book

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Until we really understand the nature of serious mental illness,
psychiatrists need to resist fads in diagnosis and treatment. The best
antidote lies in cautious conservatism and the principles of evidencebased practice.
Joel Paris is a full Professor at McGill University, and Editor-in-Chief of
the Canadian Journal of Psychiatry. His research interests lie in personality
disorders, and he has published 185 peer-reviewed articles, 17 books and 44
book chapters.
PUBLICATIONS
Cover image by Guy Undrill
Fads & fallacies
in psychiatry
Joel Paris
Fads & Fallacies in Psychiatry
This book examines fads and fallacies, past and present, that plague
psychiatry, both in diagnosis and in treatment. These include
overdiagnosis (especially of depression, bipolar disorder, ADHD,
PTSD and autism), overtreatment with pharmaceuticals and the
assumption that neuroscience has all the answers.
Paris
Aspects of mental illness are still a mystery. Answers to the most
important questions in psychiatry may require decades of further
research, so it is important to critique contemporary practice –
especially as fads in psychiatry have occurred not only on the fringe,
but in the very mainstream of theory and practice. Some of the
trendiest theoretical paradigms may turn out to be unsupported
by data. In diagnosis, some faddish approaches to classification
are unlikely to last. In treatment, both psychopharmacology and
psychotherapy sometimes embrace interventions with a weak base in
evidence that run the risk of doing harm to patients.
Fads and Fallacies
in Psychiatry
Joel Paris
RCPsych Publications
© The Royal College of Psychiatrists 2013
RCPsych Publications is an imprint of the Royal College of Psychiatrists,
17 Belgrave Square, London SW1X 8PG
http://www.rcpsych.ac.uk
All rights reserved. No part of this book may be reprinted or reproduced or utilised in any form
or by any electronic, mechanical, or other means, now known or hereafter invented, including
photocopying and recording, or in any information storage or retrieval system, without permission
in writing from the publishers.
British Library Cataloguing-in-Publication Data.
A catalogue record for this book is available from the British Library.
ISBN 978 1 909726 06 2
Distributed in North America by Publishers Storage and Shipping Company.
The views presented in this book do not necessarily reflect those of the Royal College of
Psychiatrists, and the publishers are not responsible for any error of omission or fact.
The Royal College of Psychiatrists is a charity registered in England and Wales (228636)
and in Scotland (SC038369).
Printed by Bell & Bain Limited, Glasgow, UK.
Contents
 1 Introduction
1
Part I. Origins
 2 Medicine
11
  3 Psychiatry 24
Part II. Effects
 4 Aetiology
37
 5 Diagnosis
45
  6 Epidemiology 59
 7 Psychopharmacology
65
  8 Psychotherapy 79
 9 Prevention
88
Part III. Antidotes
10 Evidence-based psychiatry
11 Overview 97
103
References108
Index
120
iii
Chapter 1
Introduction
Mental illness is a mystery. That is why I chose psychiatry as a career, and
why I love it. It is still a pioneer field, and answers to the most important
questions about mental illness will probably require another century of
research. But becoming a psychiatrist was one of the best decisions I ever
made. Fifty years later, I have no interest in retirement.
As I grow older, I have become interested in the history of my specialty.
As a medical student, I did not understand why we were taught the history
of medicine. Once ideas go out of date, why learn them? Now I have come to
realise that progress is not linear. Impeded by false beliefs, medical science
sometimes goes off on serious tangents. Understanding past mistakes helps
us to be appropriately sceptical about current theories and practices.
I have always been the type of person who questions everything. When
I was young, this trait got me into trouble. Teachers saw me as a rebellious
young man, but I had a strong need to question all received wisdoms.
Now, in my old age, I am called a curmudgeon for saying some of the same
things. Although psychiatrists do a lot of good for patients, it is important
to criticise contemporary practice, especially its susceptibility to fallacies
and its penchant for fads. That is the passion that drives this book.
The title is a deliberate paraphrase of a classic volume by Martin
Gardner (1957), Fads and Fallacies in the Name of Science. Fads are temporary
bursts of enthusiasm, based on fallacies that reflect cognitive errors or
wishful thinking. When we think of fads, bizarre ideas come to mind, and
Gardner’s book focused on very strange theories. But fads in psychiatry
have occurred not only on the fringe, but in the very mainstream of theory
and practice. Some of the trendiest theoretical paradigms may turn out
to be unsupported by data. In diagnosis, the many faddish approaches to
classification are unlikely to last. In treatment, both psychopharmacology
and psychotherapy sometimes embrace interventions with a weak base in
evidence that run the risk of doing harm to patients.
This is not to say that psychiatry consists of nothing but fads and fallacies
– far from it! In spite of enormous gaps in knowledge, we do at least as well
as physicians in other specialties in helping our patients. The problem is
1
fads and fallacies in psychiatry
that psychiatry does not fully understand mental disorders, the causes of
which remain as obscure as ever.
Should we be surprised? No. The brain is the most complicated structure
in the entire universe. Neuroscience will not solve these problems quickly.
We are told that answers are just around the corner, but that is where they
tend to stay. The most important questions in psychiatry remain unanswered.
Since psychiatrists have so much to learn, they should remain humble.
The current rage to reduce everything in psychiatry to a neuronal level is
an idea that has some degree of merit, but it is oversimplistic and hubristic.
