzsche describes in his book where he compares the business model of the drug
companies with criminal organisations.” This was free fantasy, which Cochrane
rejected: “We have not at any time expressed any opinion about Gøtzsche’s views
about drug companies.”
It was scary to see the extent to which some
journalists can sometimes distort their stories when they smell blood. This
newspaper article gave people the impression that what I had documented so
carefully in my book, e.g. that the drug industry engages in organised crime,
wasn’t correct.
The second Cochrane letter contained this very
important information: “The Cochrane Collaboration currently has nearly 34,000
members in over 100 countries. Every member, including Professor Gøtzsche, is
entitled to express their personal opinions and do work that is independent of
The Cochrane Collaboration.”
After this experience I felt like the senator in
ancient Rome who said that people wouldn’t succeed stabbing him in the back, as
he had so many scars already that the knife wouldn’t get through.
Allow me to say at this point that I am a member
of several networks of critical psychiatrists and that I get invitations to
hold talks for psychiatrists worldwide. This would hardly be the case if there
was no substance in what I say. My article on psychiatry’s ten myths32
has been translated into English, Spanish, Norwegian and Finnish and can be
found on several websites, including those of David Healy and Robert Whitaker
who know a good deal more about the harm done by psychotropic drugs than those
who criticise me.
Ten months after the witch hunt, a BMJ paper with views very similar to mine appeared.38 The paper addressed strategies in lowand
middle-income countries but its suggested solutions should be adopted
everywhere. It noted that wealthy countries have created expensive and
inefficient mental healthcare and that government, industry, and experts make
decisions at the top for people at the bottom who are left out of the
decision-making process and often out of the care system entirely. Even with
the exorbitant healthcare spending in the United States, the mental health
system fails to reach more than half the people with the most serious mental
disorders.
The paper also mentioned that we should start by
listening to people and empowering them so that they can define their needs and
design the systems they want.
We should train lay health workers and
generalists rather than specialists.
Lay health workers, backed up by medical
generalists (primary care nurses and doctors), currently provide over 90% of
mental health-care worldwide. They can learn to manage depression, anxiety,
psychosis, and substance misuse, just as they learn to manage malaria, HIV, and
tuberculosis. Specialists tend to develop a selective inattention to matters
outside their expertise, thereby missing context and creating silos of care,
overdiagnosis, and overtreatment. Wealthy countries are now spending billions
of dollars trying to convert systems that are based on specialists back into
integrated models of care so that they can control excessive treatments.
Community based psychosocial interventions
should be emphasised, rather than drug treatments.
Peer and family support, meditation, employment,
and technology tools are generally effective, have few side effects, and are
more durable than psychiatric drugs. Wealthy countries spend huge resources on
medications, mainly because of advertising and lobbying rather than because
they are effective; a rational mental health system would rely on judicious use
of generic drugs.
It’s difficult to argue against this paper. An
ancient practice of dealing with the mentally ill was to throw them into a pit
of snakes. The theory was that if something like that would make a normal
person insane, then it must work in reverse as well.39 But hold on; isn’t that what we are still doing?
Treating the mentally ill with drugs that can make normal people crazy, hoping
that the opposite will miraculously occur?39
Lecture tour in Australia
In February 2014, I received an email from a
Victorian farmer in Australia whose only son took his life at age 19 a year
earlier when he was on venlafaxine. He wanted to inform people about how
dangerous SSRIs are and asked if I would be willing to go on a lecture tour,
which he offered to arrange. After having purchased over 20 different books on
malpractice in big pharma, he said that my book2 “shone the
strongest light on the issues.”
I wish to do what I can to reduce the harms
caused by psychiatric drugs and felt it would also be a good opportunity to
strengthen our network in Australia. The farmer was a superb organiser and in
just 11 days, I gave 17 lectures on four different subjects including Cochrane
and mammography screening at public venues, hospitals and universities in
Australia and was also interviewed for radio, TV and newspapers.
People were very interested and I learned a lot
from those I met – psychiatrists, other doctors, patients, relatives of
patients, politicians, civil servants in the Ministry of Health, and
filmmakers. I found the power structure in Australian psychiatry very
disturbing, as there are many examples of how it had prevented an open debate
about issues of crucial public health importance. Two psychiatric professors
stand out: Ian Hickie and Patrick McGorry, once the Australian of the Year, and
both with huge influence on national policies.
In 2011 psychiatric epidemiologist Melissa Raven
and four academic colleagues including psychiatrist Jon Jureidini and two
ethicists lodged a complaint to the University of Sydney about a clinical trial
called The Beyond Ageing Project led by Ian Hickie. They had serious concerns
about the ethics and the methodology of the trial, which investigates whether
sertraline can prevent depression in older people who are not depressed. The
University sought the advice of two expert reviewers and claimed that they had
now addressed the problems. The University refused on several occasions to
share the reviewers’ report and other relevant documents with the lame excuse
that there was an overriding public interest against disclosure.
In contrast to this Australian
closed-mindedness, my research group has been granted access to current trial
protocols in Denmark via our research ethics system. Raven appealed this
decision to an outside body, under the New South Wales freedom of information
legislation, and it found that the University had not established an overriding
public interest against disclosure. Of course it hadn’t, as it cannot be done!
The public always has an overriding interest in
knowing what goes on in clinical trials and why. However, the University still
refused to hand over the documents, and the matter still hasn’t been resolved
but is now dealt with by the judicial system. It’s unbelievable. In my opinion,
if Hickie or others have anything against disclosing what they do and why, they
shouldn’t be allowed to conduct or approve trials.
There surely was something of interest to
reveal. The Human Research Ethics Committee at the University of Sydney, to
which Raven and her colleagues first complained, found major problems with the
trial. A 50 mg dose of sertraline was abruptly stopped and this was justified
as common practice! Furthermore, the Committee noted that a telephone call two
weeks after cessation of therapy was rather late to pick up withdrawal effects
and requested a telephone call three to five days after withdrawal. The
Committee also found that the Participant Information Statement should be
modified to clearly state the known risks of the study and that current
participants should be re-consented, after being informed of these risks.
Given what we know about antidepressant drugs, I
find the idea of trying to prevent depression in older people totally absurd.
Patrick McGorry has spearheaded equally absurd trials about using antipsychotic
drugs in order to prevent people who have never had a psychosis from developing
a psychosis. There is no good reason whatsoever to believe that these drugs can
prevent psychosis; in fact, they cause psychosis in
the long run and when people try to get off them. But McGorry has published at
least one such trial,40 while another trial, of quetiapine in children as
young as 15 “at risk” of psychosis, was halted after international protests.41 Some of McGorry’s peers said that his youth early
intervention model had been ‘’massively oversold’’ and Allen Frances was
particularly harsh in his criticism.42 Frances attacked the Australian Government’s plan to
spend $222 million expanding McGorry’s programme by funding another 16 Early
Psychosis Prevention and Intervention Centres and called it a “vast untried
public-health experiment.” He also noted that the false positive rate in
selecting pre-psychosis as a precursor for psychosis is at least 60-70% in the
very best hands and may be as high as 90% in usual practice. It’s like
performing bilateral mastectomy on all women to prevent breast cancer, as also
in this case about 90% would never have developed the disease.
So, these are the two silverbacks the
Australians have to guide them in psychiatry, both with numerous conflicts of
interest in relation to the drug industry. Other views than theirs are not
welcome. Maryanne Demasi from the Australian Broadcasting Corporation (ABC)
worked on a documentary about antidepressants and interviewed among others
David Healy and me. We used a lot of time refuting Ian Hickie’s arguments and
explaining to Demasi why he was wrong. Ten months later, the ABC’s leadership
cancelled the documentary. Hickie had teamed up with McGorry and they refused
to appear on camera, but that’s not a valid excuse for dropping a highly
relevant programme; journalists routinely say that someone has refused to
comment. Demasi had worked hard to get the scientific facts right, which meant
that I saw a good deal of Hickie’s emails. Hickie’s denial of the facts was
otherworldly:
Hickie denied that antidepressants increase the
suicide risk in children and adults and recommended Demasi read Gibbons’ work,
noting that suicide rates increase when antidepressant use decreases (Hickie
sent 10 of Gibbons’ papers to Demasi); he asked what evidence there was that actual
suicide is a side effect; he claimed that FDA’s black box warning wasn’t
justified and might have caused harm; he noted that antidepressants are not
over-prescribed; he said that suicidal thoughts are not the same as completed
suicides; he evaded the question about the chemical imbalance but said that
antidepressants do not cause a chemical imbalance; he rejected the idea that
general practitioners don’t have time for full mental health histories and
follow ups; he claimed that a very extensive literature showed that
antidepressants can prevent relapse; and he opined that there was no wide
debate about psychiatry, as the critique comes from fringe groups.
What a mouthful. Australians are not supposed to
know the truth about antidepressants and they are not given the opportunity to
hear views other than those cherished by the silverbacks. But this censorship
has cracks. Some of my talks were filmed and the one from Melbourne is publicly
available (see my website for links, www.deadlymedicines.dk).
By refusing to appear in the TV programme,
Hickie also got off the hook in another matter. He knew that Demasi would ask
him about his conflicts of interest in relation to a highly dubious,
unsystematic review he published in the Lancet as
first author.43 It was about melatonin-based drugs for depression,
but “In particular, we highlight agomelatine,” which got four pages, whereas
four other drugs only got one page in total. Both authors had numerous ties to
Servier, which sells agomelatine, and there were possibly honoraria that
weren’t declared in the paper. The second author, Naomi Rogers, had received an
“unrestricted educational grant” from Servier, which in my view is a euphemism
for corruption, as the industry doesn’t just give its money away.2 Hickie and Rogers
claimed that fewer patients on agomelatine relapsed (24%) than do those on
placebo (50%), but a systematic review by other psychiatrists found no effect
on relapse prevention, no effect as evaluated on the Hamilton depression scale,
and that none of the negative trials had been published.44 Three pages of letters – which is extraordinarily
much – to the editor in Lancet (21 January 2012)
pointed out the many flaws in Hickie’s review.
Psychiatry is not evidence-based
medicine
Instead of a science of madness, we
documented a mad science.
KLRK, GOMORY AND
COHEN IN MAD SCIENCE45
We all want to practice evidence-based medicine,
which rests on three pillars: reliable research, clinical expertise and the
patient’s values and preferences. Psychiatry is not
evidence-based medicine, as none of these apply:
1) The research is unreliable. The diagnoses are
unscientific and arbitrary; the placebo controlled drug trials are unreliable,
as they have not been effectively blinded; the placebo groups have been harmed
by introduction of withdrawal effects; drug harms are being misinterpreted as
disease symptoms, particularly when drugs are being withdrawn; harms are being
vastly underreported; and almost all trials are controlled by the drug
industry.
2) The clinical expertise is totally unreliable.
Doctors almost always credit the drugs for any spontaneous improvement and puts
the blame for any untoward symptoms on the disease, or they think they are
caused by a new disease. This leads to additional psychiatric diagnoses and is
a major reason why so many patients receive several types of psychotropic
drugs.
3) Patient values and preferences are almost
totally ignored. Patients and their relatives are rarely listened to,
particularly when they complain about drug harms, and patients are subjected to
forced treatment with drugs even when they know it will harm them.
Not even when the evidence is crystal clear is
it being respected. In Denmark, SSRIs are recommended for children who are at
risk of suicide46 and for old people with depression,47 although SSRIs increase mortality in these age
groups (see Chapter 3). In just 14 years, from 1996 to 2010, there was a
nine-fold increase in total dispensed psychotropic medication for children and
adolescents in Denmark.48 The two authors downplayed this horrible development
by stating that it was only a two-fold increase after adjusting for increasing
patient numbers. So, have the number of children in Denmark increased 4.5-fold?
No. What they mean is that 4.5 times more children are sent to the mental health
services, which in itself is wrong. It is therefore meaningless to adjust for
this, but it could be related to the fact that one of the authors had ties to
companies selling psychotropic drugs.
Considering the unblinding bias, it is not
surprising that psychiatric drugs seem to work for virtually everything, e.g.
antidepressants are used for all sorts of things including urinary
incontinence, pain, premenstrual symptoms, premature ejaculation, hot flashes
in menopause, and they even seem to work for shopaholics.2
Some effects are of course real, e.g. the sexual
harms of antidepressants may explain why some men find them useful for
premature ejaculation, but most measured benefits are non-existing. Consider,
for example, a trial that showed that escitalopram reduced the number of hot
flashes in menopausal women.49 The number of hot flashes at baseline was 10 and
after eight weeks there was a difference of 1 between drug and placebo. This
tiny effect is likely just bias, as most women have guessed which drug they
receive. And even if it were true, who cares? It cannot possibly be clinically
relevant, particularly not considering all the harms that SSRIs inflict on
women.
In 2014, the FDA approved paroxetine for hot
flashes based also on one less flash a day.50 The approval ran counter to the recommendation of
the FDA’s advisory committee, which concluded that the overall benefit-risk
profile of paroxetine was unfavourable. The FDA opined that doses don’t have to
be tapered before use is discontinued, but the dose was 7.5 mg, close to the
starting dose for depression, which is 10 mg. Due to its short half-life,
paroxetine is one of the worst SSRIs for giving people abstinence symptoms! The
FDA also allowed a new name, Brisdelle, which means that most patients won’t
know that Brisdelle is an antidepressant drug. The drug maker, Noven, doesn’t
exactly reveal this on its US home page:51
“If you’re one of the millions of women dealing
with hot flashes, you’re not alone. They can be disruptive, uncomfortable, and
embarrassing. And for some women, they can last for years. So why suffer more
than you have to? You can do something different because there’s a non-hormonal,
prescription treatment option for moderate to severe hot flashes due to
menopause called Brisdelle® (paroxetine).” Nowhere does Noven
tell the women that it is the same drug as Prozac and nowhere is it written
explicitly that Brisdelle is an antidepressant drug. I consider this
consumer fraud. The homepage says: “Have a conversation with your doctor
today.” By all means, but tell your doctor not to use Brisdelle or any other
antidepressant for hot flashes.
One of the new fads in psychiatry is the idea
that some diseases are caused by inflammation, and a systematic review of 14
trials of celecoxib, a so-called nonsteroidal anti-inflammatory drug, showed an
effect on depression, effect size 0.34.52 An effect of this magnitude can easily be caused by
unblinding bias, and by the way, nonsteroidal anti-inflammatory drugs are not
anti-inflammatory at all; it’s just a misleading name.2 And if the
patients have pain some-where, which many depressed patients have, painkillers
might seem to reduce the “depression.” Many of the patients had arthritis, and
in another study, of depressed patients treated with duloxetine, the patients
also had substantial levels of pain.53 Finally, we should not treat depression with
nonsteroidal anti-inflammatory drugs, some of the most deadly drugs we have.2
Psychiatrists are usually paid per patient
enrolled in clinical trials and may not bother to go through all the items on
the rating scales, such as Hamilton’s depression scale, with the patient but
may use their overall impression to score some of the items without having
asked, or to score later based on memory.54 Patients cheat, too. Some people participate in
trials without being ill just to pocket the money, as a healthy person told a
doctor on a train ride:55
“I’m not depressed … the trials are advertised,
the best pay about £100 a day to volunteers. For a 20 day trial that’s £2000 …
it’s nice to see your regular friends.”
Can we reform psychiatry or is a
revolution needed?
When will psychiatrists finally accept that
we are dealing with sensitive, delicately poised human beings, not machines to
be tinkered with; that the very definition of life is one of self-organisation
and self-management? The only real lasting change comes when we help a person
to bring about the painful work of change within themselves.
IVOR BROWNE,
IRISH RETIRED PSYCHIATRIST56
There is a vast disconnect between what
psychiatrists think about their treatments and what patients think about them.
In a large survey of 2,031 people from 1995, people thought that
antidepressants, antipsychotics, electroshock and admission to a psychiatric
ward were more often harmful than beneficial.57, 58 This view concurs with the best evidence we have,
but the social psychiatrists who had done the survey were dissatisfied with the
answers, and argued that people should be trained to arrive at the “right
opinion.” In what way? More brainwashing?
In another survey from 1991, 91% of 2,003 lay
people thought that people with depression should be offered counselling; only
16% thought they should be offered antidepressants; only 46% said
antidepressants were effective; and 78% regarded antidepressants as addictive.59 The psychiatrists’ view on these responses was that,
“Doctors have an important role in educating the public about depression and
the rationale for antidepressant treatment. In particular, patients should know
that dependence is not a problem with antidepressants.” I fully understand why
the survey also found that “the word psychiatrist carried connotations of
stigma and even fear.”
It’s not the patients that need training, it’s
the psychiatrists and other doctors, but psychiatry is so much out of touch
with reality that I am afraid that no amount of training will get us even close
to where we want to be.