Neural processes can only be understood in the context of interactions with
psychological adversities and sociocultural stressors. Although multivariate
models are complex, they explain why research on the origins of mental
illness and their treatment is so difficult.
Ironically, the main source of psychiatric fads is that practitioners
want so badly to help their patients. Human nature being what it is,
clinicians are uncomfortable with doubt and seek certainty. They have
trouble maintaining a cautious stance in the face of scientific ignorance.
Practitioners do not want to wait a hundred years for answers, and are
tempted to believe they know enough already. That is the main reason why
psychiatry has been infected by fads and fallacies. This book will document
how and why this happens.
Why I have written this book
I began my career as a clinician and an educator. In spite of doubts, I largely
accepted the point of view my teachers had given me. With time, I came
to realise the older generation was wrong about many things. I became
committed to a scientific perspective, and trained myself to become a
researcher. I became a passionate convert to evidence-based medicine. I no
longer took clinical experience, even my own, for granted. For this reason, I
have taken care to ensure that most ideas in this book are at least consistent
with the empirical literature, and refer the reader either to relevant
studies or to comprehensive reviews. However, since the subject is so vast
(psychiatry as a whole), I have had to be very selective about references.
This book will also draw on my 40 years of work as a consultant.
Describing these clinical encounters is not intended to contradict one of
the main themes of this book, which is that one cannot base practice on
clinical experience. I will use consultations to illustrate points that can be
confirmed by empirical data. Since 1972, I have been in charge of a hospital
clinic that sees hundreds of patients every year referred from primary care.
I also worked in a university health service for 25 years, and after setting
up a specialty clinic for personality disorders in 2001, conducted thousands
of consultations on patients with these conditions. Although I still treat
sicker patients in specialised clinics, like many of my colleagues, I spend
more time than I did in the past on consultations to primary care.
2
introduction
In total, I estimate that I have seen 25 000 patients over the past 40 years.
When my students ask me how I seem to understand problems and make
diagnoses rapidly, I tell them that things get easier after the first 25 000
cases. But even the most extensive experience does not make you right.
You could be making the same mistakes thousands of times. That is why I
so strongly support evidence-based psychiatry.
If you want to practise scientific medicine, you have to give up certainty
and embrace doubt. In the first 10 years of my career, I aimed for radical
changes in my patients. With experience, I learned that although I could
help many people, psychiatry lacks the tools to achieve consistent and stable
remissions of many mental disorders. The field is only beginning a very long
journey. And since the specialty still has a relatively thin knowledge base,
I went into research to do my part in broadening it.
My second career in research started quite late, in my 40s, so I could
not reach the same level as others who started earlier, and I am only one
soldier in a vast army. But I benefited from clinical experiences that some of
my colleagues, tied to their labs and desks, lacked. Being an active clinician
helped me to ask more relevant questions. In turn, conducting research
affected my practice. The doubt that characterises the scientific culture is
the best antidote to fads. I brought its world view back to my clinical work
and my teaching.
The clinical trenches are far from the ivory tower of academia. Although
I aim to practise, as much as possible, in an evidence-based way, some of
the most crucial questions cannot be answered by empirical data. Thus,
when I treat patients, I keep in mind what I can and cannot do. And even
though I teach students to follow the research literature, I advise them to
remain cautious about generalising from one or a few published studies.
Unfortunately, not all my colleagues share this perspective. Some jump
on bandwagons and pretend unjustified certainty. Most simply follow the
crowd, and join in a consensus, however uncertain, if it is shared by their
colleagues.
Psychiatric fads, then and now
When I was young, two theoretical models shaped psychiatry, and both
became sources of orthodoxy. One was the psychoanalytic model. I began
training in the late 1960s, during the heyday of psychoanalysis in the USA
and Canada. At many universities, including my own, analysts were leaders
in academic psychiatry. Trainees revered them. That was because they had
an answer for everything. Analysts may have been arrogant, but students
were attracted to their confidence and certainty. These were teachers who
could provide plausible (or not so plausible) explanations for symptoms of
all kinds. They also insisted, without evidence, that their treatment method
was highly effective. When analysis did not work that was only because
it had not lasted long enough, or was not conducted with sufficient skill.
3
fads and fallacies in psychiatry
The psychoanalytic fad was never as powerful in Europe. It had some
influence in the UK, but never dominated psychiatry there. Disinterest in
research ultimately proved to be its downfall. Neither the theory nor the
method could stand up to empirical scrutiny. Today, although the analytic
movement remains alive, it plays a marginal role in psychiatry, both in the
USA and in Europe.
Although psychoanalysis was a fad, one cannot say that it was only a
fad. Many of its concepts and methods have been incorporated into other
forms of psychotherapy that have undergone clinical testing and have been
shown to be effective. Research supports brief courses of psychoanalytic
psychotherapy, and cognitive–behavioural therapy (CBT) makes use of
some aspects of the same theory. Also, my ability to listen empathically to
patients and to understand what they might be thinking comes from having
been trained in this model. (It is also a skill that cannot be entirely turned
off, even in private life.)
Following the rejection of psychoanalysis, modern psychiatry returned
to its medical roots. Even in my student days, biological psychiatry
had become an alternative orthodoxy. But psychiatry did not yet take
psychopharmacology to an extreme. Although drugs are often effective,
clinicians today may only treat symptoms in this way, losing interest
in people and their life histories. That is why I expect and hope that
psychotherapy will eventually make a comeback.
The 1960s was the golden age of psychopharmacology. The dramatic
success of treatment for severe mental disorders gave biological psychiatry
an enormous boost. Healy (2002) has described the medical management
of psychosis as one of the most inspiring developments in human history. I
entirely agree. I visited mental hospitals as an undergraduate student, and
saw what patients with psychosis were like before drugs to control their
symptoms were discovered. Yet only a few years later psychiatrists had
highly effective treatments for most of them. I saw such patients discharged
and maintained in the community after years of serious illness. This was
indeed a time of miracles.
Biological psychiatrists were less colourful than psychoanalysts, but they
kept psychiatry within the scientific mainstream. Instead of tradition and
authority, they relied on research studies and clinical trials. Yet although
neuroscience became the dominant force in psychiatry, it did not really
explain why psychiatric drugs are effective (Healy, 2002). Moreover, the
neuroscience community took a very narrowly biological approach, assum­
ing that mental disorders are ‘nothing but’ brain disorders. That is both true
and untrue. There can be no mind without brain, but psychiatry needs to
study mind on its own level. Moreover, neuroscience should not ignore the
powerful effects of psychological and social forces, which also shape the brain.
In this way, biological psychiatry, if associated with an almost total
dependence on drug treatment, can be as dogmatic as psychoanalysis ever
was. Its ideas are based on a core of truth that can be stretched to the
4
introduction
point of faddishness. Drugs are useful tools, but almost never cure mental
disorders, most of which remain chronic. Psychiatrists, rushing to gain the
respect of medical colleagues, embraced an ideology that is triumphant
for now, but covers vast ignorance with a gloss of science. In spite of all
the progress of recent decades, neuroscience is still in its infancy. Brain
research has not even begun to explain how psychological symptoms
develop (Hyman, 2007). It will eventually do better. But it will never be
able to reduce all mental phenomena and symptoms to a cellular level, or
to neural networks. Unless psychiatry embraces a broader model, it will
suffer from a crippled perspective.
Fads in contemporary psychiatry
I wish I could say that psychiatry has outgrown the fads and fallacies of
my youth. But it has not. This book will focus on three areas that remain
problematic.
The first is its diagnostic system. The International Classification of Diseases
(ICD) published by the World Health Organization (1993) is official in
most countries, with a revision (ICD-11) expected in 2015. This system is
standard in European countries. But over the past 30 years, the Diagnostic
and Statistical Manual of Mental Disorders (DSM), developed by the American
Psychiatric Association, has become the dominant model in the USA, and
has had a strong influence on research and practice all over the world. The
latest version (DSM-5), which was published in 2013, does not radically
differ from earlier editions. But both ICD and DSM diagnoses have become
reified with constant use, even though they are replete with conceptual and
practical problems.
Diagnostic manuals are rough-and-ready guides to complex phenomena.
Current systems are based almost entirely on observable signs and
symptoms, not confirmed by laboratory tests as in the rest of medicine.
Some categories are faddish and can expect a short life. At the same
time, psychiatric diagnosis has been expanding, sometimes threatening
to medicalise the human condition. Mental disorders are being seriously
overdiagnosed, leading to inappropriate treatment and unnecessary stigma.
We lack a basis for establishing the true boundaries of illness, and as time
goes on, diagnosis has crossed into normal variation, leaving hardly anyone
free of mental disorder at some point in their life.
A second area of concern is that the current trend in the USA for an
almost exclusive reliance on drugs is putatively based on the application
of a neuroscience model to practice. The most serious mental disorders
(psychoses and melancholic depression) absolutely require medication.
However, in the management of common mental disorders (anxiety and
depression) drugs are only one of the tools, and many patients do not
respond to them. A lot of data on treatment for these conditions support
either psychological treatment or a combination of pharmacotherapy and
5
fads and fallacies in psychiatry
psychotherapy. Unfortunately, that is not necessarily what happens in
practice. Instead, symptoms may be treated ‘aggressively’ with one or more
pharmacological agents, and little time is spent talking about the context
of the patient’s life.
Thus, practice has swung wildly – from talking without a clear purpose
to not talking at all. Contemporary psychiatrists are rarely interested
in conducting formal psychotherapy, and even those who have received
training in these kinds of interventions may not use them. Talking therapy
takes time and commitment. In the USA, the medical insurance system is
organised in a way that encourages psychiatrists to offer drug treatment
only, accompanied by a brief chat. Even where psychotherapy is covered
by insurance in principle, for example in the UK, psychiatrists pass on
procedures to psychologists, and these professionals are unfortunately
limited in number. Finally, faddishness continues to affect the practice of
psychotherapy. Some treatments have been marketed as cure-alls for a very
wide variety of problems.
A deeper concern is that those who only prescribe may forget how to
listen. As the American psychiatrist Leon Eisenberg once put it, psychiatry
has gone from being brainless to being mindless (Eisenberg, 1986).
Psychiatric drugs are effective when used for the right indications, but
not when applied to problems for which they lack an evidence base. For
example, antidepressants can be unimpressive in mild to moderate cases
of depression and anxiety, often not much better than placebo. But when
patients do not do well with these agents, clinicians are often advised to
press on with augmentation and switching. That means prescribing agents
originally designed for other problems, which often leads to ineffective
polypharmacy associated with highly problematic side-effects. These
practices remind me of the way psychoanalysts used to add on more therapy
when treatment failed, stubbornly refusing to consider alternatives to their
paradigm.