The self-delusion, denial and hype in psychiatry
run really high. Just before fluoxetine reached the market in 1988, NIMH had
surveyed the public about its views on depression, and only 12% wanted to take
a pill to treat it.60 However, the leaders of NIMH were determined to
change this attitude and launched a totally misleading, so-called public
awareness campaign: Depression is a serious disease that can be fatal if
untreated; depression is underdiagnosed and undertreated; and 70-80% get better
on drug and only 20-40% on placebo. This postulated 45% difference in effect is
fraudulent; even the industry-friendly FDA found only 10%, and the true
difference is close to zero (see Chapter 3). The campaign was immensely
successful, and the media praised Prozac as the new wonder drug.
The hype was extreme even by American standards.
A popular trick is to underline the seriousness of depression by saying that
the suicide risk in major depression is 15%.61 Every major textbook quotes this high suicide risk,
which comes from a 1970 study, but the true lifetime risk is only 2-3%.61
Many patients are called treatment-resistant. It
isn’t that the medication didn’t work, the patient was treatment-resistant.
This is very convenient for psychiatrists, as it puts the blame on the victim
and not on the drug or on them, although they failed by endlessly trying new
drug combinations and higher and higher doses, instead of taking patients off
the drugs and talking to them, which might have led to recovery. The term
treatment-resistant should be banned, as it is a cover-up for the system’s own
failures. If psychiatrists insist on using this term, they should accept that
we might call them fact-resistant. Psychological research has shown that the
more facts people are exposed to showing that their beliefs are wrong, the more
steadfast they often become in their erroneous beliefs. This is where
psychiatry is today. Thus, the fact-resistant psychiatrists are also
treatment-resistant.
Psychiatry doesn’t deliver what patients want
and what they believe is most helpful to them. A meta-analysis of 34 studies
showed that the patients, of which almost 90% had depression or anxiety,
preferred psychological treatment three times as often as drugs.62 However, few patients get psychotherapy; almost all
of them get drugs. David Healy is right when he says that psychiatric drugs are
poisons that have been rebranded as fertilizers to be used as widely and early
as possible.63 The chemical pollution from psychotropic drugs is
vastly more dangerous for our health than the chemical pollution of our food
and environment.
General practitioners cannot handle psychiatric
diseases either.64 In relation to depression, for example, the chairman
for the Danish Association for General Practitioners said in 2014 that they
didn’t have “oceans of time” and couldn’t set aside a whole hour for one
patient, as they also needed to think of their economy. But that is exactly the
point. What is needed is plenty of time, in order to avoid drug treatment and
to heal patients, not only for people with depression but for virtually
everyone with a psychiatric disease or who is suffering from difficult life
circumstances.
What should be done about this? Is there any
hope that doctors can learn to handle psychiatric drugs in a way that creates
more good than harm? Given the evidence we have, we will have to conclude that
this cannot be done. Furthermore, all the initiatives I know about where
pioneering psychiatrists or psychologists have tried to use drugs as little as
possible – and rather consistently have gotten better results than mainstream
psychiatrists – have been strangled. What people do in healthcare has little to
do with what is right or wrong, but a lot to do with who holds power. There are
strong guild interests to protect, and politicians and administrators loathe
going against powerful specialist groups, as it gives them so much trouble. It
is far more convenient to support psychiatric leaders when they say that
initiatives for using drugs far less are unethical experiments on people with
serious diseases and in great need of drugs. Specialists always say this when
their guild interests come under threat.
In order to restructure psychiatry even a little
bit, we need to work primarily with lawyers, journalists, patients and their
relatives, and young psychiatrists in training who have not yet been spoiled by
the silverbacks. We need nothing less than a revolution in psychiatry. Like in
all revolutions, those in power must go and we must carefully construct a
completely new curriculum for future psychiatrists.
14
Deadly psychiatry and dead ends
I’ve spent most of my professional life to
evaluate the quality of clinical research, and I think it is particularly poor
in psychiatry. Industry-sponsored studies … are selectively published, are
often transitory, are designed to favor the drug and demonstrate such small
benefits that they probably do not outweigh the long-term damage.
MARCIA ANGELL, FORMER EDITOR OF
NEW ENGLAND JOURNAL
OF MEDICINE1
Psychiatry’s almost manic obsession with
ineffective, addictive drugs has led to a disaster in public health so big that
nothing I have seen in other areas of medicine comes close.
Robert Whitaker is convinced that most
psychiatric patients would be better off not receiving drugs at all.2, 3
Whitaker once invited me to give a lecture at the Safra Center for Ethics at
Harvard University in Boston, to which he belongs, and I have lectured with him
on several occasions in different countries. Every time there have been
psychiatrists in the audience who shared our views that the way we currently
use psychiatric drugs causes far more harm than good.
On one such occasion, I gave an invited talk in
Los Angeles at the annual conference of the International Society for Ethical
Psychology and Psychiatry, which has been described as North America’s leading
organisation of critical thinkers in the mental health field.4 The title of the meeting was punchy, “Transforming
Mad Science and Reimagining Mental Health Care,” and the press release
announced that the plenary speakers “shared the controversial belief that a
‘medical model of care’ – the idea that distress and misbehavior have physical
causes that are best treated with physical means like medications – is causing
more harm than good to individuals and to society.” These speakers included
leading psychiatrists like Allen Frances and David Healy, psychologists,
psychotherapists, social workers, neuroscientists, and a previous patient.
Peter Breggin, who was not at the meeting, has also concluded that psychiatric
drugs do more harm than good.5
It was a fascinating meeting that made it clear
that we need a revolution in psychiatry. Psychiatric survivor Laura Delano
described how small groups of people gather to support each other in coming off
psychiatric medications, de-indoctrinating themselves from the biological model
of mental illness and supporting each other through psychological crises and
social change. When she read Whitaker’s book, Anatomy of an
Epidemic,2 which won the 2010 Investigative Reporters and
Editors book award for best investigative journalism, it suddenly dawned on her
that she should reclaim her humanity and free herself from the prison of
psychiatric “care.” She had become dehumanised by psychiatry, she was called
treatment-resistant, was on five drugs, and her drug-induced weight increase
was even given a psychiatric diagnosis: binge eating! Whitaker’s book saved her
and helped her live with her pain more peacefully, until she had built up
enough faith in herself to heal, so that she no longer felt the need to remind
herself over and over again that she didn’t need to believe everything her mind
was telling her, as it was still under the influence of drugs.
Laura has connected with many practitioners who
are slowly coming to understand the inefficacy and harm of the current
“treatment” standard, but who feel powerless and afraid to do anything
differently, fearing they could lose their licenses, face a lawsuit, get fired,
or not get promoted. We must find ways to change this so that it becomes
acceptable not to medicate people, which mainstream
psychiatry considers “irresponsible,” “dangerous,” or even “life-threatening.”
We need to create a heightened consciousness around just how oppressed and
harmed the patients have been by the “quick fix” mentality we have as a
society, and to realise how false the “quick fix” story is in the first place,
so that the demand for “psychiatric care” will lessen.
The organiser of the meeting, psychologist David
Cohen, wasn’t surprised to hear that people coming from different backgrounds
independently had arrived at similar perspectives on the problems we’re facing
in psychiatry and how to go about solving them. He also reminded the audience
that, over the last few years, mental health authorities have acknowledged an
absence of findings from biological or genetic research that have translated
into a difference in patient care. They have recognized that 50 years of
increasingly sophisticated treatments have not reduced the burden of mental
disorders; in fact they have increased it substantially.2 At the same time,
powerful conflicts of interest have been exposed that keep practitioners and
patients uninformed about the true effects of drug treatments.
Usually, people who are extreme are few in
number, but in this case it is the vast majority of psychiatrists that are
extreme. It is truly extreme that psychiatrists have built their specialty on a
number of myths, lies and highly flawed research, which have harmed our nations
to the extent we have seen. Marcia Angell has noted that psychiatrists should
consider that other medical specialists, unlike psychiatrists, would be very reluctant
to offer long-term symptomatic treatment without knowing what lies behind the
symptoms, e.g. if a patient suffers from nausea or headache.1 In my own
specialty, internal medicine, we are on much safer ground when we intervene.
Furthermore, apart from chemotherapy for cancer, it is difficult to identify a
class of drugs in general use as toxic as antipsychotics.
In 2014, a senior psychiatrist at
Rigshospitalet, the national university hospital in Denmark, which is where I
work, underlined involuntarily just how necessary the revolution is. He was
interviewed by a newspaper and said that SSRIs protect against suicide, with
reference to observational studies. He also said we didn’t overuse SSRIs, as
the consumption reflects the number of ill patients. This is a sick system,
which we must fight with all the means at our disposal.
Psychiatrists are slowly waking up to the
tragedy they have created, and mainstream psychiatric journals, such as the British Journal of Psychiatry, now publish papers that are
highly critical of the current model of biological psychiatry. For example, one
paper stated that the research into biological mechanisms of mental and
behavioural responses has failed to deliver anything of value to clinical psychiatrists
and is very unlikely to do so in the future,6 and another predicted that the current biology-based
model will be ruinous to the profession due to its consistent failure to
deliver.7 It is noteworthy that these pessimistic statements
come after more than 60 years of research in biological psychiatry.
It seems that many billions of research money
have been wasted on false leads. Even Thomas Insel, the director of NIMH, is
critical. He has pointed out that there is no evidence for reduced morbidity or
mortality from any mental illness from new drugs developed over the last 20
years, in striking contrast to the steadily decreasing mortality rates for
cardiovascular disease, stroke and cancer, and that there is little evidence
that the prospects for recovery have changed substantially in the past century.8 That’s a strong statement, but it’s actually an
understatement, as there is solid evidence that the prospects for recovery have
worsened substantially because of the drugs we use.
But what the public has heard about are reforms, revolutions, progress,
innovations and paradigm shifts.8 Empty barrels make the loudest
noise.
The connection between psychotropic
drugs and homicide
Whether they are legal or illegal, it’s
unhealthy to perturb normal brain functions with drugs, and psychotropic drugs
can lead to violence, including homicide.9-13 An analysis of
adverse drug events submitted to the FDA between 2004 and 2009 identified 1,937
cases of violence, 387 of which were homicide.11 The violence was particularly often reported for
psychotropic drugs (antidepressants, sedatives/hypnotics, ADHD drugs and
varenicline, a smoking cessation drug that also affects brain functions).
We know that antidepressants and ADHD drugs can
lead to homicide,11 but if we read the newest scientific literature, we
are led to believe that it isn’t clear whether antipsychotics increase or
reduce violence. However, the observational studies in this area are just as
problematic as the observational studies that claim that the use of
antidepressants reduce the risk of suicide (see Chapter 3). We therefore
shouldn’t pay much attention to them, but I shall comment on a 2014 study from
Sweden published in the Lancet that linked a crime
register with a prescription register.14 The authors acknowledged that the evidence that
drugs can reduce the risk of violence is weak. But they also said that in their
own study, violent crime fell by 45% in patients receiving antipsychotics
compared with periods when participants were not on medication.
Such studies are highly misleading. Patients
might stop taking the drug because it gives them bad feelings that predispose
to crime. Withdrawal effects also predispose to crime, and patients with severe
psychopathology might have committed a crime and avoided taking drugs.
I debated with Norwegian psychiatrists in 2015
in a newspaper, and one of them wrote that it is the untreated patients that
are dangerous. However, the study he referred to cannot be used to substantiate
this claim.15 It showed that the risk for murder is greatest in
first episode psychosis and decreases when patients are treated. But we don’t
know whether this risk would have been reduced equally, or perhaps even more,
if the patients had not been treated with antipsychotics.
Curiously, our most prestigious journals have
published some of the most misleading studies or commentaries I have ever
found. An NIMH study reported that patients with serious mental illness –
schizophrenia, major depression, or bipolar disorder – were two to three times
more likely to be assaultive as people without such an illness. A professor of
psychiatry who commented on the study in the New England
Journal of Medicine mentioned that although it didn’t specifically
monitor the treatments, “it seems possible that treating psychiatric illness
does not just make patients feel better; it may also drastically reduce the
risk of violent behavior.”16 This wishful thinking is contrafactual.
Antipsychotics and antidepressants can cause violence and it will usually be
the drugs, not the disease, that on rare occasions can make psychiatric
patients commit horrendous acts. Studies that do not separate medicated from
unmedicated patients are not worth the paper they are written on, and these
patients were medicated!
In
contrast to such flawed studies, it is pretty revealing to look at studies
conducted before the advent of antipsychotics.3 Before 1955, four
studies found that patients discharged from mental hospitals committed crimes
at the same or lower rate than the general population, whereas eight studies
conducted between 1965 and 1979 found higher rates.
Akathisia, the well-known causal factor for
violent actions and crime, was given little attention in these years, and
physicians generally interpreted the restless behaviour as a sign that patients
needed a higher dose of the drug, which only increases the risk of crime. When
the psychiatrists finally took an interest in their patients, the results were shocking.
In one study, 79% of mentally ill patients who had tried to kill themselves
suffered from akathisia.3 A 1990 study reported that half of
all fights at a psychiatric ward were related to akathisia and another study
found that moderate to high doses of haloperidol made half the patients
markedly more aggressive, sometimes to the point of wanting to kill their
torturers, the psychiatrists.3
Psychotropic drugs can cause people to lose some
of their conscience, so that they lose control over their behaviour.10 Such people are at greatly increased risk of
committing acts of crime and violence.
Several high-profile homicides have been
committed by patients in a drug-withdrawal state, which also may cause
akathisia,5, 10
and a clear sign that the psychiatrists generally don’t know what they are
doing and what they are causing is that they have virtually always interpreted such
events as meaning that the patients need to be kept on their drug, rather than
acknowledging the peril of using the drug in the first place.3 It is therefore
their fault that the media have failed to write about it or investigate it. As
David Healy says: “Violence and other potentially criminal behaviour caused by
prescription drugs are medicine’s best-kept secret. Never before in the fields
of medicine and law have there been so many events with so much concealed data
and so little focused expertise.” When one of the teenage shooters in the
Columbine High School massacre, Eric Harris, was found to have an
antidepressant in his blood, the American Psychiatric Association immediately
denied a causal relation and added that undiagnosed and untreated mental
illness exacts a heavy toll on those who suffer from these disorders as well as
those around them.17 This sickening marketing speak comes right from the
drug industry, which provides generous funds to the association (see Chapter
13). Harris’ partner, Dylan Klebold, had taken sertraline and paroxetine.
Adam Lanza killed 20 school children, six
members of staff, his mother and himself in Newtown, Connecticut, in 2012.
After this crime, the International Society for Ethical Psychology and
Psychiatry called for an inquiry into the connection between such acts of mass
murder and the use of psychotropic drugs.18 The media had noted that Lanza was taking
prescription drugs to treat a neurological-development disorder, but nothing
was revealed about the nature of these drugs. The society mentioned a number of
other mass killings where psychotropic drugs might have had a causal role and
noted that in 14 recent school shootings, the acts were committed by persons
taking or withdrawing from psychiatric drugs, resulting in 58 killed and over
100 wounded.18
In other school shootings, information about the shooters’ prescription drug
use and other medical history was kept from public records.
It is difficult to know when psychotropic drugs
are the major factor in these crimes, as the people who take them may suffer
from severe personality disorders. But there is no doubt that these drugs can
cause homicide, and the mass murders should therefore be routinely investigated
for this possibility. There is enough evidence, for example, that
antidepressants increase the risk of suicide and violence for the US Food and
Drug Administration and its Canadian counterpart to require that drug companies
include a black box warning to that effect on their packages. Antidepressants
appear to more than double the risk of hostility events in adult and paediatric
placebo controlled trials,18 and in our systematic review of
studies in human volunteers, we found that antidepressants double the incidence
of activating effects19 (see also Chapter 3).
How few drugs do we need?
We could have a much better psychiatry almost
without drugs. Some psychiatrists hardly use any drugs at all. One is Lois
Achimovich, Australia, a child psychiatrist for 40 years, who has never used
stimulants or antipsychotics. He only uses diazepam, in low doses and only
short-term, when a child cannot sleep in an acute situation, e.g. after the
death of a parent. Peter Breggin once had a debate with a paediatrician who
tried to look very judicious by stating that he only medicated a small number
of children each year. He challenged Breggin to say what was wrong with that,
and Breggin replied, “Doctor, I would not know which child to poison.”
Several psychiatrists I have met have never used
antidepressants, as they don’t believe they work while they cause much harm.
Like Achimovich, the only drugs Peter Breggin uses are benzodiazepines, and
only temporarily, if people feel badly during drug withdrawal. Perhaps people
like them don’t see the worst cases, but they have nevertheless demonstrated
that we very rarely need drugs.
One way to go, which David Healy and David Cohen
have suggested, could be to make psychotropic drugs freely available over the
counter. This is an interesting suggestion, provided that marketing to the
public became forbidden of course. If there were no doctors as intermediaries,
with all their false beliefs about chemical imbalance, targeted therapy and
false reassurances about safety and drugs producing recovery and preventing
relapses, many patients would give up taking psychotropic drugs very quickly,
as their side effects are so horrible.