Faddish clinical practices derive from overly simplistic theories.
Contemporary views about the aetiology of mental disorders favour the
idea that mental symptoms are due to a ‘chemical imbalance’ or aberrant
neural circuits. These theories could turn out to be correct, but are currently
not well supported by solid evidence. Even so, many practitioners, and
many patients, believe these ideas to be scientific truth. The result is that
treatment aims to correct putative imbalances with a ‘cocktail’ of drugs.
Many patients are being given treatments they do not need.
The antidote to fads
The enterprise of science encourages debate and doubt, which are the
best correctives for faddish ideas. In the basic sciences, even the most
powerful paradigms decline when the weight of evidence fails to support
them, but change is slower in medicine. Sick people can be desperate, and
6
introduction
physicians may also seek desperate remedies. I have great sympathy for
front-line clinicians who deal with highly distressed patients. But that is
why psychiatry, which deals with poorly understood illnesses that cause
profound suffering, is so susceptible to faddish ideas. A scientific world
view implies a commitment to test all theories before accepting them,
and to subject all treatments to clinical trials. Practitioners can emphasise
virtues such as patience, humility and caution.
The antidote to fads is thinking scientifically and conducting evidencebased practice. This influential concept, developed by the great Scottish
physician Archibald Cochrane, is a principle to which we all pay lip service.
But people are prone to preconceptions, and tend to see the world in a way
that confirms them. These confirmation biases lie at the heart of fallacious
thinking in clinical work. Close attention to the scientific literature helps
keep these biases in check, and leads to a more cautious and conservative
way of working with patients. Adopting an evidence-based perspective
helps us to be comfortable with uncertainty, makes us less likely to harm
patients and more likely to help them.
Acknowledgements
Edward Shorter, who read an earlier version of this book, made many useful
recommendations for revision. Peter Tyrer was supportive of the project at
all stages.
This book is dedicated to family and friends who encouraged me to go into
psychiatry.
7
Part I. Origins
Chapter 2
Medicine
Fads are novel ideas that are rapidly adopted and followed enthusiastically –
for a time. By and large, fads are based on bad ideas. Science moves slowly,
and caution makes progress more certain. Yet since they can appear new
and attractive, fads initially earn great attention. Most end by disappearing
from view, sometimes with barely a trace. The American sociologist Joel
Best (2006) described these phases as ‘emerging, surging, and purging’.
Not every new idea is a fad. There are real breakthroughs in knowledge,
but it can take years to determine how they pan out. As a rule, it is best
to remain cautious about concepts that spread rapidly, and to be more
welcoming to those that gain support gradually and withstand the test
of time. In the end, fads are addictive ideas that short-circuit the slow
progress of science. Similarly, fallacies are mistaken conclusions that may
be embraced incautiously, but do not bear close inspection. Both fads and
fallacies are based on cognitive errors.
Fads, fallacies and cognitive errors
Most people assume that even though others can be foolish, they themselves
are rational and show good judgement. This principle has been supported
by research (Tversky & Kahneman, 1982). A lack of critical perspective on
the self is the most prevalent of all fallacies. One would like to assume that
intelligent clinicians and scientists are less susceptible to fads, and that
they only appeal to uneducated non-professionals. If only that were so!
This book will show how stubbornly wrong ideas can be held, even by the
most brilliant people. It also takes time for fads to decline and disappear,
often only after the death of influential founders of schools of thought and
their disciples.
One of the earliest books on this subject was Charles Mackay’s (1841)
Extraordinary Popular Delusions and the Madness of Crowds, still in print after
over 170 years. Mackay made fun of faddish ideas, but implicitly assumed
that his readers would be immune to them. Over a century later, Martin
Gardner’s (1957) Fads and Fallacies in the Name of Science showed how science,
11
fads and fallacies in psychiatry
or at least popular science, can also be infected by fads. Most of Gardner’s
examples were fringe ideas that have died out, but a few remain current:
extrasensory perception, homeopathy and food fads.
The evolutionary theorist Richard Dawkins (1976) made a useful
contribution to the understanding of fads by introducing the term ‘meme’,
a concept later expanded by the psychologist Susan Blackmore (1999).
Dawkins and Blackmore suggested that ideas can spread through society
almost like genes, and are replicated even more rapidly. The difference, of
course, is that the mechanism is entirely social and cultural. The concept
of a meme remains controversial, but it goes some way to explaining how
false conclusions spread rapidly. In common parlance, we often speak of
ideas ‘going viral’.
To explain why people are attracted to fads, we could begin by considering
mechanisms of thought that promote incorrect conclusions. Fads gain
adherents because they seem promising, even if they are based on false
reasoning. These cognitive errors have been the subject of a large body
of research by cognitive scientists, most recently in the new discipline of
behavioural economics (Ariely, 2008; Kahneman, 2011). This is a timely
subject in a period of financial turmoil driven by misjudgements and
unjustified optimism. What research shows is that most opinions and
judgements are based on emotion, not reason, and that arguments are used
to justify conclusions already reached. This explains why it is often a waste
of time to try to change another person’s mind by arguing – whether in
politics and religion, or in scientific debate.