We could also take the opposite approach. More
than 40 years ago, Archie Cochrane, whom the organisation I work for is named
after, wrote:20
“I would ban the prescription of amphetamines
and put a large number of other psychotropic drugs on a list which could only
be prescribed by psychiatric consultants. I do not suggest this because I think
consultants know better than GPs which of these drugs will do more good than
harm in the long run. I do not think anyone knows, but they may know more about
side effects and, much more importantly, there are fewer consultants than GPs
and it will make the prescriptions more difficult to get. Psychiatry, in my
view, must be criticized as using a large number of therapies whose
effectiveness has not been proven. It is basically inefficient.”
It’s remarkable that Cochrane wrote this so long
ago, as it’s still the case today that psychiatric drugs are pretty
inefficient.
Peter Breggin has suggested that we should
prohibit giving psychiatric drugs to children, just like we have prohibited
physical and sexual abuse.21 I agree completely that psychiatric drugging of
children is a form of child abuse that should be prohibited, with very rare
exceptions. We are not allowed to beat our children but are allowed to destroy
their brains with drugs. We medicalise the inevitable conflicts that arise
between parents and children, and methylphenidate (Ritalin) has become the
modern version of the cane. This is a flagrant abuse of a faulty disease model
and a serious violation of the children’s human rights, which must be stopped.
The drugged child’s brain cannot develop in its
intended manner but develops in response to a toxic internal environment.
Furthermore, the stigmatisation and loss of self-esteem, which often follows
psychiatric diagnosis and treatment (see Chapter 6), is especially ominous in
children who have yet to shape their personalities, and it can hamper future
opportunities even without considering the potential brain damage caused by the
drugs. Children may learn to view themselves as physically or genetically
disabled, with impaired self-determination and increased feelings of
helplessness.21
It’s horrible.
Also for adults, psychiatric drugs are a
dangerous weapon that doctors cannot handle and most of them do far more harm
than good. We could therefore take them off the market and spare a few for
acute situations and for legitimate purposes outside psychiatry, e.g. for
induction of anaesthesia and for treatment of epilepsy. This would mean
tremendous progress for mental health, as far fewer people would be in
treatment and far fewer would be harmed.
I shall try to estimate how little we need
psychiatric drugs. I will leave out epilepsy drugs, as I don’t know how much of
the usage is for psychiatric purposes (at any rate, I believe these drugs
shouldn’t be used for psychiatric diseases). This leaves us with five drug
groups: antidepressants, ADHD drugs, antipsychotics, anti-dementia drugs, and benzodiazepines
and similar sedatives.
As antidepressants likely don’t work, whereas
they actually cause much harm, including deaths, personality changes, sexual
disturbances and addiction, we shouldn’t use them at all.
We shouldn’t use ADHD drugs either. They might
give some short-term relief but are clearly harmful when used long-term, which
they almost always are.
Antipsychotics kill many people and destroy many
more people’s lives, and it’s likely we could use benzodiazepines for the same
indications. Whitaker has estimated that we could halve the two million adults
disabled by schizophrenia in the United States if we used antipsychotics in a
selective, cautious manner.2 I have no doubt he is right. But it
can be discussed whether we need this class of drugs at all.
Anti-dementia drugs shouldn’t be used, as they
don’t work and are pretty harmful.
Benzodiazepines and similar drugs are also very
harmful but we need drugs for sedation in acute situations and they are less
harmful than antipsychotics.
I shall use Danish statistics (http://medstat.dk/) to
illustrate how little we need psychiatric drugs. Currently, we use so many of
these drugs that one out of seven Danes could be in treatment with a psychiatric
drug every day for their entire life, from cradle to grave, if they took one
drug each (Table 14.1).
Table
14.1. Usage of psychotropic drugs in Denmark in 2013. Defined daily doses per
1000 inhabitants per day; sales in million DKK.
Antipsychotics are used long-term although they
are very harmful when used this way. We should only treat acute conditions,
which is roughly about 5% of current usage, or less. The current usage is 14.3
defined daily doses per 1000 inhabitants per day (DDD), of which 1.1 is
lithium. Lithium is perhaps an important drug, as it perhaps reduces suicides
(see Chapter 7).22 On the other hand, most cases of bipolar disorder
are caused by antidepressants and ADHD drugs, and if we stop using these, there
wouldn’t be much need for lithium; 0.5 DDD would seem more than enough. Thus,
the 14.3 DDD could be reduced to 0.5 plus 5% of 13.2, which is 1.2 DDD.
It is not very often we would need a drug for
acute anxiety or sleeping problems, and it should be short-term. Since most
people on anxiolytics take them for years because they have become dependent on
them, we could somewhat generously say that only 5% of current usage is needed.
If we used psychotropic drugs prudently, we
would not need 135.3 DDD but only 2.7, which is 2% of current usage (see Table
14.1).
Our current usage of psychotropic drugs could
be reduced by 98%.
In Denmark, 97% of all psychotropic drugs are
used outside hospitals. We should therefore primarily target doctors who work
in specialist practice, particularly general practitioners who prescribe most
of the drugs by far. If we restricted psychotropic drug usage to hospitals, we
could curb our drug epidemic. I am aware that this proposal seems radical but
it actually isn’t. We don’t usually give chemotherapy outside hospital, and
psychotropic drugs are also toxic and dangerous. This would be too restrictive,
though, as psychiatrists in specialist practice need the possibility to use
drugs in acute situations.
The potential financial savings are even larger
than 98%. Our costs would only need to be 3% of current expenditure (Table
14.1), but this is before we have taken into account that clinicians often use
drugs that are five to ten times more expensive than equivalent drugs. We could
therefore easily save 99% of our current expenditure. For Denmark, this would
mean annual savings of around DKK 1.5 billion; for the United States it would
mean annual savings of a good deal more than $15 billion, as there is virtually
no price control in that country.
Note that the contest is not between drugs and
psychotherapy or any other specific mental health approach. The potentially
earth-shaking contest takes place between drugs and real life, between an
artificially distorted mental life and a clear mind and spirit.10 Peter Breggin
has cautioned that the people most in need of help are the least likely to
benefit from any form of help. Being drugged only pushes them deeper into
helplessness, further crippling them psychologically and socially. Although he
is himself a psychiatrist, Breggin advises that the most disturbed patients
need to be protected from psychiatrists.10
How many people are killed by
psychotropic drugs?
Psychiatric drugs are much, much more
dangerous than you have ever, ever been led to believe by the doctors who are
prescribing them. I genuinely believe that if most people knew how dangerous
the psychiatric drugs really were, most people would never start on them, and I
also believe that if most prescribers had even the faintest idea how dangerous
they were, they would stop prescribing them. How is it that so many people can
be ignorant about psychiatric drugs? Well, the truth is that’s because they are
all getting their information from the drug companies.
PETER BREGGIN23
Likely all psychotropic drugs can lead to
confusion and impaired coordination and balance, which can lead to falls and
traffic accidents.24-29 Antidepressants are by far the most used
psychotropic drugs (Table 14.1). They can cause orthostatic hypotension,
sedation, and confusion and they double the risk of falls and hip fractures in
a dose-dependent manner.28, 29 Hip fractures
are often deadly, which makes psychotropic drugs a silent killer, as we will
rarely suspect that it was the drug that caused the fall.
If we want to find out how many people
psychiatric drugs kill, we might think that placebo controlled randomised
trials would be ideal, but that’s not the case, and schizophrenia is a prime
example. The cold-turkey design of most of these trials has caused some
patients to commit suicide in the placebo group (see Chapter 6). We therefore
need to find patients who were not already in treatment with antipsychotics
before they were randomised.
In trials in dementia, pre-treatment is not so
likely. A meta-analysis of such trials proved that antipsychotics kill people,30 but the authors of a study about antipsychotic
prescribing in UK primary care toned down the unwelcome news when they quoted
this metaanalysis by saying that dementia “may be associated with” increased
all-cause mortality.31 No “may be” and no “associated with” are
appropriate here; the meta-analysis proved that antipsychotics kill people.
The meta-analysis included trials of newer
antipsychotics, aripiprazole (Abilify), olanzapine (Zyprexa), quetiapine (Seroquel)
and risperidone (Risperdal), in patients with Alzheimer’s disease or dementia,
and deaths were recorded up till 30 days after discontinuing the double-blind
treatment. For every 100 patients treated, there was one additional death on
the drug (3.5% versus 2.3% died, P = 0.02). Elderly patients are often treated
with several drugs and are more vulnerable to their harmful effects, which
means that the death rate is likely higher than in young patients. On the other
hand, the trials generally ran for only 10-12 weeks although most patients in
real life are treated for years. Furthermore, deaths on drugs are often
underreported in industry-sponsored trial reports.13 I therefore believe a death rate of 1% is a
reasonable estimate to use.
The authors of the meta-analysis also reported
that 32% dropped out on the drug and 31% on placebo. Discontinuation rate is a
good outcome, as it combines perceptions of benefits and harms from the drugs,
and the result indicates that the drugs are pretty useless.32 So elderly patients are killed in huge numbers for
no benefit, and yet, in the United States, a third of people in nursing homes
take antipsychotics.32
With regard to benzodiazepines and similar
drugs, a cohort study of 34,727 patients found that increased doses increased
mortality, and the drugs doubled the death rate, although the average age of
the patients was only 55.33 The excess death rate was about 1% per year.
Another large cohort study of such drugs used for sleeping problems also found
increased mortality with higher doses.25 The authors did not report on absolute death rates
but estimated that sleeping pills kill between 320,000 and 507,000 Americans
every year.
With regard to SSRIs, a UK cohort study of
60,746 patients older than 65 showed that they led to falls more often than the
older antidepressants or if the depression isn’t treated, and that the drugs
kill 3.6% of patients treated for one year.34 The study was done very well, e.g. the patients
were their own control in one of the analyses. Some may argue that since it was
an observational study, it hasn’t been proved that antidepressants kill elderly
people. But it’s a strong message that even when the patients were their own
control – which is a good way to remove the effect of confounders – the lethal
effect was clear. Another cohort study, of 136,293 American postmenopausal
women (age 50-79) participating in the Women’s Health Initiative (WHI), found
that antidepressants were associated with a 32% increase in all-cause mortality
(hazard ratio 1.32, 95% CI 1.10 to 1.59) after adjustment for confounding
factors.35 This corresponded to 0.5% of people killed by SSRIs
when treated for one year. Thus, the death rate was only one seventh of that
found in the UK cohort but there are good explanations for this. The authors
warned that their results should be interpreted with great caution, as the way
exposure to antidepressant drugs was ascertained carried a high risk of
misclassification, which would likely make it more difficult to find an
increase in mortality. Further, the patients were much younger than in the UK
study, and the death rate increased markedly with age (0.3% for 50-59 years,
0.6% for 60-69 and 1.4% for 70-79).35 Finally, the women who were
exposed and not exposed were different for many important risk factors for
early death, whereas the people in the UK cohort were their own control.
Table
14.2. Usage of antipsychotics, benzodiazepines and similar, and antidepressants
in Denmark in 2013 in people aged at least 65 years, and estimated number of
drug-induced deaths. Defined daily doses per 1000 inhabitants per day. The
estimated use at hospitals (1-3%) has been included.
I therefore find that the 3.6% annual death rate
is more reliable than the 0.5% rate but will use a conservative estimate of a
2% death rate.
We can now estimate how many patients are killed
each year by antipsychotics, benzodiazepines and similar drugs, and
antidepressants. I will use Danish data again, as they are pretty typical for
psychotropic drug use in the western world, e.g. 12% of those aged 65 to 79 are
in treatment with an antidepressant drug (Table 14.2); in the United States,
usage is 14.5% in those at least 60 years of age.36
Table 14.2 shows the estimated number of
drug-induced deaths per year in those aged 65 and above caused by
antipsychotics, benzodiazepines or similar, and antidepressants. The total
number of deaths per year correspond to 209,000 deaths in the United States and
to 539,000 deaths in the United States and the European Union combined.
Psychotropic drugs kill more than half a
million people every year aged 65 and above in the western world.
There are some uncertainties related to this
estimate. Some people are in treatment with two or even three different types
of drugs and you can only die once. There is also survivorship bias, i.e. those
who continue for years are those who tolerate the drug. On the other hand,
death can occur at any time, also in people who have taken a drug for years.
For example, both antipsychotics and antidepressants prolong the QT interval on
the ECG, and these drugs topped the list among all drugs in the FDA’s Adverse
Events Database for this side effect;37 thus, a patient might die when another drug is
added. We also know that benzodiazepines increase the mortality of
antipsychotics,38 so this combination is also risky. Furthermore, far
more people are exposed to the dangers of these drugs than the data in the
table shows, as I have assumed that all patients are treated for a full year.
Even focusing only on those aged 65 and above,
the estimates show that psychotropic drugs are the third major killer after
heart disease and cancer, which in 2010 killed 600,000 and 575,000 Americans,
respectively.13
I have deliberately been conservative, and have not factored in deaths
occurring in those under 65.
Based on studies in Europe and the United
States, I previously estimated that our prescription drugs kill 200,000 people
every year in the United States.13 This estimate now seems to be far
too low, as psychotropic drugs alone kill more than this.
We could also look at the total sales figures
for drugs, for example for Eli Lilly’s best-seller, fluoxetine. In 2004, the
company was under attack and sent this written statement: “Prozac has helped to
significantly improve millions of lives. It is one of the most studied drugs in
the history of medicine, and has been prescribed for more than 50 million
people worldwide. The safety and efficacy of Prozac is well studied, well
documented, and well established.”39 When drug companies face trouble, they often try to
escape by using big numbers. Prozac has not improved millions of lives. Prozac
has made millions of lives miserable, so let’s estimate how many patients the
drug has killed. In Denmark, 45% of total usage of antidepressants occurs in
those aged 40 to 64, and 31% in those aged 65 and above, and using the same
assumptions as above, Prozac has killed 311,000 people worldwide in the age
group 65 and above up to 2004.
15
Forced treatment and involuntary
detention should be banned
Of all tyrannies, a tyranny sincerely exercised
for the good of its victims may be the most oppressive. It would be better to
live under robber barons than under omnipotent moral busybodies. The robber
baron’s cruelty may some-times sleep, his cupidity may at some point be
satiated; but those who torment us for our own good will torment us without end
for they do so with the approval of their own conscience.
C.S.
LEWIS, NORTHERN IRELAND WRITER (1898–1963)
Forced treatment is the biggest ethical issue in
psychiatry. Although it goes against our deepest instincts, it is commonly
used, not only for severe cases of psychosis, but sometimes also for people who
say they are thinking about suicide and for people who are not particularly
psychotic. As free citizens, we vehemently oppose oppression and tyranny in all
its forms. However, it is human nature to dominate and take control of others,
which lies deep in our genes, as it carries a great evolutionary advantage.
Striving for dominance is one of the strongest driving forces in nature, and to
have power over others gives us emotional satisfaction and more offspring,
which we can observe so clearly among our cousins, the great apes.
As power corrupts, there needs to be a power
balance in human relations. In psychiatry, however, involuntarily admitted
patients are totally powerless. This extreme power imbalance is a recipe for
disaster, and there is nothing psychiatric patients fear more than forced
treatment. They have been the victims of punitive measures for centuries
without their consent, and the mere threat of such measures has often terrified
patients to such an extent that they become docile in order to avoid them. Some
psychiatrists have administered shocks to patients they disliked the most, and
doctors have regularly prescribed shocks for those who were fighting, restless,
noisy, quarrelsome, stubborn and obstinate.1
Because of the extreme power imbalance, there is
a high risk that forced treatment is being used to benefit staff rather than
patients, in order to make their work less stressful. Many patients have
reported how the threat of mechanical restraints has been used to discipline
them into taking drugs, which they didn’t want because of their terrible side
effects. And the threat continues when the patients have left hospital and live
in a treatment home. If they refuse to take their medication, they might be
kicked out of the facility and involuntarily re-admitted to hospital;1
they might lose their social benefits; and they might even be denied access to
a mental healthcare centre. This happened to a four-year-old child when a nurse
practitioner in New York said she was bipolar and had a chemical imbalance, and
suggested three drugs: valproate (an epilepsy drug), risperidone and lithium. Her
parents refused this dangerous cocktail and she got well without drugs.2
Human rights in Europe
Patients often perceive forced treatment as
torture, and in Europe the oversight of forced treatment comes under the
convention prohibiting torture. Article 3 in the European Convention on Human
Rights is very short but to the point: “Prohibition of torture. No one shall be
subjected to torture or to inhuman or degrading treatment or punishment.”3
What this means is detailed in another document,4 and to ensure that the convention is not just window
dressing, a European Committee was set up, which, by means of visits, examines
the treatment of persons deprived of their liberty with a view to
strengthening, if necessary, the protection of such persons from torture and
from inhuman or degrading treatment or punishment.5
Regarding psychiatry, the committee noted in its
2013 report5
that working with the mentally ill will always be a difficult task and that it
has observed a dedication to patient care among the overwhelming majority of
staff in most psychiatric establishments. However, the committee also observed
that deliberate ill-treatment of patients in psychiatric establishments occurs.
I shall convey the key messages in the 2013
report in the next two sections and will thereafter give my comments on them.
Forced treatment
The admission of a person on an involuntary
basis should not be construed as authorising treatment without his or her
consent. The restraint of agitated or violent patients may on occasion be
necessary, but this is an area of particular concern to the Committee
for the Prevention of Torture (CPT), given the potential for abuse and
ill-treatment. The restraint of patients should be based on a clearly defined
policy that should make clear that initial attempts to restrain patients
should, as far as possible, be non-physical (e.g. verbal instruction) and that
where physical restraint is necessary, “it should in principle be limited to
manual control.” Talking to the patient to calm him or her down is the
preferred technique.
Instruments of physical restraint (straps,
straitjackets, etc.) should only very rarely be justified and must always be
either expressly ordered by a doctor or immediately approved by a doctor. Such
instruments should be removed at the earliest opportunity, and they should
never be applied, or their application prolonged, as a punishment.
Every psychiatric establishment should have a
comprehensive, carefully developed policy on restraint. The policy should also
contain sections on issues such as staff training, complaints policy, internal
and external reporting mechanisms, and debriefing.
Patients have repeatedly said they felt the
whole ordeal to be humiliating, a feeling at times exacerbated by the manner in
which the restraint was applied.
The CPT often finds that patients are
restrained, usually with mechanical restraints, as a sanction for perceived
misbehaviour or as a means to bring about a change of behaviour.
In many psychiatric establishments, the
application of restraints is resorted to as a means of convenience for the
staff. The usual justification is lack of staff but this reasoning is unsound.
The means of restraint require more – not fewer – medical staff, as each case
necessitates a member of staff to provide direct, personal and continuous
supervision. Clearly, video surveillance cannot replace such a continuous staff
presence.
A specific register should be established to
record all instances of recourse to means of restraint. Reducing its use to a
minimum often requires a change of culture.
In many psychiatric establishments, the use
of restraint can be substantially reduced, and programmes set up in some
countries for that purpose seem to have been successful, without this having
led to an increased resorting to chemical restraint or manual control. The
question therefore arises whether complete (or almost complete) eradication of
mechanical restraint might not be a realistic goal in the longer term.
Patients’ rights
The Committee for the Prevention of Torture
states that psychiatric patients should be treated with respect and dignity,
and in a safe, humane manner that respects their choices and
self-determination. An introductory brochure setting out the establishment’s
routine and patients’ rights should be issued to each patient on admission, as
well as to their families. Any patients unable to understand this brochure
should receive appropriate assistance.
Further, as in any place of deprivation of
liberty, an effective complaints procedure is a basic safeguard against
ill-treatment. Specific arrangements should exist enabling patients to lodge
formal complaints with a clearly designated body, and to communicate on a
confidential basis with an appropriate authority outside the establishment.
Patients should, as a matter of principle, be
placed in a position to give their free and informed consent to treatment. Any
derogation from this fundamental principle should be based upon law and only
relate to clearly and strictly defined exceptional circumstances.
Of course, consent to treatment can only be
qualified as free and informed if it is based on full, accurate and
comprehensible information about the patient’s condition and the treatment
proposed; to describe ECT as “sleep therapy” is an example of less than full
and accurate information. All patients should be provided systematically with
relevant information about their condition and the treatment which it is
proposed to prescribe for them.
The maintenance of contact with the outside
world is essential, not only for the prevention of ill-treatment but also from
a therapeutic standpoint. Patients should be able to send and receive correspondence,
to have access to the telephone, and to receive visits from family and friends.
Confidential access to a lawyer should also be guaranteed.
The patient should be able to consult his or her
file, unless this is unadvisable from a therapeutic standpoint, and to request
that the information it contains be made available to his or her family or
lawyer. In the event of discharge, the file should be forwarded – with the
patient’s consent – to a treating doctor in the outside community.
Once means of restraint have been removed, it is
essential that a debriefing of the patient take place. For the doctor, this
will provide an opportunity to explain the rationale behind the measure, and
thus reduce the psychological trauma of the experience as well as restore the
doctor-patient relationship. For the patient, such a debriefing is an occasion
to explain his emotions prior to the restraint, which may improve both the
patient’s own and the staff’s understanding of his behaviour.
Psychiatric treatment should involve a plan for
each patient that includes a wide range of rehabilitative and therapeutic
activities, including access to occupational therapy, group therapy, individual
psychotherapy, art, drama, music and sports. Patients should have regular
access to suitably equipped recreation rooms and have the possibility to take
outdoor exercise on a daily basis; it is also desirable for them to be offered
education and suitable work.
The CPT all too often finds that fundamental
components of effective psychosocial rehabilitative treatment are
underdeveloped or even totally lacking, and that the treatment provided to
patients consists essentially of pharmacotherapy.
Regular reviews of a patient’s state of health
and of any medication prescribed is a basic requirement, which will enable
informed decisions to be taken as regards a possible dehospitalisation or
transfer to a less restrictive environment.
My comments
The European approach provides a blueprint for
all nations to follow. The maintenance of contact with the outside world is
absolutely essential but not always respected, e.g. a social worker in Norway
told me about a patient who wasn’t allowed to phone anyone outside the
hospital. Such isolation increases the risk of abuse and of the Stockholm
syndrome, where captives express empathy and sympathy with their captors. Such
feelings are irrational in light of the danger endured by the victims, e.g. a
Norwegian psychiatrist used forced treatment with olanzapine, arguing wrongly
that untreated schizophrenia causes brain damage.
I oppose vehemently the European Committee’s
standpoint that a patient should not be able to consult his file if this is
unadvisable from a therapeutic standpoint. The Committee doesn’t explain what
this means, and the exception to patients’ right to their file is abused
pervasively. US lawyer Jim Gottstein has told me that he doesn’t know of a
single patient who obtained the file by just asking for it. Therefore, people
give an Authorisation for Release of Information to provide the file to PsychRights
(see below) that then gives it to the patient. This works about half the time.
One of the things providers do to try to prevent the patient from getting their
own file is to charge for the copies, which can be prohibitive, as most
patients are quite poverty stricken.
In the United States, many patients are
unnecessarily imprisoned or are homeless on the streets.6 Some US states still have the death penalty, and a
mentally ill patient can be executed by the state, if a committee decides that
the patient wasn’t insane when he killed someone. This has happened but it is
morally repugnant. A patient under the influence of a psychiatric drug may
seemingly act in a rational fashion when he kills, but can nonetheless behave
totally irrationally and out of character.7 Thus, by stating that a person wasn’t insane in a
forensic report to a court, which is a highly arbitrary decision, a
psychiatrist may contribute to murder by the state. This is about as far from
being a doctor as one can get, and psychiatrists should refuse to play kings or
gods that decide over life and death.
I was involved as an expert witness in a much
publicised court case where Graham Bishop, an Englishman, almost stabbed his
two daughters to death in the hospital where I work. He was sentenced to 11
years in prison and permanent expulsion from Denmark, but the case was
appealed. The forensic committee had acknowledged that methylphenidate
(Ritalin) could lead to “increased irritability and emotional instability” and
that they could not exclude the possibility that the drug could have influenced
his psychological state when the act was committed. However, they considered
this unlikely, arguing that he had previously taken similar doses without
problems.
There were several issues with this argument.
The fact was that he had never before taken such a high dose as he took just
before he stabbed his daughters, but even if he had not increased the dose, he
could still have reacted out of character under the influence of the drug
because the events that led up to the misdeed were very stressful. Further, the
harms of methylphenidate are far worse than the committee’s euphemistic note
about “increased irritability and emotional instability.” Methylphenidate can
cause violence, including homicide.8
I asked the forensic committee whether they
considered it the standard of care that Bishop’s psychiatrist had apparently
said that Bishop could increase the dose without problems and with no upper
limit. This question, and several others I had posed, was ignored by the
committee, and their reply to my question: “Does the forensic committee think
that intake of methylphenidate can increase the risk of violence, including
homicide?” was: “The question is of a general character.”
Yes, it was of a general character but relevant
for the case. I was pretty uncomfortable about getting no answers and also
about the committee being in a position where it was essentially asked to
evaluate its own previous judgment. This constitutes an unacceptable conflict
of interest, as few people are willing to admit their mistakes and overrule
themselves. No one knows whether Bishop would have committed his hideous crime
had he not been on methylphenidate.
I find the laws about forced treatment highly
problematic. In many countries, a person considered insane, or in a similar
condition, can be admitted to a psychiatric ward on an involuntary basis if the
prospect of cure or substantial and significant improvement of the condition
would otherwise be significantly impaired.
But is this ever the case? Are there any
treatments that can cure insane patients, or which can lead to such substantial
improvements that the patient’s condition would be significantly impaired if
she is not forced to go to hospital immediately? I don’t think so, and,
considering the abuse that takes place at psychiatric wards, this clause should
be removed from the law of all nations. There is already a clause that, if
patients present an obvious and substantial danger to themselves or others,
they can be involuntarily admitted. We don’t even need this. According to the
National Italian Mental Health Law, a reason for involuntary treatment can no
longer be that the patient is dangerous. If people are dangerous, it is a
matter for the police.
Thus, we don’t need forced treatment for
patients under any circumstances. We don’t need forced admission to hospital
either, as patients in Italy can decide that they want treatment elsewhere.
Our physicians cannot give us insulin without
our permission, not even if the lack of insulin might kill us, and they cannot
force us to take any other drugs than psychiatric drugs. This discrepancy
doesn’t make sense.
There is a common law assumption of course, that
if a person is unable to give consent, the health professional acts in
accordance with what she herself would have preferred, e.g. by giving an
unconscious person bleeding to death life-saving blood transfusions. But we
cannot assume that a severely psychotic person would want psychotropic drugs,
or that she is unable to understand what is being proposed or its consequences,
e.g. she might decline drugs because of previous experiences of serious harm.
Our laws about forced drug treatment build on
the terribly harmful misconception that antipsychotics have a specific effect
on psychosis, which is good for people.1 However, starting in 1975, patients
took their fight to US state courts and battled for their human rights. At the
same time, Soviet dissidents smuggled out manuscripts describing neuroleptics
as the worst sort of torture, which made it tricky to explain how the same
substance could be a poison in one country and a helpful remedy in another,1
particularly as the poison was used as forced “treatment” in both countries.
The idea that it is permissible to drug
incompetent people against their will ends up as being the justification to
drug everyone who doesn’t agree to it in those kinds of settings. This cannot
be defended from an ethical perspective, as it – quite objectively – usually is
not in the person’s best interest. Furthermore,
competence is about autonomy, which is not an all-or-nothing condition. People
can be incompetent for some purposes and competent for others, and I firmly
believe everyone is competent to decline psychotropic medication and
electroshock, especially after they have had any experience with it. Thus, the
key word is negotiation.
Psychiatric patients are the real experts and
judges and it is only they who can provide a credible insight into the
sometimes confusing chaos caused by injured feelings, just like only the
sufferer knows what it feels like to have physical pain and can describe it.
These are private feelings, and there can be great value in finding a meaning
in the madness instead of rejecting it and knocking the patients down against
their will with dangerous drugs and making zombies out of them. That won’t help
them recover and tackle the symptoms of madness. It’s a slippery slope if
psychiatrists assume that patients lack insight into their disease and the
drugs used to treat it because of their psychiatric disorder, and that their
judgments therefore shouldn’t count because they don’t know what is best for them.
It opens the floodgate for health professionals to decide on everything, which
short-circuits the good intentions of involving patients in their own treatment
and increases the risk of abuse.
Psychologist David Rosenhan has drawn attention
to the Catch 22 position of psychiatric patients.9 Some patients have found that they should avoid
mentioning certain things to their psychiatrist when hospitalised because it
may lead to additional diagnoses and more medication, which the psychiatrist
will rarely be interested in stopping again.
What should a patient then do when convinced
that the drug and not the disease is the cause of her symptoms? If she says
anything about having the dose reduced, she might end up having it increased,
or having another drug prescribed on top of the current one, with the argument
that she lacks insight into her disease.
Many of the emails I have received from patients
and relatives describe exactly this. The power the psychiatric set-up gives to
the health professionals is often abused in a way that makes patients helpless
and deprives them of their dignity as a person; they are reduced to a “thing.”
Here is what a former patient wrote to a psychologist I collaborate with:
I am a nurse but have experienced psychiatry
from the patient’s side since 1999. I can “only” say that if I had ever treated
any person like what I have seen and been exposed to myself, I would not have
been able to live with the bad conscience this would have given me. I happened
to sit next to someone whose son was admitted to a psychiatric ward and who
said that he only saw the staff when they came to tell him that he needed to
take his medication. I escaped psychiatry’s “captivating spiral” in 2004, and
it makes me so sad to hear that there has been no significant evolution in the
system. I know that psychologists have offered their help, but they have had to
attend courses before they could be included in the care system. I fail to
understand this, as what is most important is to show an interest in the
patients, and if you do this, the patients will surely reveal the traumas that
might have caused their mental disorder.
We don’t help people by stigmatising them,
locking them up, and drugging them, and it is noteworthy that it is patients
that have demanded drug-free alternatives. For their doctors, becoming
“stabilised” means using drugs to calm them down, which is very different to
meeting the patients with their bewildered thoughts and allotting time to work
through them without medication.
Psychiatrists have experienced that assertive
communication, which involves taking a step back rather than running after the
patient and intervening in turmoil, can considerably reduce the use of forced
treatment. One such programme is Basal Exposure Therapy,
which is used by Åse Lyngstad and her colleagues in Norway.10 It has similarities to the treatment of phobia, as
it exposes patients to those factors that cause them to panic. The staff’s role
is to be on equal terms with the patients and it is the patients’ own
experience with drugs that is being discussed, instead of the usual top-down
approach where the doctors ignore patients’ complaints about side effects and
their wish to stop the drugs. This approach enforces a different way of
working, and a drug-free alternative is offered to the patient, always with a
plan for tapering off drugs.
Why are there so few shining lights in
psychiatry who understand that psychiatry is not so much about drugs as it is
about human relationships?
Forced treatment must be banned
As for all interventions in healthcare, the
overriding question is whether forced treatment does more good than harm. I
have no doubt it does vastly more harm than good and that we will never be able
to prevent widespread abuse if we keep it, and I shall explain why.
Not a single randomised trial has compared
seclusion or mechanical restraint with no such intervention,11, 12 but these measures can be fatal.11 Electroshock can
also be fatal, but what is most worrying is that forced drug treatment kills
many patients.
The fact that forced treatment can be fatal was
recently underlined in a Danish register study of 2,429 suicides.13 It showed that the closer the contact with
psychiatric staff – which often involves forced treatment – the worse the
outcome. Compared to people who had not received any psychiatric treatment in
the preceding year, the adjusted rate ratio for suicide was six for people
receiving only psychiatric medication, eight for people with psychiatric
outpatient contact, 28 for people with psychiatric emergency room contacts, and
44 for people who had been admitted to a psychiatric hospital. Patients
admitted to hospital would of course be expected to be at greatest risk of
suicide because they were more ill than the others (confounding by indication),
but the findings were robust and most of the potential biases in the study were
actually conservative, i.e. favoured the null hypothesis of there being no
relationship. An accompanying editorial noted that there is little doubt that
suicide is related to both stigma and trauma and that it is entirely plausible
that the stigma and trauma inherent in psychiatric treatment – particularly if
involuntary – might cause suicide.14 The editorialists believed that a proportion of
people who commit suicide during or after an admission to hospital do so
because of conditions inherent in that hospitalisation.
A tragic case where a trial participant stabbed
himself to death while on an antipsychotic drug at the University of Minnesota
illustrates several of the ethical issues involved in the extreme power
imbalance at psychiatric institutions.15 Dan Markingson agreed to enrol in a trial while
committed involuntarily to hospital, raising questions about his ability to
consent, and the lead researcher on the trial was also his treating
psychiatrist. An independent review of the research practice at the university
found only a single instance where consideration of the dual and potentially
conflicting role of the treating psychiatrist/investigator was addressed.
Faculty and staff in the Department of Psychiatry told the reviewers that they
worked in a “culture of fear.” It took bioethicist Carl Elliott from the same
university and others almost ten years of pressure before the university agreed
to the investigation, but the review team was expressly forbidden to look into
the Markingson case!16 It seems that fraud was involved, with photocopying
of consent forms with identical answers supposedly given by different trial
participants, fake signatures and incorrect diagnoses. Markingson’s mother had
repeatedly raised concerns about his condition, questioning his involvement in
the trial, but her pleas were ignored.