Thus, the most important cognitive errors derive from preconceived
beliefs. The idea that we discover the truth from reason is beloved of
philosophers, but evidence shows that people adopt a view of the world
based on intuition, not data (Haidt, 2012). Many years ago, Festinger
(1957) introduced the term cognitive dissonance to account for how people
explain away discrepancies between expectations and facts. He studied
why followers of a failed prophet became even more fanatical when their
prediction about the end of the world did not come about. Once they were
committed to a point of view, it was hard for them to admit they were
wrong or foolish. Instead, they held on to their original opinions more
strongly than ever. Strangely, scientists sometimes do the same thing. When
presented with contrary evidence, they find a way to explain why the data
prove they were right in the first place, or why contrary data cannot be relied
on because of methodological flaws. And if scientifically trained people
can sometimes be fanatical, those who are mainly trained as clinicians are
even more likely to be credulous. Physicians with strong beliefs about the
effectiveness of treatment methods can be very good at finding ways to
explain away contradictory evidence.
A general term used to describe these phenomena is confirmation bias
(Oswald & Grosjean, 2004). Once you have already made up your mind,
new information is interpreted in the light of preconceived ideas. One
might think this kind of error does not happen in research, where data, at
12
medicine
least in principle, are the final arbiter. In the words attributed to the 19thcentury biologist Thomas Huxley, ‘many a beautiful theory is killed by an
ugly fact’. Unfortunately, some scientists hold on to favourite theories with
religious fervour.
Many researchers writing scientific papers will have had the experience
of having trouble publishing results that challenge a current consensus or
paradigm. Peer review is a necessary part of science, but can sometimes
be used by experts who do not want data contradictory to their own views
to appear in print. Thus, when a submitted paper challenges a broadly
held consensus, that is, is ‘counterintuitive’, the immediate reaction of
a peer reviewer could be negative, an intuition that may be backed up
by pointing out inevitable shortcomings in research methods. Similarly,
anyone who has ever attended a scientific congress can attest to the
way that researchers hold on to favourite ideas for dear life. It has long
been observed that theories only change when old scientists die, and are
replaced by younger ones. In this way incorrect conclusions linger on
through simple inertia.
Mahoney & DeMonbreun (1977) carried out a useful empirical study of
confirmation bias in the peer review of scientific papers. They sent the same
submission to 75 expert readers, modifying only what the data showed.
The results showed that reviewers had a much more favourable opinion
of studies with results that confirmed their own theoretical views, and a
poorer opinion of those that disconfirmed them. As editor of a psychiatric
journal, I have seen peer reviewers demonstrate their scientific potency by
tearing apart papers that do not support their views (or that simply fail to
quote their own work). In another provocative study, researchers sent out
several classical high-quality research papers from years in the past under
different names (Peters & Ceci, 1982). Only a few journals recognised the
deception, and 89% of the submissions were rejected on methodological
grounds. The same process occurs in grant submissions. I have known
researchers who spend almost as much time on predicting who will be their
reviewers as in writing a proposal. If a hypothesis is too controversial, one
may be better off withholding submission.
In a widely read book, Kahneman (2011) described the nature of
cognitive biases. One of the most important is the ‘availability heuristic’.
In that scenario, error comes from depending on what comes easily to
mind, rather than on what is most probable. This type of cognitive bias
frequently afflicts clinical practice. Even the most intelligent people tend
to be impressed by a lively anecdote or a recent personal experience. But as
the witticism goes, ‘the plural of anecdote is not data’. This kind of error
is all too frequent in treatment decisions. If you have just seen a series of
patients with a particular diagnosis and have given them a certain therapy,
you may be tempted to view future patients as having the same condition
and requiring the same intervention. This is how patients get incorrect
diagnoses of depression, bipolar disorder or attention-deficit hyperactivity
disorder (ADHD), leading to incorrect forms of treatment.
13
fads and fallacies in psychiatry
The human mind is programmed to find patterns in the world (Bloom,
2004). Sometimes people see hidden faces in natural landmarks, and in
medicine any explanation tends to be better than none. When I was a young
teacher, I passed on many of these ‘just-so stories’ to my trainees. Since
I believed them myself, enthusiasm made me a popular teacher. Today,
embracing the scientific culture of doubt, I find myself telling students that
we have little idea why many patients fall ill, and often do not know what
to do for them. The price I pay is being less popular as a teacher. Colleagues
who, such as my younger self, have an answer for everything, tend to be
more attractive.
Establishing cause and effect
The simplest cognitive error concerns the nature of cause and effect. The
basic fallacy is post hoc, ergo propter hoc (‘after this, therefore because of this’).
In plain English, correlation does not prove causation. Although everyone
understands this principle, it is surprising how often it is flouted. As a
journal editor, I (and my peer reviewers) often have to remind authors to
tone down conclusions and avoid making causal inferences out of simple
associations. This happens all too often in research, and is an even more
serious problem in practice.
Let us consider one of the most common errors in medicine: attributing
change in a patient’s condition to the most recent intervention. A physician
prescribes a drug and the patient gets better. Is that not good enough?