One of psychiatry’s many unfortunate fads is
community treatment orders, often called assisted outpatient treatment in the
United States, which are legal regimes making outpatient treatment compulsory.
A 2014 Cochrane review (three trials, 752 patients) didn’t find any differences
in service use, social functioning or quality of life compared with standard
voluntary care.17 In clinical practice, this initiative has also
failed. In the UK, it was hoped that these treatment orders, which came into
force in 2008-09, would lead to fewer hospital admissions but the admissions
increased.18 Another problem has been the great variation in
their use, with some areas discharging 45% of the patients with treatment
orders and others none at all, which indicates a good deal of arbitrariness and
uncertainty. Some psychiatrists find treatment orders unethical and,
unsurprisingly, many patients find them stigmatising.
The UK mental health charity, Mind, has many
concerns about community treatment orders.19 If a community patient’s distress is manageable,
the professionals may well argue that the set-up is working and should be
continued, but at what point will it be stopped? Without the natural cap on
hospital detention provided by the finite number of beds, these orders will
undoubtedly be used for too long and for too many people, like a “lobster pot”
– easy to get into but very difficult to ever get discharged from. Community
treatment orders mean that many people who do not wish to take drugs for the
rest of their lives are no longer able to make that decision. There is no
escape from this Catch 22. If the patient remains
well, this is taken to mean that the drugs are working, and if not, forced
drugging is often increased, causing even more misery and more deaths. This is
totally unacceptable.
When I lectured in Australia in 2015, I was told
that only 3-5% of the patients come off the treatment orders again and I met
with a doctor who had been on such an order on and off for 20 years. He gave me
a copy of an evaluation by a psychiatrist who in 1995 deemed him insightless
because he had alerted the community to the brain-damaging effect of
antipsychotics! Another person I met was a psychiatrist who was also considered
insane by her colleagues, also because she spoke out about the harms from
psychotropic drugs. They tried to have her involuntarily confined to hospital
but failed. Not much different from Stalin’s incarceration of political
opponents with the “help” of psychiatrists.
An increase in the use of compulsion in the
community will inevitably result in an even greater reliance on drugs, in
particular the dangerous use of depot injections of antipsychotics, which are
commonly used for community patients, e.g. for the doctor I just mentioned.
In 2014, the Danish Ministry of Health issued
what looks like a licence to kill. It allowed psychiatrists to use
extraordinarily large doses for forced treatment and said that this applies
especially to patients who have been in prolonged treatment and where smaller
doses have been tried without a good therapeutic result.20 It’s unbelievable. These patients should have their
drug withdrawn. Giving more of what was already not working doesn’t help, it
harms.
Forced drugging prevents people from making
their own evaluations of the benefits and harms of the drugs and from stopping
medication, although this would often have been the most rational decision.
According to Mind, people deemed fit to live in the community should be trusted
to make such decisions for themselves, with support, and the approach to
working with them should be based on gaining their trust; not on compelling
them to take drugs, which will undermine the valuable therapeutic relationship
with doctors, nurses and social workers that might otherwise be established.
Many people consulted by Mind feel their relationships with professionals would
be harmed by the increased threat of compulsion, with those professionals being
turned into “Mental Health Act police officers.”
Forced treatment is very common. About 1% of all
Americans are subjected to coercion in the name of mental health every year,21 which is a large-scale violation of the deeply
treasured American freedom rights, and in Denmark 21% of the patients in
psychiatric hospital departments were exposed to forced treatment in 2007.22 Forced drugging is far more common than any
official statistics will tell us, however. Rule number one in psychiatric
institutions is that patients must comply with the medication regimen, and the
patients know that if they refuse they might not be discharged, or other
unpleasant things might happen to them. This makes forced drugging look
“voluntary.”
As I explained above, forced drugging isn’t
needed. Only about 10% of patients refuse treatment, and most do so for only a
short time, often because they don’t like the drugs or are afraid of their
harms, which are very good reasons for refusing.23
Extremely rare cases like forced feeding for
life-threatening anorexia are already covered by other laws than those that
apply specifically to psychiatry. We should therefore protest against forced
treatment until it is banned by law and we can use the law to accomplish just
that.
Professor Loren Mosher’s testimony in an Alaska
court case about forced drugging is particularly lucid.24 He stated that the therapeutic relationship is the
single most important thing, and if you have been a cop and have used force, it
becomes nearly impossible to change that role into the traditional role of the
physician as a healer and advocate for the patient. This is why psychiatrists
should stay out of the job of being police. Another reason is that violence
breeds violence.
Mosher explained that if somebody is about to do
themself or others grievous harm because of some altered state of
consciousness, he would stop them in whatever way he needed to. He would prefer
to do it with the police, and an Icelandic psychiatrist told me that this is
what the hospital staff would do in Iceland. It is important that the police
are unarmed, which is the case in Iceland, and that there are very clear rules
about their engagement (which can only be requested by the consultant),
including that they cannot put a person in jail. In extreme cases, they would
have to stay. This is a sign of respect. The police are called upon to deal
with the risk of violence, whether people with mental health problems are
involved or anyone else. Same laws for everyone, and in Iceland people trust
the police as servants of the people. This is the natural way of handling a
difficult situation, as it means that the staff doesn’t get involved in serious
fights with their patients.
Mosher reported that in his whole career he had
never acted as a police officer. He formed the kind of relationship and an
ongoing treatment plan, which was acceptable both to him and the patient, and
which avoided their getting into a fight.
What makes Mosher’s testimony so pertinent is
that he is likely the person in the western world who has seen more acutely
psychotic people without medication than anyone else. In his Soteria project,
which he headed for 12 years, he sat for hours on end with psychotic but
unmedicated patients, whom he found were among the most interesting of all
people.
The Alaska Supreme Court decided that the
government cannot drug someone against their will without first proving by
clear and convincing evidence that it is in their best interests and there is
no less intrusive alternative available.
The crucial point in this decision is what it
means to be “available,” and in another case, the court decided that if an
alternative is “feasible,” the state has to either provide it or let the person
go.
I have met with Jim Gottstein, the lawyer who
convinced the Supreme Court to rule as it did. He is currently president of The
Law Project for Psychiatric Rights in Alaska (http://psychrights.org/), a public interest law firm
that says on its homepage that it is:
“Devoted to the defense of people facing the
horrors of forced psychiatric drugging and electroshock. We are further
dedicated to exposing the truth about these drugs and the courts being misled
into ordering people to be drugged and subjected to other brain and body
damaging interventions against their will. Currently, due to massive growth in
psychiatric drugging of children and youth and the current targeting of them
for even more psychiatric drugging, PsychRights has made attacking this problem
a priority. Children are virtually always forced to take these drugs because it
is the adults in their lives who are making the decision. This is an unfolding
national tragedy of immense proportions.”
Gottstein has noted that the public’s opinion is
that the drugs work, and that if people weren’t crazy, they would know that the
drugs are good for them.2 Accordingly, at court hearings,
where hospitals apply for sanction of forced treatment, psychiatrists argue
that no sound person would refuse medically sound treatment, and the courts
comply with their wish.
It was therefore essential for Gottstein’s
success to use scientific data to convince the Supreme Court that this isn’t
true. The court ruled that, “Psychotropic medication can have profound and
lasting negative effects on a patient’s mind and body” and “are known to cause
a number of potentially devastating side effects.”
This was a stunning victory for human rights in
psychiatry. It happened in 2003, and in 2009 Gottstein succeeded to persuade
the authorities to fund a seven-bedroom Soteria home in Alaska where psychotic
patients can recover with minimal or no use of drugs. But there is a long way
to go. On the web page, “Psychiatry: Force of Law,” Gottstein explains that
psychiatrists, with the full understanding
and tacit permission of the trial judges, regularly lie in court to obtain
involuntary commitment and forced medication orders.
The experts frequently and openly subvert
statutory and case law criteria that impose rigorous behavioural standards as predicates
for commitment, and insurmountable barriers are raised to insure that the
allegedly “therapeutically correct” social end is met.
Traditionally, lawyers assigned to represent
state hospital patients have failed miserably in their mission. And the
psychiatric profession explicitly acknowledges that psychiatrists regularly lie
to the courts. Fuller Torrey, likely the most prominent proponent of
involuntary psychiatric treatment, has said that it would probably be difficult
to find any American psychiatrist who has not exaggerated the dangerousness of
a mentally ill person’s behaviour to obtain a judicial order for commitment.
It is clear that the legal protections for
people diagnosed as mentally ill are illusory and the court proceedings are
fairly characterised as a sham. Indeed, our laws contribute to creating a Catch 22 situation. For example, according to Alaska’s
forced drugging statutes, “competent” means that the patient appreciates that
he has a mental disorder or impairment, if the evidence so indicates; and
denial of a significantly disabling disorder or impairment constitutes evidence
that the patient lacks the capability to make mental health treatment
decisions. In other words, denying that one is mentally ill is evidence that
one is mentally ill!
The worst of all this is perhaps that very many
of the patients, sometimes far more than half, are wrongly diagnosed with
schizophrenia (see Chapter 6). This fact alone makes forced treatment totally
reprehensible.
Psychiatrists usually say that it would be
impossible to practice psychiatry safely without having the option of using
forced drugging, restraints with belts and straps, and seclusion. But this is
false. Studies have shown that, with adequate leadership and training of staff
in de-escalation techniques, it is possible to
practice psychiatry without using force.25, 26 Studies have also demonstrated that use of coercive
measures is based much more on culture, traditions, and policies than on
medical or safety requirements.27 For example, in a 398-bed state psychiatric
hospital in North Carolina, the use of mechanical restraints was reduced by 98%
at the acute adult unit and it was eliminated at the community transition unit.28 Overall, combining the two groups, the number of
injuries was reduced and this was accomplished without an increase in the use
of seclusion, manual holds, or drugs.
Another example is the Living Room in Arizona.29 By welcoming involuntarily admitted patients in a
living room where they could feel respected and at home, the staff abolished
the use of seclusion and restraint almost entirely and far fewer patients
needed to be sent to psychiatric hospitals. Initially, there was considerable
resistance from the medical staff, but the experience from other peer-operated
recovery programmes had shown that most of what the staff were saying would
prove not to be true. The focus is almost exclusively on the person’s problems
and when the peers (recovery mentors) listen to them, they can say that they
have had the same experiences and have recovered. So the focus is on recovery
and on the patients’ strengths instead of illness and of finding faults with
them, and the patients value having a place they can come back to if they start
to slip, without worrying about being locked up or subjected to restraint or
forced drugging.
One of the Living Room programmes was eliminated
when the regional health authority took over the crisis services. It wanted to
redirect the focus to be more of a traditional medical model service and
changed the name from Psychiatric Recovery Center to Urgent Psychiatric Care. I
have seen this happen in many countries. Whenever some clear-sighted pioneers
have introduced a model that builds on respect for patients and preservation of
their autonomy, and that model has demonstrated far better results than the
traditional medical model, the “system” destroys it. It is unspeakably tragic.
What does it take to wake people up to the fact that they do the wrong things
in psychiatry? Why are people against a humane psychiatry?
A psychosis usually involves a devastating loss
of confidence and trust in other human beings, and an acute psychotic break
often responds to skilled human intervention, but instead of building rapport
with their patients, psychiatrists reflexively resort to pressuring or forcing
them into hospitals against their will, and drugging them, further humiliating
and alienating them.30 A few hours or days of disturbed behaviour are
treated as a cause for a lifetime sentence to drug treatment, and psychiatrists
in training will hardly ever see a patient who is not already snowed under with
drugs and therefore get a wrong impression both of the patient and his
strengths and of the potential for cure without drugs.
Psychiatrists should consider the fact that some
patients don’t tell them about their thoughts, how they feel, and what they
experience, because they are afraid that if they are honest, it could lead to
forced treatment. This is not a healthy therapeutic relationship. It is not
laudable either that the staff often “justify” their actions by saying that,
were it not for the forced treatment, the patient might have died. The evidence
we have tells us the opposite. Forced drugging kills. A patient told me that
she likened forced treatment to rape and said that there cannot be good rapes.
This patient was raped by a man in her family when she was only nine years old
with the remark: “Will you take off your pants yourself, or shall I do it?” She
became terrified whenever the staff subjected her to forced treatment.
In Iceland, seclusion and restraint were
abolished in 1932 and never used again.11 That year, Helgi Tómasson, the
first modern psychiatrist in Iceland, took the shackles, straightjackets and
other physical restraints that existed in the mental hospital, Kleppur, and
burnt them in a furnace – all except one set, which he sent to the Parliament
where it is still on display.
The Icelandic psychiatrist who informed me about
how difficult situations are handled in Iceland told me that he once worked in
a hospital in England where seclusion was used rather a lot. He got a
maintenance man to lock the room and put up a sign saying “Out of order!” which
remained for about a month. When he took it down, the staff didn’t use the
seclusion room any more, as they had gotten used to not having this option.
He also said that when he worked at a psychosis
ward in London, he and his colleagues waited on average about two weeks before
starting antipsychotic medication on newly admitted people, who had
unfortunately nearly always been involuntarily admitted. They didn’t want to
force treatment on anyone, but most people did in the end, however, choose to
take some medication, often in very small doses, so it is very well possible
that it was respect, time and shelter that helped the patients, not the
“sub-treatment threshold doses.”
Practices vary enormously between countries.
Involuntary hospital admissions in Europe range from 12 per 100,000 inhabitants
in Italy to 233 in Finland.25 Once admitted, rates of coercion
also vary enormously. In the UK, mechanical restraint isn’t allowed and
seclusion is used rarely. In Austria, mechanical restraint is used 45 times
more often than in the Netherlands, where forced drugging is also very little
used, as the view is that involuntary medication is more invasive and threatens
the personal integrity more than seclusion or mechanical restraint.11
The Dutch mental health legislation is very restrictive regarding involuntary
medication. It is allowed only in cases of acute emergency, and an emotional
crisis is not a medical emergency. Psychiatrist Simon Wilkinson from Akershus
University Hospital in Norway has told me that they don’t have a regime for
rapid tranquillisation and have never needed one in the last 20 years, which is
in stark contrast to UK conditions. The staffing is better in Norway and
difficult situations are foreseen and managed within the existing care culture.
Patients are of course against forced drugging,
and if they are given the option of choosing between two evils, most patients
prefer mechanical restraint for forced medication.31 But there should be no evil. According to
psychiatrist Peter Breggin, forced medication is not therapy but coercion and
should have no place in mental health practices.7 I shall also
quote Jim Gottstein:32
A commonly-held belief is that locking up and
forcibly drugging people diagnosed with mental illness is in their best
interests as well as society’s as a whole. The truth is far different. Rather
than protecting the public from harm, public safety is decreased. Rather than
helping psychiatric respondents, many are greatly harmed.
I have explained throughout this book why drug
treatment of psychiatric disorders increases violence instead of decreasing it,
also in patients with schizophrenia. All the evidence we have tells us that
forced treatment increases the harm done not only to patients but also to
others.
Only soldiers at war and psychiatric patients
are forced to run risks against their will that might kill them. This is
perhaps the strongest argument against forced drugging. In rare cases force may
be needed, e.g. if a patient is dangerous, but restraint without belts, i.e.
holding the patient firmly, will suffice.
Forced treatment can be avoided, and rather than
claiming it would be impossible to practice psychiatry without it,
psychiatrists should consider that it’s impossible for some patients to live after having been exposed to this humiliating and dehumanising
treatment. Some patients commit suicide after such an experience.13
Until we have outlawed forced treatment, we
should monitor carefully the use of coercive interventions as an indicator of
the quality of psychiatric inpatient treatment.11 But we don’t
have to wait, in fact, we are obliged to stop these practices now. See next
section.
United Nations forbids forced
treatment and involuntary detention
The fundamental human right to equal recognition
before the law applies to everyone, also to people with mental disorders. This
is clear from the Universal Declaration of Human Rights, the International
Covenant on Civil and Political Rights and the United Nations Convention on the
Rights of Persons with Disabilities, which has been ratified by virtually all
countries.33
In 2014 the Convention specified that member
states must immediately begin taking steps towards the realisation of the
rights by developing laws and policies to replace regimes of substitute
decision-making by supported decision-making, which respects the person’s
autonomy, will and preferences.33
At all times, the individual autonomy and
capacity of persons with disabilities to make decisions must be respected,
which means that “mental health laws that permit forced treatment must be
abolished.” People have the right to be free from involuntary detention in a
mental health facility and not to be forced to undergo mental health treatment;
the right to respect for one’s physical and mental integrity; the right to
liberty of movement and to choose where and with whom to live; and the right to
consent to medical treatment. “States parties have an obligation to require all
health and medical professionals (including psychiatric professionals) to
obtain the free and informed consent of persons with disabilities prior to any
treatment.”