Unfortunately, it is not. There can be many reasons for improvement. One
is spontaneous remission. Another is the natural course of disease. Still
another is a favourable change in life circumstances or the removal of a risk
factor. Physicians make this mistake because they want to believe that what
they do is of value. Patients also prefer to think in this way. If they get better
after taking a medicine, they assume cause and effect. If they get worse
after taking (or stopping) a medicine, the same assumption is made. Maybe
the drug worked, but maybe all you are seeing is a coincidence or a placebo
effect. You cannot be sure about causation unless you conduct an experiment
with proper controls. That is why clinical trials are so essential in medicine.
Physicians want to see that problems are treatable, and to stick with the
treatments they know. They like to make diagnoses that provide a basis for
such treatments. In other words, if all you have is a hammer, everything
else looks like a nail. On a broader level, problems in determining cause and
effect have led to a profound misunderstanding of the causes of illness. The
idea of a single cause for a single disease is attractive. That model has long
been based on infectious diseases, in which Koch’s postulates for identifying
an organism eventually led to the discovery of effective treatments. But even
this example is misleading, in that it fails to take into account resistance
factors that determine whether even the most virulent infections become
pathogenic. Hardly any diseases in medicine have a single cause.
14
medicine
The multifactorial nature of illness often gives physicians trouble. The
human mind is programmed to favour single causes and single effects. But
the real world is different. To take multiple factors into account, there has
been a vast change in the way research data are analysed statistically. When
I was an undergraduate, we learned to carry out t-tests and chi-squares.
Today journals may not accept papers unless the analysis is multivariate.
We need to know how much of the variance is captured by each variable in
a study. I have come to the conclusion that the world as a whole is a kind
of multiple regression. Everything has many causes, and few effects are
easily predictable.
Oversimplification of complexity affects research. When a single risk
factor is identified, whether biological or psychosocial, it can sometimes
be seen as the cause of illness. That conclusion is usually wrong. A good
example is attempts to find viral infections in patients with chronic
fatigue, which may not play any causative role in the syndrome, but
reflect contributory risks, secondary effects or incidental findings (Afari
& Buchwald, 2003). This example illustrates the tendency in medicine
to view every disorder in the light of biomedical reductionism. Disease is
not a software glitch that just needs to be tweaked. Complex interactions
between multiple risk and protective factors require complex forms of
treatment.
Fads and good intentions
Many years ago, when I was training on an in-patient ward, I suggested
to one of my teachers that since schizophrenia has a strong genetic basis,
psychotherapy for psychosis has limited therapeutic value. His reply was,
‘If I accepted your view, I would have to consider the condition hopeless’.
But my teacher’s assumption that genes strictly determine outcomes
was wrong. Even in the most severe illnesses, genes are rarely the only
determinant of outcome. Moreover, research in epigenetics describes
mechanisms by which the environment can switch genes on or off (Szyf et
al, 2009).
My teacher’s comment also made me realise how important hope is for
clinicians. He was a psychoanalyst who had spent his life treating the sickest
patients. He sincerely believed that if you had enough skill, anything was
possible. This led him to make serious mistakes, such as analysing medical
colleagues who had developed a bipolar disorder.
Ultimately, medical fads arise because practitioners have good intentions.
For reasons of training, idealism and professional pride, physicians
passionately want to help their patients. Admittedly, they often succeed,
but most are less comfortable with chronic illness than with acute disease.
Managing chronicity requires patience and an acceptance of limitations.
When I was a medical student, a painting was prominently displayed
at the entrance of the faculty building. It showed a heroic physician at the
15
fads and fallacies in psychiatry
bedside of a child, physically struggling with a skeleton representing death.
This is an image that medical graduates want to believe in. Doctors aim to
conquer disease, even as they learn that this is not the only service they
can give their patients. In a famous saying (attributed, like so many other
sayings, to Hippocrates), the role of the physician is to cure sometimes, to
treat often, but to care always.
Medicine and science
The idea that medicine should be practised on scientific principles is
relatively new. Over most of history, clinical work was more of an art than
a science. Then, in the 19th century, pathology and bacteriology developed
methods to confirm medical diagnoses. But treatment methods in medicine
were still not particularly evidence based. Practice was based on clinical
experience, or on the consensus of experts. There was no formal concept
of evidence-based medicine until the mid-20th century. Even today, it is
not possible to conduct practice entirely on the basis of empirical data. The
evidence we have is rarely conclusive, and many important questions have
never been studied.
Scientific medicine is associated with advances that have reduced the
burden of disease and increased the human lifespan. But it is still necessary
to ensure that empiricism rules. Medical journals set the standard for
what is accepted as scientific. But as empirical data became required for
deciding what valid diagnoses are and what effective treatment is, the bar
has constantly been raised. Peer review is much more critical today. Many,
if not most, articles published 25 years ago would today be rejected. We
expect larger, more representative samples, and journals have statistical
consultants to ensure that the most advanced methods of analysis have
been used. The top journals pride themselves on a high rejection rate, which
can approach 80–90%.
When I peruse medical journals of previous generations, I observe
a very different standard. Journals in the past were replete with papers
whose methods were almost entirely unscientific and unreliable. One still
sees these kinds of publications in lower-impact journals – case series
without control groups, associations reported as percentages, with few
hypotheses and no formal statistical tests. For many years, prominent
journals still published reports of single cases, from which one can conclude
almost nothing. (Case reports can sometimes be heuristic if they generate
hypotheses that stimulate systematic research, but most journals, including
the one I edit, refuse to publish them, and those that do put them in the
letters column.)