“Forced treatment by psychiatric and other
health and medical professionals is a violation of the right to equal
recognition before the law and an infringement of the rights to personal
integrity (art. 17); freedom from torture (art. 15); and freedom from violence,
exploitation and abuse (art. 16). This practice denies the legal capacity of a
person to choose medical treatment and is therefore a violation of article 12
of the Convention.”
States parties must respect the legal capacity
of persons with disabilities to make decisions at all times, including in
crisis situations; must ensure that accurate and accessible information is
provided about service options and that non-medical approaches are made
available; and must provide access to independent support. Substitute
decision-making regimes, in addition to being incompatible with article 12 of
the Convention, also potentially violate the right to privacy of persons with
disabilities, as substitute decision-makers usually gain access to a wide range
of personal and other information regarding the person.
“States parties must abolish policies and
legislative provisions that allow or perpetrate forced treatment, as it is an
ongoing violation found in mental health laws across the globe, despite
empirical evidence indicating its lack of effectiveness and the views of people
using mental health systems who have experienced deep pain and trauma as a
result of forced treatment.”
The Convention makes it clear that
“unsoundedness of mind” and other discriminatory labels are not legitimate
reasons for the denial of legal capacity, and that the concept of mental capacity
is highly controversial in and of itself.
“Mental capacity is not, as is commonly
presented, an objective, scientific and naturally occurring phenomenon. Mental
capacity is contingent on social and political contexts, as are the
disciplines, professions and practices which play a dominant role in assessing
mental capacity.”
“In most of the State party reports that the
Committee has examined so far, the concepts of mental and legal capacity have
been conflated so that where a person is considered to have impaired
decision-making skills, often because of a cognitive or psychosocial
disability, his or her legal capacity to make a particular decision is
consequently removed. This is decided simply on the basis of the diagnosis of
an impairment (status approach), or where a person makes a decision that is
considered to have negative consequences (outcome approach), or where a
person’s decision-making skills are considered to be deficient (functional
approach). The functional approach attempts to assess mental capacity and deny
legal capacity accordingly. It is often based on whether a person can
understand the nature and consequences of a decision and/or whether he or she
can use or weigh the relevant information. This approach is flawed for two key
reasons: (a) it is discriminatorily applied to people with disabilities; and
(b) it presumes to be able to accurately assess the inner-workings of the human
mind and, when the person does not pass the assessment, it then denies him or
her a core human right — the right to equal recognition before the law. In all
of those approaches, a person’s disability and/or decisionmaking skills are
taken as legitimate grounds for denying his or her legal capacity and lowering
his or her status as a person before the law. Article 12 does not permit such
discriminatory denial of legal capacity, but, rather, requires that support be
provided in the exercise of legal capacity.”
A person’s mode of communication must not be a
barrier to obtaining support in decision-making, even where this communication
is non-conventional, or understood by very few people. States must take
measures to provide access to the support required and must ensure that support
is available at nominal or no cost. The person must have the right to refuse
support and terminate or change the support relationship at any time.
The ability to plan in advance is an important
form of support, whereby persons with disabilities can state their will and
preferences, which should be followed at a time when they may not be in a
position to communicate their wishes to others. The point at which an advance
directive enters into force (and ceases to have effect) should be decided by
the person and included in the text of the directive; it should not be based on
an assessment that the person lacks mental capacity. Where, after significant
efforts have been made, it is not practicable to determine the will and
preferences of an individual, the “best interpretation of will and preferences”
must replace the “best interests” determinations.
All people risk being subject to “undue
influence”, yet this may be exacerbated for those who rely on the support of
others to make decisions. Undue influence is characterized as occurring, where
the quality of the interaction between the support person and the person being
supported includes signs of fear, aggression, threat, deception or
manipulation. Safeguards for the exercise of legal capacity must include
protection against undue influence; however, the protection must respect the
rights, will and preferences of the person, including the right to take risks
and make mistakes.
States have the ability to restrict the legal
capacity of a person based on certain circumstances, such as bankruptcy or
criminal conviction. However, the right to equal recognition before the law and
freedom from discrimination requires that when the State denies legal capacity
it must be on the same basis for all persons.
With respect to children, the best interests of
the child must be a primary consideration and their views must be given due
weight in accordance with their age and maturity, so that the will and
preferences of children with disabilities are respected on an equal basis with
other children.
Police officers, social workers and other first
responders must be trained to recognise persons with disabilities as full
persons before the law and to give the same weight to complaints and statements
from persons with disabilities as they would to non-disabled persons.
The denial of the legal capacity of persons with
disabilities and their detention in institutions against their will, either
without their consent or with the consent of a substitute decision-maker, is an
ongoing problem. This practice constitutes arbitrary deprivation of liberty and
violates articles 12 and 14 of the Convention. States parties must refrain from
such practices and establish a mechanism to review cases where persons with
disabilities have been placed in a residential setting without their specific
consent.
My comment: If you still accept forced treatment
and involuntary detention, I hope you will change your mind after having read
the next section, which is a summary of a book that describes virtually
everything that is wrong with psychiatry. It moved me so greatly that whenever
I open it again, I get overwhelmed with sadness because I know that many
psychiatric patients are abused and die under similar circumstances.
Dear Luise
In Dear Luise, Dorrit
Cato Christensen writes about her daughter who was killed by psychiatry.34 In his foreword, “You need to be strong in order to
be vulnerable,” former Danish Prime Minister Poul Nyrup Rasmussen describes the
book as heartbreaking. It truly is, and it should be obligatory reading for all
doctors contemplating becoming psychiatrists. If they get through it without
crying, they should find themselves another job.
Luise’s hospital admissions always involved
troubleshooting, never finding out what strengths she had. It was only when she
attended an alternative type of school that people were more interested in her
strengths than her weaknesses, and she flourished while there. Her teachers had
the necessary patience with her minor oddities, which quickly evaporated if she
was given a little time. Psychiatry killed her because the psychiatrists didn’t
listen to her, or her mother, or psychologists, or other health professionals,
or even to their own staff that knew her much better than they did.
Most unfortunately, Luise’s story isn’t atypical
at all. It started when she was seven and had socialising problems and
displayed absentmindedness. This led to a series of wrong diagnoses and harmful
treatments, starting with valproate for an assumed hidden epilepsy. The
neurologist and psychiatrist both said she had improved on valproate, while the
psychologist who knew her better said she had deteriorated. She gained 25 kg in
weight, which became 6 kg in her chart.
Aged 11, Luise was admitted to a psychiatric
ward for adjustment of valproate but ended up at a psychiatric treatment
facility where she was raped by another patient. The way she was treated was
utterly dehumanising right from the beginning. She was accused of lying and
living in a fantasy world, even though what she told was absolutely true. Her
“fantasies” were reported to the social services as being a big problem and a
sign of her disease. She was bullied by the staff. Dorrit overheard Luise
saying: “I have a headache,” and a staff member said: “Listen, Luise has a
headache, isn’t that funny? What are we going to do about it?” whereupon the
staff and the inhabitants all laughed. Luise also attempted suicide while she
was home on a weekend leave, as she did not want to go back to the institution.
Almost without exception, whenever Luise or
Dorrit complained about side effects, the dosage of the suspect drug was
increased, and in several instances what was written in the patient’s chart was
plain wrong but made the staff’s actions look better. On several occasions,
inconvenient correspondence with the authorities simply “disappeared.”
The staff noted that every time Luise had been
home over the weekend, they experienced increased problems with her when she
came back. It didn’t dawn on them that this was because she would rather stay
with her mother. One day, a doctor stopped valproate cold turkey, although this
is dangerous.
Reaching the age of 18, Luise was considered an
adult who should now take care of her own matters. She was not prepared for
that because of her former “protected life” in the treatment system. Her doctor
suggested a psychiatric evaluation, so she could get the paperwork updated
about what she needed help with.
When Luise kept on talking about some friends
coming to visit, which wasn’t correct, Luise and her mother interpreted this as
a delusion and sought admission to Rigshospitalet, Denmark’s National
University Hospital, to have an evaluation done. Dorrit made sure that the
receiving psychiatrist dictated into the tape recorder that Luise should not
get psychiatric drugs but should merely be observed. The next day, however,
Dorrit found Luise on the floor in her own urine, heavily intoxicated by drugs,
and the staff refused to answer Dorrit’s question about which drugs Luise was
on. There was nothing in Luise’s chart about observing her without drugs;
instead, there was false information that she was already in treatment with an
antipsychotic when she arrived, and the dose of this non-existing drug was then
“increased.” This was a tremendous and dire error. Luise had never received an
antipsychotic before. The psychiatrist asked Luise many leading questions and
got answers that had nothing to do with her but which confirmed the doctor’s
own prejudices. After eight days on that heavy medication, Luise developed a
malignant neuroleptic syndrome, which carries a high mortality.
The psychiatrists apparently ignored this, as
they continued the heavy drugging, which turned Luise into a helpless baby that
put everything into her mouth. They interpreted these iatrogenic symptoms as
signs of very poor intelligence and regression to childhood and started forced
drugging her. Dorrit reluctantly accepted it, as she was told that otherwise
Luise’s condition could become permanent!
Luise fought against the huge doses, but as it
ended with forced treatment every time, she stopped her resistance. After 12
days, she was broken: “Today, the patient offers no physical resistance but is
anxious about being medicated and holds hands, and afterwards she is somewhat
tearful.”
When Luise was close to being discharged, a new
psychiatrist came by and saw all sorts of problems and she was subjected to
forced medication and belts for 22 days, during which she didn’t breathe fresh
air. After this, Luise was given a 30-minute leave but didn’t return. A week
later, the laconic note in her chart was: “Since the patient is discharged,
mandatory treatment is discontinued.” I really wonder why all this forced
treatment was so important when Luise apparently could discharge herself, and
after that nothing was important?
After six months without drugs, Luise was picked
up by the police, while wandering around in Copenhagen airport one night. She
often did so, because the airport reminded her of travelling, which she loved.
When they said they would transport her to Rigshospitalet, she shouted and
screamed. Why didn’t they just drive her home?
The psychiatrists didn’t believe Dorrit when she
told them that Luise only hallucinated when she was on drugs. Luise didn’t want
drugs, but the psychiatrists noted in her chart that if she refused they would
force her to take drugs. No true conversation seems to have taken place, and
there was nothing in her files about how it had been for Luise during the six
months she was not on drugs. It was totally absurd. The psychiatrists made her
psychotic with antipsychotic drugs and then increased the dose because she was
psychotic.
Three months later, after three weeks of forced
drugs and belts at St. Hans Hospital, she escaped and went home to her mother.
Three days later she got the ultimate punishment at Rigshospitalet after having
been admitted for less than two hours: a diagnosis of paranoid schizophrenia,
apparently without any kind of proper diagnostic process and with no
questioning of why Luise had run away from St. Hans Hospital. The psychiatrist
didn’t know and didn’t investigate which drugs Luise was on but gave her a
tranquilliser and four different antipsychotics, including the drug that might
have killed her earlier, as it caused a malignant neuroleptic syndrome.
Luise was sent back to St. Hans Hospital but to
another department. They didn’t know which drugs she had received earlier,
neither at Rigshospitalet, nor at their own hospital, and they started four new
antipsychotics.
Two months later Luise fell asleep in her bed
while smoking a cigarette after an extraordinarily large dose of an
antipsychotic, probably as a result of a medical error. The bed caught fire but
a member of staff quickly extinguished it. In court, she got a forced treatment
order which, in principle, could be for life. No one asked the staff who knew
her but a chief physician who didn’t know her gave testimony, which sentenced
her. Her sentence was used by the staff even many years later to overmedicate
her, arguing how dangerous she was.
Luise moved to a treatment home, mostly
inhabited by people with senile dementia. She often had nightmares about
doctors holding her while they gave her injections, and she once dreamt that a
particular doctor inserted the needle directly into her brain with an evil
laugh. Due to the heavy drugging, she spent most of her time in bed. Tapering
was sometimes discussed but the problem was that the psychiatrists changed all
the time so a long-term plan was never made.
Dorrit asked to have the medication reduced and
the nurse who was deputy chief at the treatment home also argued strongly for a
dose reduction. Dorrit asked whether Luise could have been hallucinating
because of the drugs, as she had never hallucinated without taking drugs, but
the psychiatrist replied that this was unthinkable. Luise once told the psychiatrist
that another patient had sent her evil thoughts, which was interpreted as
insanity and led to an increase in drugs. However, that patient often screamed
at night things like, “Get out of here – I’ll kill you!” which Dorrit had heard
herself and told the psychiatrist, but the psychiatrist didn’t listen. Half an
hour was set aside for this important conversation with Luise, Dorrit and the
nurse, but the psychiatrist left after five minutes and there was nothing in
the chart about the nurse having been present.
Luise now got a permanent psychiatrist, Sofus
(not his real name), assigned to her but that didn’t mean progress. He tried 11
different antipsychotics in just two years and changed the dose 26 times up or
down. She sometimes got three times the highest recommended dose and the
psychiatrists were puzzled that she had hallucinations. Luise vomited and this
symptom was also ignored and explained as a sign of her illness. Dorrit was
told that it was common that patients wouldn’t accept that they were ill, and
therefore vomited to avoid medical treatment.
When Dorrit asked for a second opinion with
another psychiatrist, Luise’s assigned psychiatrist wrote to her:
“I think it will be difficult to find a
psychiatrists who would be willing to make such an evaluation … If his
evaluation were materially different from mine, I would of course take it into
consideration, though I cannot promise to follow it – as long as I am
responsible for the treatment, I also want a free hand. The situation would be
extremely inopportune for our future collaboration. And it would not really
benefit Luise.”
Dorrit read about a test for slow metabolism,
which might explain why Luise tolerated the drugs so poorly, as the drugs would
then accumulate in her body. She contacted a chief of research, who agreed
entirely that Luise should get tested because of her symptoms. However, he
later said on the phone – speaking non-stop for an hour and 18 minutes – that
someone like Luise could not take the test because, even though it might be positive,
it was still the psychiatrist’s duty to prescribe this much medication
considering how ill she was. He was careful to add that since Dorrit had now
been informed, she would not receive a letter about the matter.
It was clear that the research leader must have
taken advice from the psychiatrist, and Dorrit wrote a letter asking for a
written response with the reasons for rejection of her request. She never got a
reply.
One month later, Luise was admitted to Amager
Hospital and after a few days, her psychiatrist wanted to transfer her to St.
Hans Hospital. Luise was terrified at the thought of going back there and
Dorrit therefore came to see her psychiatrist. She was shocked. Luise was
running around wildly, trying to avoid the snakes and fictitious blood-soaked
creatures that were coming out of the walls. A nurse who had been on duty the
last two nights told Dorrit that this was the result of the last two drug dose
increases.
But as always, the psychiatrists refused to face
the consequences of their gross incompetence. There was now a new psychiatrist
and she seemed somewhat uneasy about the situation. She was very unpleasant and
didn’t even look at Dorrit but leafed through chart notes while throwing one
accusation after another at her. It was Dorrit’s fault that Luise was not
getting better because she was against drug treatment. It was Dorrit’s
influence that set Luise against going to St. Hans Hospital. The psychiatrist
recommended Dorrit stop visiting Luise since, according to the staff, she felt badly
after her visits. The psychiatrist went on and on, her head buried in the
chart. Dorrit never got the chance to ask questions since she had to defend
herself against all the accusations.
The chart note from the same day said: “I speak
with the patient who urgently asks for more Seroquel [quetiapine], which is
also indicated.”
Luise did not request more Seroquel; she had no
idea what was being talked about, being too busy dodging bloodthirsty monsters
coming out of the walls. Dorrit wrote to the psychiatrist and pointed out that
the staff would certainly not vouch for her claim that Luise felt worse after
Dorrit’s visits – in fact, quite the opposite.
Two years before she died, Luise said to her
mother: “You can write on my tombstone that it was the medication that killed
me.”
Now the reprisals began. Nobody on the ward
would talk to Luise or Dorrit. The daytime staff was dismissive of Luise and
made no positive contact. They were cold, as Luise put it, and Dorrit was also
frozen out when she came to visit; the staff didn’t even say hello but turned
their backs on her. One day, Luise asked Dorrit to ask her contact person, a
nurse, whether they had increased the dose the previous day. The nurse sat in
the courtyard with her feet up on a chair, reading a magazine; she hardly
looked up, replying that she really didn’t know.
Luise was sent to St. Hans Hospital again,
against her wishes. It was essential of course to provide a detailed
description of her problems and her history, but this never happened. There was
a short chart note speaking of a 30-year old woman with “schizophrenia and
mental retardation” who was in treatment with two antipsychotics, three minor
tranquillisers, and a drug against drug-induced Parkinsonism.
The first psychiatrist that turned up was
shocked at the large doses of medication Luise had been getting at Amager
Hospital and decreased the drugs. Later, another psychiatrist came by and
increased the medication again.