Fifty years ago the case series was one of the most common types of
articles published in journals. A physician would describe and report on a
number of patients. There would be no control group for comparison, and
no effort to show that they were in any way representative of larger clinical
16
medicine
populations. If the article proposed an association between a disease and an
aetiological factor, one had no way to determine whether the observations
were of real significance, could be explained in some other way or were
only chance findings. If the article described a new method of treatment
and claimed it was effective, it might not be replicated, since so many such
reports were based on unrepresentative samples, or actually described
placebo effects. This change has produced angst among researchers
who now have more papers rejected. But a high bar is good for medical
science.
The stakes of publishing misleading data in medical journals are
higher than they are in the basic sciences. If physics, chemistry, biology or
academic psychology produce faulty research findings, there are no direct
effects on health. But patients suffer real damage when medical researchers
get things wrong. Sometimes, as in the claim that certain vaccines cause
autism (Taylor et al, 1999), public health can be at risk. To prevent incorrect
and dangerous conclusions, peer review must assure that research methods
were properly followed and that conclusions are justified.
Even under the stringent standards of modern medical journals, papers
will be published that eventually prove to have misleading findings. In
most cases, unrepresentative samples are the problem. That may be why,
as the noted epidemiologist John Ioannidis (2005) has shown, most
research articles published in medical journals are never replicated. That
is also why the media almost always get medical science wrong. They
are looking for a story, particularly anything that looks like a dramatic
breakthrough. When a new finding comes out in a top journal, medical
reporters jump on it. However, we may not learn that, later on, the results
were not replicable. Over 20 years ago, one of my colleagues became
briefly famous for finding a gene that he claimed controlled a major
personality trait. The finding was duly written up in Time magazine, but no
one was ever able to replicate this report. Needless to say, non-replication
is not a story for the media.
For the same reason, we should be cautious about the expert consensus
that lies behind formal treatment guidelines, even the very high-quality
recommendations published by the National Institute for Health and
Care Excellence (NICE). These guidelines are more reliable than anything
produced in the USA, probably because British culture has always valued
empiricism and common sense. Even so, although NICE guidelines and
Cochrane reports represent the best we can do at any given time, they
cannot guide practice. Many become dated within a decade or so.
Feinstein (1988) once remarked: ‘the consensus of experts has been a
traditional source of all the errors that have been established throughout
medical history’. But imagine the plight of physicians of the past who had
nothing to rely on but the opinions of senior clinicians and unscientific
reports in medical journals. Let us go back in history and consider
examples of how practice, when not evidence based, went seriously astray.
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fads and fallacies in psychiatry
Medical fads in historical context
Forty-five years ago, working at a summer camp in a remote area of Canada,
and reading by kerosene lamp, I encountered a copy of William Osler’s
The Principles and Practice of Medicine. This famous textbook, first published
in 1892, eventually went into an 8th edition (Osler, 1916), and was still
an instructive read in the 1960s. Osler acknowledged how little was then
known about illness, or how to treat it. That made him ahead of his times
in many ways. He criticised the fads of his era, and did not approve of a
‘shotgun’ approach in which every symptom was treated with a separate
drug. (That kind of practice remains common today.)
Reading a book published before the First World War made me wonder
what our own textbooks would look like 50 or 100 years hence. This is
an example of how the history of medicine offers a useful perspective on
present errors. Future readers may shake their heads, wondering how
physicians of the 21st century could have so totally misunderstood and
mismanaged disease.
Physicians of the past were foolish to rely on methods such as bleeding
and purging as mainstays of therapy for so many diseases. But they lived in a
climate of opinion in which the most respected members of their profession
promoted these practices. American psychiatrists still admire Benjamin
Rush, a signee of the Declaration of Independence. But Rush advocated
bleeding and purging to the very end of his days, no doubt killing patients
along the way (Fruchtman, 2005). This was ignorance, but the failure on
the part of medicine as a whole to challenge such ideas is chilling.
In another cognitive error, called ‘groupthink’, people adjust their views
to those of peers with whom they work (Janis, 1972). It is difficult to stand
against received wisdoms without being branded a renegade. Practitioners
generally accept the consensus of their colleagues unless they are offered
alternative options.
A good example is pharmacology. Even in the past, drug treatment was
fairly aggressive, in spite of the fact that most agents available in the 19th
century were not effective. An American physician of the time, Oliver
Wendell Holmes, is believed to have once said, ‘If the entire pharmacopeia
were thrown into the ocean, it would be much better for mankind and much
worse for the fishes’. Only a few drugs from the previous century have stood
the test of time, the most prominent being digitalis and morphine. Even
today physicians may prefer to prescribe ineffective agents than to stand
around helplessly in the face of serious illness.
Once diseases are understood, therapy becomes more rational. Even
before the era of antibiotics, once the organisms causing infectious diseases
were identified, patients were less likely to receive treatment that could
make them worse. Often, once effective therapy became available, fads died
out entirely. That was the ultimate reason for the disappearance of bleeding
and purging. And most drugs of unproven value also disappeared, once
physicians had a modern pharmacopeia.