A third psychiatrist who was going to be in
charge of Luise, listened to Dorrit and was very surprised to hear that Luise
could be a fully functioning girl when she wasn’t heavily drugged. Dorrit told
her that Luise would have been transferred to a home for the mentally retarded
if Dorrit hadn’t intervened. This psychiatrist was highly exceptional since she
not only treated Luise as a human being, not some impersonal diagnosis, but
also gradually reduced her medication, which clearly improved Luise’s
condition.
One day the staff phoned Dorrit and asked her to
come, as they couldn’t understand what had happened to Luise. She fought and
raved, shouting “No, I won’t.” For a very good reason. The ward she had just
moved to was the same place where she was poisoned for two years while strapped
down, subjected to forced injections, and where her bedding caught fire. These
buried traumas now resurfaced.
The good psychiatrist took Luise seriously and
arranged conferences with the psychologist. Luise was very happy about this and
never missed a conference, no matter how tired or ill she was. She started to
talk again about travelling, followed what was happening in the city’s cultural
milieu and wanted to see an exhibition of Turner’s landscapes, which she and
Dorrit had seen previously in London.
The reason for Luise’s transferral to St. Hans
Hospital was to adjust and stabilise her medication. After 18 months, she was –
in Dorrit’s words – sent back to Hell. The discharge letter says in part:
“During hospitalisation, we found no evidence of
mental retardation. The patient appears of normal intelligence, well-oriented,
and can problem-solve … Our experience is that the patient is
treatment-resistant to the medication. Treatment with antipsychotics has been
reduced because of side effects … There is still a mild form of tardive
dyskinesia (involuntary grimacing) … no change should be made for the next one
to two years, and then further reduction since the patient should be regarded
as treatment-resistant.”
This expert guidance wasn’t respected at Amager
Hospital. Luise returned to her treatment home, where she had the same
psychiatrist as at the hospital, and in less than a year the hospital had
killed her.
While at St. Hans Hospital Luise finally took
the tests that were earlier denied her and they showed that she was a poor
metaboliser and therefore accumulated drugs. She was still on drugs, as the
good psychiatrists had had only six months to taper her heavy medication, and
when Sofus, Luise’s assigned psychiatrist at Amager Hospital, called for a
meeting to discuss Luise’s stay at St. Hans Hospital, Dorrit and her companion
came armed to the teeth with good arguments for reducing the drugging further.
Dorrit reminded Sofus about Luise’s worrisome tendency to throw up, which she
still did because of the drugs, but in the written record of the meeting, Sofus
said that he could not remember the vomiting and that it was contrary to his
position to reduce the medication. In actual fact, Sofus had himself mentioned
this problem in her chart notes several times and had sent Luise for countless
unpleasant gastrointestinal examinations.
The next day, the staff had a meeting with
Sofus, which they had arranged because of Luise’s vomiting. Luise’s contact
person, Dorte, was present and told Dorrit afterwards that Luise led the
discussion herself and that she’d never seen Luise so strong and focused as in
this conference. Dorte had declared at the meeting that, “Luise felt better and
was more clear-headed than l’ve ever seen her before – one hundred per cent.”
However, the record of the meeting doesn’t even
indicate that Dorte was present or what she said:
“The patient says that she must stick a finger
down her throat to induce vomiting. In addition, the patient is very talkative,
digressive and somewhat disconnected. She reports that there are several people
inside her room who are friendly, having a hard time and homeless. They are
friendly but do not talk to her because they are invisible … I [Sofus] ask
about her orientation: The patient doesn’t know what day of the week it is.
When asked about the month, she replies the month before December, when
Christmas is. I ask what year it is, and get no reply.”
What Sofus wrote about Luise’s lack of
orientation wasn’t true. Luise always knew the dates. Dorrit felt that Sofus
depicted Luise as mentally retarded, as lack of orientation about time and
place is one of the criteria for making the diagnosis.
A month later there was a new meeting and Dorte
described that the staff had observed that Luise behaved very differently from
other residents diagnosed with schizophrenia. She stressed that it was as if
Luise was a complete outsider (which staff at the various wards where Luise had
stayed over the years had also said). Dorte reported that the care team had
observed how much better Luise felt after prolonged vomiting (i.e. in a less
drugged condition). Sofus said that regardless of whether the diagnosis was
right or wrong, it could never be erased. It was a very long meeting where
Dorte argued well for the staff’s position.
At the meeting, Dorrit and Dorte asked to see
the record of Luise’s conference with Sofus three weeks earlier. Dorrit was
shocked to see Sofus’s record stating that there had been a so-called urgent
call from the staff: “The patient has been increasingly psychotic recently and
has been vomiting. If the patient does not improve, she should be
hospitalised.” This was not at all correct, so Dorte brought out the chart and
started to recite from the staff’s daily patient notes, which indicated Luise
had been very sociable and happy. She had helped with the daily chores and had
not received any additional medication, as she normally did. Therefore, there
was no evidence of increasing psychosis. Dorrit asked how it was possible to
observe increasing psychosis at a single meeting since, if it were increasing,
it would be happening gradually. Sofus said he had met Luise in the hallway and
that she seemed psychotic.
Dorrit was very worried and didn’t understand
Sofus’ motives. Why did Sofus write that Luise was increasingly psychotic when
she was feeling better than she had for a long time? Was he perhaps setting
Luise up for an imminent increase in her medication?
The minutes of this meeting included a great
deal about the World Health Organization’s diagnostic utterings about
schizophrenia and little about Dorte’s and the staff’s views on Luise’s
diagnosis. It was all written rather vaguely. Dorrit got access to the record
two weeks later, only to discover a whole new version of it. The key passage
about the urgent call from the staff and Luise becoming increasingly psychotic
had been deleted.
The new minutes now only dealt with Luise’s
vomiting and the text was more or less a copy of a letter Dorrit had written to
the psychiatrist about her worries about Luise’s vomiting and recent increase
in medication. Dorrit’s paragraph where she predicted that Luise would be
hospitalised within a month if things went as usual wasn’t included.
Luise was admitted to Amager Hospital after her
vomiting ceased and she became intoxicated with drugs again. Sofus contributed
to a dose increase despite the fact that he had been involved in the discharge
conference three months earlier at St. Hans Hospital where he learned that
Luise should take as little antipsychotic medication as possible. Luise lost
all hope and asked her mother at one of her visits: “Mom, do you think it’s
better in Heaven?”
Luise’s best friend at the care home, who was
also admitted to the hospital, and stayed in the room next to her, suddenly
collapsed at the floor and died within a few minutes. Luise was completely
shattered and all she said to her mother was: “I’ll be next.”
The staff didn’t offer any psychological help,
arguing that Luise appeared completely untouched by the shocking death.
Instead, Luise’s medication was increased because, as the nursing record said,
“Rather troubled because of the commotion in the ward this morning. Seems
everything is wrong with her and she’s asking us to take her blood pressure.”
So, the psychiatrists had just killed a patient
with their drugs, but this was called “commotion,” and the staff apparently
didn’t have even the most elementary knowledge about the drugs being used, e.g.
that they take away people’s emotions so that they don’t respond like people
who are not drugged. In addition, the lack of reaction from the other patients
to the screams when Luise’s friend died was likely also related to their fear
that they might be next to die from overmedication. They made every effort not
to react emotionally to the situation, as they knew so well that the treatment
offered for an intense reaction is rarely soothing conversation but rather
restraints, possibly supplemented with a syringe. This reminds me of the
ubiquitous fear that prevailed in Nazi concentration camps where everybody did
their utmost not to show any emotions to avoid becoming the next corpse. A
third reason that Luise didn’t react was that psychiatry had broken her.
Initially, she fought back, which resulted in long-term coercive measures.
Eventually, just the threat of forcible measures was enough to make Luise
simply give in. On several occasions, Luise asked to be strapped down, which
she preferred to the even worse alternative: extra medication or drugs by
injection.
One would think that talking was a normal part
of treatment at a psychiatric ward, but this wasn’t the case for Luise. When
psychiatrists perceive the patients’ problems as misfiring neurons as a result
of some brain defect, talking becomes irrelevant. It would have given her a
chance to tell how she felt about her treatment and why she was afraid of the
antipsychotic medication. Dorrit found it amazing how much better Luise felt
when the good psychiatrist at St. Hans Hospital listened to her, and how things
got even better in her sessions with a psychologist.
The Council of Europe’s Committee for the
Prevention of Torture and Inhuman or Degrading Treatment or Punishment visited
Denmark in 2002 and again in 2004, where it noted that the use of forced
measures had increased. Four months after Luise’s death, however, the practice
of strapping patients had decreased significantly. Psychiatrists had realised
that the “patients can take much more responsibility than we had assumed” and
also that by talking to them and respecting them, far less restraint was needed
and for far less time.
Over the years, Dorrit has written to several
prominent psychiatrists asking if they could help her with a second opinion.
None welcomed her request but asked her to talk to Luise’s psychiatrist again.
It is abundantly clear to me that doctors are very reluctant to put themselves
in a position where their independent statements can be seen as a criticism of
one of their colleagues. Dorrit finally found one, and he concluded that Luise
suffered from Asperger’s syndrome. It is quite common that such patients are
misdiagnosed as having schizophrenia. He said he would contact Luise’s
psychiatrist (Sofus) and was sure that the two of them together could devise a
long-term drug discontinuation plan for Luise. A month later, he phoned Dorrit
and informed her that Luise’s psychiatrist had refused to cooperate. Dorrit
cried on the phone and said she might just as well wait for Luise to die. That
came to pass four days later.
Early one morning, Dorrit got the phone call she
had feared and had had nightmares about for years. Luise had fallen to the
floor like her friend six months earlier, with convulsions, and died. Dorrit
screamed and shouted: “No, no, no, it can’t be. You’ve killed her with your
medicine. That’s what I always said. You were going to kill her.”
Dorrit informed her sister Elsebeth who promised
to come as quickly as possible. In the next call from the hospital, a cold
female voice said that if they wanted to have flowers on Luise’s deathbed, they
had to bring them themselves.
Ninety minutes after the death call, Dorrit got
a third call where a voice said that “if you want to see Luise before she’s
taken away, you have to come now.” Dorrit yelled back tearfully: “I can’t just
come out there alone to see you people who have killed her, and say my final
farewell to Luise, the person in my life I love the most!”
Luise’s death was described as an “unintended
event” by the doctor in the intensive care unit who was the one who had ordered
the lethal injection. At his side sat Luise’s regular consultant (Sofus). There
was no offer of condolences. The doctors seemed angry, dismissive and
insensitive. Elsebeth asked why they had not listened to Dorrit’s warnings. A
week earlier, Dorrit had told them that more drugs – and especially
prolonged-release medication – would be Luise’s death, because she couldn’t
throw them up. Dorrit had argued that no psychiatrist knew how much medication
Luise could tolerate since she always vomited.
The answer to Elsebeth’s question was: “We went
by the book.” But they had not acted by the book. Luise was given a new
antipsychotic drug on top of the three she was already taking, which
contravened the guideline from the National Board of Health that says that
doctors should avoid giving more than one drug at a time and that two drugs
could be administered only in exceptional cases.
There was nothing in the record that showed what
information Luise was given on prolonged-release injections, or what she said
about it. On the day the injection was given, less than ten hours before Luise
died, the chart said laconically:
“The patient was persuaded today to take
prolonged-release medicine.” Then a few words about the dose and about her
feeling well. The autopsy revealed marks around her body, which the coroner
could not explain. Dorrit had no doubt these marks stemmed from what happened
when Luise got the injection. Luise did not want medicine by syringe, which is
crystal clear in the chart note from a week earlier, where she says no, never
in my life do I want an injection.
Dorrit had called Luise in the afternoon on the
day she received the lethal injection. Luise was angry and did not want a
visit, which worried her mother who phoned the ward and was told that Luise was
doing fine and just did not want a visit. When Dorrit then asked if there had
been a change in her medication – she dreaded the injection the doctor had
talked about and said it would be Luise’s death – they replied that they had
decided to inform her about any medication changes only once a week, so she
would find out a week later. Now Dorrit got really scared, but the next morning
Luise was already dead.
There was nothing in the record about the
injection, except the time, although it is required by law that a patient’s
chart must record what information the patient has received about a new product
and what the patient has articulated about it.
After Luise’s death, everyone advised Dorrit not
to bother filing a complaint, as it is a degrading and exhausting process, and
that she would never get anywhere with it, as psychiatrists are as thick as thieves.
Dorrit reported Luise’s death to the police, to
the Patient Complaints Commission and to the Patient lnsurance Association. She
felt there surely was at least the possibility of a negligent homicide
investigation. The police contacted her by letter nine months later stating
they had concluded their investigation. By contrast, they had had regular
contact with the Copenhagen Hospital Corporation and, through them, Amager
Hospital. Three months after Luise’s death they had stated that they found no reason
to interview the doctor Dorrit had reported to the police, but that they were
awaiting the National Board of Health’s medical assessment of Luise’s
treatment.
The Board of Health concluded that Luise had
been treated in accordance with the standards of good specialist practice,
which it certainly wasn’t, as it so clearly violated the Board’s own guideline.
Dorrit’s complaint to the Patient Insurance
Association, with the headline “Death from drug poisoning,” led nowhere either.
According to the Association’s psychiatry expert, Luise had received the
highest standard of specialist treatment. If that is really the case, I
understand better why psychiatrists kill so many of their patients. The
psychiatrist noted that, “the risk inherent in the medical treatment must be
weighed against the suffering Luise Hjerming Christensen would have undergone
without treatment.” It’s utterly unbelievable that the truth can be twisted in
this way. Luise’s suffering and death were caused by the drugs the
psychiatrists had enforced upon her. She would have done well without the
drugs, which amounted to three times the highest recommended dose, and on top
of that, in a person who metabolised them poorly.
The Patient Complaints Board took three years to
come to a decision. Again, Luise had been treated in accordance with the
standards of good specialist practice.
The “licence to kill” in James Bond movies has a
perverse meaning in psychiatry. It is considered the highest standard of
specialist treatment to kill people after having tortured them for many years
with the drugs that ultimately killed them, and which they begged their
torturers not to use. Further, this “high standard” took no account of public
statements by leading pharmacologists from Denmark and the Nordic countries
affirming that the large dose of medicine without any doubt had been the cause
of Luise’s sudden death!
The absurdity of it all was total when it turned
out that the same doctor Dorrit had filed the complaint against was hired by
the Patient Complaints Board as a psychiatric expert seven months after Luise’s
death, i.e. while the case was still being considered. This means that the case
might have been settled before it ever got started, as it would have been
inconvenient for the Board to investigate a doctor they had just hired.
Several odd things happened during the
proceedings. Luise’s death certificate said “death from unknown causes” and as
contributory causes of death it had “epilepsy and mental retardation.” This was
outrageous. There was nothing about drugs. And the hospital washed its hands.
It disclaimed any responsibility for the two incorrect diagnoses and said it
was a matter for the police and forensic experts.
Oddly enough, Luise’s friend who had died six
months earlier at the same hospital also had epilepsy listed as a contributing
cause of death on her death certificate although she wasn’t epileptic either.
It’s never the drug’s fault or the psychiatrists’ fault, it’s you and your
disease.
Dorrit’s complaints led nowhere, but the massive
media coverage helped launch a wide-ranging debate about the quality of mental
healthcare in Denmark.
The system, however, congratulated itself for
its first-class homicide where everyone seems to have been immunised beforehand
against being found guilty. The officially accepted term for deaths such as
Luise’s is “natural death.”
16
What can patients do?
There is a lot patients can do to help create a
better and more humane psychiatry and to protect themselves against
ill-treatment.
1) Try to avoid being treated with electroshock
or psychotropic drugs. Remember that very few patients benefit from the drugs
they take; that many more are harmed by them; and that we don’t have safe
drugs. There is widespread corruption at the FDA, and corruption also occurs at
other drug agencies.1 David Graham, who has spent more than 40 years
working for the FDA’s Office of Drug Safety, has illustrated the regulatory
impotence and industry friendliness:2
“The way FDA approaches safety is to virtually
disregard it … The case of antidepressants and suicidality is a perfect example.
How does the FDA handle this? With labelling changes. FDA knows that labelling
changes don’t change physician behavior … what FDA says is: We can’t be 95
percent certain this drug will kill you, therefore we will assume it doesn’t –
and they let it on the market … if we wanted drugs that are safe, we could have
it tomorrow. It is easy to design those studies. But FDA is not interested in
that.”
In 2012 a former FDA scientist, Ronald Kavanagh,
also spoke out:3
“Sometimes we were literally instructed to only
read a 100- to 150-page summary and to accept drug company claims without
examining the actual data, which on multiple occasions I found directly
contradicted the summary document. Other times I was ordered not to review certain
sections of the submission, but invariably that’s where the safety issues would
be … I found evidence of insider trading of drug company stocks reflecting
knowledge that likely only FDA management would have known. I believe I also
have documentation of falsification of documents, fraud, perjury, and
widespread racketeering, including witnesses tampering and witness
retaliation.”
In contrast to drug agencies, as David Healy has
pointed out, airline pilots are critically concerned with our safety because if
we go down, they do too.4 If a patient goes down, doctors can blame it on the
patient’s illness rather than the drug and their own incompetence. When pilots
report adverse events, they are taken very seriously and it leads to change.
Doctors rarely report adverse events and if they do, their reports are filed as
anecdotal and don’t lead to change.
2) If you have a mental health problem or other
problems with your life, avoid seeing a psychiatrist unless you know that he or
she tries to avoid drug treatment and is a good psychotherapist. If you go to a
mainstream psychiatrist, you’ll likely get harmed. Perhaps not immediately, but
in the long run.
3) Ask if your doctor receives money or other
benefits from the drug industry, has shares in a drug company, is visited by
drug sales-people, or is being “educated” at industry-sponsored events. If any
of this is the case, find yourself another doctor.
4) Don’t go to the pharmacy at once if your
doctor writes a prescription, but find the officially approved package insert
on the Internet. This information can be pretty overwhelming with many
unfamiliar medical terms, so you may wish to consult with a knowledgeable
friend. It may take some time to digest all the information, but considering
that many patients are treated for years, it is well worth the effort. There
are also shorter summaries on the Internet that are easier to understand, but
they are not necessarily accurate and may have been produced by drug companies,
even if posted on seemingly neutral websites like those of patient
organisations.
Do a Google search on the name of the drug or
search on the drug regulators’ homepages, where there can be separate
information for patients and for doctors, e.g.:
http://www.ema.europa.eu/ema/ (European Medicines Agency)
http://www.fda.gov/ (Food and Drug Administration)
http://www.mhra.gov.uk (UK drug agency)
If you read the package insert, you’ll likely
know much more about the drug than your doctor does, and I am not joking. I can
assure you that if doctors knew what is written in package inserts, they
wouldn’t prescribe so many drugs.
You may also look up independent information
sources about drugs and other treatments, e.g. the Cochrane Library, www.cochrane.org.
Abstracts of Cochrane reviews are freely available and the full reviews are
freely available for half the world’s population. You should realise, however,
that almost all trials of psychotropic drugs summarised in Cochrane reviews are
flawed. You therefore need to be critical when you read reviews; in particular,
the harms of the drugs are often downplayed or missing.
You are now in a better position to decide for
yourself whether or not to take the drug. American TV commercials invariably
end with something like, “Ask your doctor whether Prozac is right for you.” But
since your doctor has very likely been influenced by the drug industry, it
would be preferable to “Ask your doctor whether Prozac is wrong for you,” or
even better, “Ask yourself whether Prozac is wrong for
you.” If you ask me, no one should take antidepressants.
5) Avoid taking new drugs the first seven years
they are on the market, as most drugs that are with-drawn for safety reasons
get withdrawn within the first seven years.1
6) If a drug is needed, ask your doctor if
cheaper drugs are available. Take the drug for as short a time as possible and
ask your doctor for a firm plan for tapering it off before you start. If your
doctor doesn’t think such a plan is needed, don’t take the drug!
7) Always remember that our prescription drugs
are the third major killer after heart disease and cancer, and that very many
unnecessary deaths are caused by psychiatric drugs.1 This is the
result of widespread crime in the drug industry, widespread corruption of
doctors, and impotent drug regulation. We have created a system that doesn’t
work as intended and which is dangerous for patients.
8) One of the most devilish problems in taking
drugs is that, quite often, you don’t realise that when you don’t feel well, it
could be a side effect of the drug. Although psychotropic drugs have many
harmful effects, doctors tell their patients very little or nothing about the
side effects when they prescribe them, or they say there are no side effects to
worry about, which is never true.
9) If you have been trapped by psychiatry,
reclaim control over your own life (see Chapter 14). You are the master of your
life, the psychiatrists aren’t and they usually make your life more miserable
than it already was.
10) Ask yourself whether you really need the
drugs you take and consider gradually reducing them, one by one, with
professional assistance (not necessarily the doctor who prescribed them, who
will usually be against stopping them). Remember it can be dangerous to stop
drugs abruptly (see Chapter 12).
11) Remind yourself that we cannot believe a
word of what drug companies tell us, neither in their research nor in their
marketing or information to patients.
12) Withdraw your membership if your patient
organisation accepts drug industry money or other favours. Patient
organisations are often set up by drug companies, although they hide this.
Between 1996 and 1999, the US National Alliance for the Mentally Ill, which
calls itself “a grassroots organisation of individuals with brain disorders and
their family members,” received almost $12 million from 18 drug companies, led
by Eli Lilly.5 It is hugely rewarding for companies to brainwash
leaders of patient organisations, as they can allow themselves to be much more
vocal and belligerent than the companies can.
13) Don’t volunteer for trials unless the
informed consent form contains a clause that the trial protocol, all analyses,
and all the raw data (in an anonymised fashion that doesn’t allow
identification of individual patients) will be made publicly available.1
Ensure – before you sign – that you have seen all agreements between the
sponsor and the investigators, including monetary amounts and conditions. If
doctors are uncomfortable about this, they have something to hide and you shouldn’t
participate in the trial.
Many industry-sponsored trials are marketing
disguised as science that exploit patients for a monetary gain, not only for
the company but also for the doctors or their institutions, and they often have
a biased design that guarantees results that are useful for the company but
which are misleading. Such trials are a breach of the implicit social contract
between researchers and patients. To be truthful, patient consent forms should
therefore often look somewhat like this:1
I agree to participate in this trial, which I
understand has no scientific value but will be helpful for the company in
marketing their drug. I also understand that if the results do not please the
company, they may be manipulated and distorted until they do, and that if this
also fails, the results may be buried for no one to see outside the company.
Finally, I understand and accept that should there be too many serious harms
from the drug, these will either not be published, or they will be called
something else in order not to raise concerns in patients or lower sales of the
company’s drug.
17
What can doctors do?
There is a lot doctors can do to help create a
better and more humane psychiatry.
1) We should work towards banning all forced
treatment by law in all nations. We have other laws that allow us to save the
lives of people, e.g. those with anorexia nervosa who are at risk of dying.
2) We should bury the DSM-5 and the
corresponding parts of ICD-10 in psychiatry’s grave and start all over again
with the diagnostic system. NIMH has abandoned the use of the DSM as a research
tool and in 2013, its president, Thomas Insel, explained why:1
“Unlike our definitions of ischemic heart
disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about
clusters of clinical symptoms, not any objective laboratory measure. In the
rest of medicine, this would be equivalent to creating diagnostic systems based
on the nature of chest pain or the quality of fever.”
No one with conflicts of interest in relation to
the pharmaceutical industry should be allowed to participate in this work. We
should narrow and restrict diagnoses so that the resources we already have
would be sufficient to allow us to take care of the really sick people in a
humane way and allow us the necessary time to listen and talk to them.
3) We need to refresh the art of being patient
and wait and see without giving the patients sticky diagnoses and addictive
drugs. “Watchful waiting over multiple visits can enable doctors to see if the
problems will resolve without intervention.”2 Good psychiatrists try to avoid prescribing drugs at
the first visit but they are very rare. One of these psychiatrists wrote to me:
“I have been appalled by the state of psychiatry
in my country. My professor is behind it all, from developing guidelines to
postgraduate education. With experience, I have begun to see what a sham this
recasting of mental distress as medical suffering really is. Reading critical
psychiatry books has helped me make sense of my clinical experience. I now
strive to have discussions and relationships with patients that are
non-coercive equal partnerships. A few patients have questioned if I am really
a doctor because I treat them like humans, smile, laugh, and give them a sense
of responsibility and ownership of their problems and treatments. I Google
things in front of them if I am not sure, usually around side effects, drug
interactions or odd withdrawal symptoms. It also made me understand my own
history. In my twenties, I had a massive breakdown. At the time, I
instinctively resisted all psychiatric labels and medical treatments. It took a
long time to get back to normal but somehow I did. When I look back now I can
easily see how, in the wrong hands, I could have been labelled schizophrenic,
as I heard voices and had delusions and severe anxiety. Now I know my breakdown
was no different to what my patients experience. Mental healthcare could be a
lot better if it embraced treatments like Open Dialogue or Soteria and listened
to the growing voice of psychiatric survivors, but the bio-maniacs have taken
over everywhere, and they have money and power, so the hegemony prevails. Most
people don’t really know how it all works. They assume the drug companies are
working for the good of humanity, so we are rather stuck.”
If someone becomes a psychiatrist after having
had their own experience with psychosis, they usually retain a warm empathy for
their patients, whereas without that experience, many psychiatrists seem almost
dismissive of their patients as human beings. This is what so many patients
complain about, that they are treated as a thing – a diagnosis – and not being
respected.
4) We need psychiatric institutions where
patients are guaranteed that psychiatric drugs will not be used under any
circumstances, and patients should be free to choose such institutions.
5) We should constantly remind people that a
life without drugs is possible and even desirable.
6) Doctors should insist on getting training in
psychotherapy and should learn to see this as more important than anything else
in psychiatry. A US psychiatrist said:3 “When I trained back in the 80s, we got 50 percent
psychotherapy training and 50 percent biologic medication training. Today, the
average psychiatric resident gets zero psychotherapy training. So all they have
to offer is a pill.”
7) We need a major culture change where we see
clinical trials as a public enterprise done for the public good, and performed
by independent academic institutions. We should stop the industry from being
its own judges and therefore should no longer accept that the industry can
conduct trials on patients. The industry could still pay for trials but should
have nothing to do with them, and a public body with patient representatives
should ensure that trials are relevant for patients and have relevant outcomes.
This could break the vicious circle where drug companies choose investigators
that have long-standing relations with the drug industry and don’t ask
uncomfortable questions. The arrangement would also be vastly cheaper for the
industry. The European Society of Cardiology has estimated that university
centres can perform drug trials for about 5-10% of the cost of industry trials
where there are numerous for-profit middlemen (including doctors and hospitals)
who take a hefty surcharge.4
8) Psychiatrists should embark on the long-term
randomised trials that they have failed to carry out for decades that can
inform us about the long-term effects of psychiatric drugs, including their
permanent harms.5 Our public funders and governments should be more
than happy with such trials, as the results will no doubt lead to huge savings
for our societies, fewer deaths and healthier patients.
9) Doctors should avoid having financial
conflicts of interest. The idea that, as long as they declare them, everything
is all right, is silly. Financial conflicts of interest distort what people say
and write,6 so how should readers handle a research report with
authors on industry payroll? Should they ignore the report completely or
downgrade it, and if so, in what way and by how much? The solution clearly is
to avoid financial conflicts of interest entirely.
Doctors should therefore say no to industry
money and favours of any kind, including meals and travel to congresses.7 If companies ask for advice, doctors can give it for
free, and they should decline to be consultants or sit at companies’ advisory
boards, as they cannot be advocates for their patients and the drug industry at
the same time. It is untenable that doctors won’t accept a court case where the
judge is paid by one of the sides whereas they willingly accept to be paid by
the drug industry.
Unfortunately, there is a culture among doctors
that allows acceptance of easy money, and companies may offer to transfer the
money in ways that cannot be traced.6 But doctors and their organisations
should consider whether they find it ethically acceptable to receive money that
has been partly earned by organised crime that has harmed and killed many of
their patients.6
We need to reverse this culture into one of professional ostracism so that a
person on industry payroll would no longer show their face in places where
their academic colleagues gather. It’s unbelievable that doctors cannot see
that acceptance of easy money is corruption. This corruption has many
euphemistic names, e.g. “discretionary funds,” “no strings attached,” or
“unrestricted educational grants.”
Doctors should also avoid accepting any surplus
money generated by collaborative research with the industry, which they can use
for their own research, as this impairs their judgment and critical sense and
can lead to coercion of patients into trials with harmful drugs. The same
applies to hospitals.
10) Institutions should not accept gifts from
the industry, as such gifts distort the institutions’ agendas.6, 8, 9 This will be hard to avoid, as the amounts can go up
to one hundred million Euros for just one institution, which has happened in my
country.
11) All countries should have publicly
accessible and easily searchable websites of doctors’ collaboration with
industry, detailing the monetary amounts and other benefits, and there should
be stiff penalties for missing information or incorrect amounts.
12) Doctors should not “educate” other doctors
at industry-sponsored meetings. Such events have no genuine educational purpose
but are just marketing, and the industry wouldn’t sponsor these activities if
they didn’t increase sales. It carefully controls the content, although it
tries to conceal this fact.6
13) Doctors should not add their names to
ghost-written papers, which is fraud, as it gives them false credibility and
misleads readers deliberately.6
14) Doctors should not meet with drug
salespeople, as this leads to higher drug costs and irrational prescribing in
other ways, and the more frequent the contacts with salespeople, the worse the
outcome is for public health and our national economies.6, 10 As an example, general practitioners in France
prescribed an antipsychotic three times as often if they had been visited by a
salesperson in the last month touting such drugs.11 I often wonder why any doctor is willing to believe
anything drug companies tell them.
15) Medical journals should stop publishing drug
trials. Instead, the protocols, results and the full dataset should be made
available on publicly owned websites.6, 12 Our most prestigious journals earn a vast amount of
money by selling reprints to the companies of their trial reports, and the
editors have a huge conflict of interest when they allow flawed research and
flawed abstracts to be published, which often occurs.6 Instead of
publishing trials, journals could concentrate on critically describing them.
I will end my book with a quote by biologist
Richard Dawkins, Oxford, author of The God Delusion, who said: “Apparently,
when you’ve become the establishment, it ceases to be funny when someone
punctures the established bag of wind.”13 I hope that, with this book, I have punctured
psychiatry’s established bag of wind effectively, as this will benefit patients
and enable the coming generations of psychiatrists to do a more meaningful job.
18
Helpful websites
There are many websites about what psychiatry
has done to people and about what people can do to reduce their risk of getting
harmed by psychiatry and to come off psychiatric drugs. I have described some
of them on my own website, www.deadlymedicines.dk, where there are also links to
some of my lectures, patient stories and other information.
www.madinamerica.com Award winning science journalist
Robert Whitaker’s website about why psychiatry hasn’t delivered what it
promised. New posts appear almost every day.
http://davidhealy.org/ Psychiatrist David Healy’s
website about the risks of taking prescription drugs and much else. RxISK.org is about
research on and reporting of drug side effects, and about which drugs have been
related to suicides. http://econsult.rxisk.org/
offers consultation with a medication specialist for a fee.
http://www.breggin.com/ Psychiatrist Peter Breggin’s
website: What your doctor may not know: psychiatric drug facts. There is a lot
about why and how to avoid psychiatric drugs.
http://www.mindfreedom.org/ MindFreedom International
unites grassroots groups to win human rights and alternatives for people
labelled with psychiatric disabilities.
http://psychrights.org/ is Jim Gottstein’s homepage,
with information about the force of the law, a search function with many
pivotal research papers, and a long list of everyday horror stories from the
mental health system.
http://www.psychintegrity.org/ The aim of the International
Society for Ethical Psychology and Psychiatry is to promote safe, humane, and
life-enhancing approaches to those problems, which are often diagnosed as
psychiatric disorders.
http://cepuk.org/
Council for Evidence-based Psychiatry communicates evidence of the harmful
effects of psychiatric drugs and works to reduce psychiatric harm by informing
policymakers and practitioners, by sharing the testimony of those who have been
harmed, and by supporting research into areas where evidence is lacking.
http://www.ssristories.org/ is a collection of over
5,000 stories that have appeared in the media and where prescription drugs were
mentioned as a possible cause for a variety of adverse outcomes including
suicide and homicide.
http://www.woodymatters.com/ is Kim Witczak’s website
with links to psychiatric drugs in relation to the FDA, big pharma, corruption,
political reactions, and lawsuits (from 2003 to 2008).
http://recoveringfrompsychiatry.com/ Psychiatric
survivor Laura Delano’s website with tips about how you can recover from
psychiatry.
www.whocaresinsweden.com is a documentary by Jan
Åkerblom in three parts about the risks of antidepressant drugs.
www.depression-heute.de is a website in German about
depression.
© Peter C. Gøtzsche og People’sPress, København
2015
© This edition: People’sPress, 2015
Cover: Stine Trampe
ePub produktion: Rosendahls - BookPartnerMedia
ISBN: 978-87-7159-62-43
1. Edition
All rights reserved. No part of this publication
may be reproduced,
transmitted, or stored in a retrieval system, in
any form or by any means,
electronic, mechanical, photocopying, recording
or otherwise,
without the prior permission of the publishers.
This book is sold subject to the condition that
it shall not,
by way of trade or otherwise, be lent, re-sold,
hired out or
otherwise circulated without the publisher’s
prior
consent in any form of binding other than that
in which it is published
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condition
being imposed on the subsequent purchaser.
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CHAPTER 1 REFERENCES
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