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medicine
Diagnostic fads in medicine
The most common and most intractable symptoms that patients present
with to physicians are those that are most likely to attract fads. I need not
discuss the endless number of diets that have been promoted by physicians
over the years. Food fads have never entered mainstream practice, although
some physicians have made fortunes recommending them. One could write
volumes on methods used to manage chronic insomnia, some of which also
lie beyond the boundaries of medicine. But let us narrow our focus to two of
the most frequent presentations seen in any physician’s clinic: unexplained
fatigue and unexplained chronic pain. These common but often intractable
problems are likely to elicit faddish remedies.
Chronic fatigue syndrome has been a subject of intensive research and
serious controversy for decades. A review of the current state of knowledge
(Holgate et al, 2011) found that the diagnosis remains controversial. As
defined by the Centers for Disease Control and Prevention in the USA,
chronic fatigue syndrome is characterised by persisting or relapsing fatigue
for at least 6 months, cannot be explained in other ways, and is associated
with four other symptoms from a list that includes post-exertional malaise,
impaired memory or concentration, unrefreshing sleep, muscle pain, multijoint pain without redness or swelling, tender cervical or axillary lymph
nodes, sore throat and headache (www.cdc.gov/cfs/).
Attempts to define chronic fatigue syndrome in other ways, such as by
the term ‘myalgic encephalopathy’, assume that a specific aetiology has
been found. But these claims have never been replicated. Viral infection is
not a cause of the syndrome, even if it can be a trigger. Holgate et al (2011)
concluded that post-viral fatigue ends up being chronic, either because of
psychosocial stressors or other unknown factors. Thus, chronic fatigue is
not an infectious disease, as claimed by some patient advocates who want
to legitimise their suffering, but an abnormal response to infection and
failure to recover.
No evidence-based treatment for chronic fatigue syndrome has ever been
established. This is not surprising, given that it is heterogeneous. Abbey &
Garfinkel (1991) concluded that chronic fatigue syndrome includes cases
with unknown organic causes, and others that represent depression, or
what 19th-century psychiatry called ‘neurasthenia’ (Shorter, 1993), as well
as what DSM-5 now calls ‘somatic symptom disorders’. One can compare
this fad with another one, the idea that fatigue is often due to low blood
sugar (Bennion, 1983). (Unfortunately, diagnosing hypoglycaemia, and
advising patients to take frequent doses of glucose to relieve symptoms,
has still not quite run its course.)
Another problem that physicians struggle with, chronic pain, can take
many forms. Today fibromyalgia is a common diagnosis in primary care.
This syndrome has a fairly specific definition (Chakrabarty & Zoorob,
2007): the presence of widespread pain for a period of at least 3 months,
as well as tender points at 11 out of 18 specific anatomic sites. However,
19
fads and fallacies in psychiatry
no lesions are found at the tender points, and there is no evidence of any
aetiological factor – or of any evidence-based method of treatment. Like
chronic fatigue, fibromyalgia overlaps with somatic disorders (Shorter,
1993), with the important difference that it is more widely accepted within
the medical profession. Even so, the concept remains controversial. Like
many mental disorders, it presents with symptoms but without signs, and
is not associated with biological markers or organic changes. There is a very
good chance that fibromyalgia will go down as a medical fad.
Surgical fads
In the history of medicine, surgery developed many heroic and effective
interventions for illness. But some of its procedures have been faddish. I
will focus on one that for decades was firmly in the mainstream of practice:
radical mastectomy.
The history of therapy for breast cancer is complex (Lerner, 2001).
This is a common disease that often kills. It therefore attracts powerful
treatment methods, as well as strong emotions. For over a hundred years,
the first line of treatment has been surgery. But it was never clear how
extensive these procedures should be. Because cancer spreads to lymph
nodes and beyond, many surgeons felt that one should go beyond removing
the tumour itself.
William Stewart Halsted, a prominent American professor of surgery at
Johns Hopkins University, was a pioneer in surgical technique, antisepsis
and effective anaesthesia (Nuland, 1988). Halsted developed the technique
of radical mastectomy, in which axillary lymph nodes, as well as chest
muscles, were removed. This method was still standard when I was
a medical student. But it was already becoming apparent that simple
mastectomy, accompanied by radiotherapy and/or chemotherapy could be
equally effective. Long-term follow-up studies lasting as long as 25 years
later confirmed this conclusion (Fisher & Wolmark, 2002).
Why was an ineffective and disfiguring surgical procedure popular for
so long? One factor was the prestige of Halsted, a pioneer working at one
of America’s top medical schools. In spite of his addiction to cocaine and
morphine (revealed only years after his death), Halsted (1961) convinced
the surgical community of the effectiveness of his methods by publishing
highly descriptive surgical papers. Yet if control groups had been required,
as they would be today, radical mastectomy might have never earned
support. Perhaps Halsted’s aggressive approach reflected the ‘can do’ beliefs
of American culture. If a disease is dangerous, you just had to fight harder
to beat it.
Was radical mastectomy, a mainstream treatment used for many
thousands of patients and a standard approach supported by clinical
consensus, a fad? I would say yes, because it persisted into an era when
better evidence could have been made available. In spite of poor scientific
20
medicine
support, radical mastectomy spread rapidly and became wildly popular,
but eventually disappeared. Perhaps it was the best that medicine had to
offer at the time, but Halsted’s operation could easily have been challenged
in his own time, by following up patients who received it and comparing
their outcomes with those who received less radical treatment. It was bad
judgement to stick with a procedure that was both aggressive and naively
ambitious.
One can readily find other examples of surgical fads. One is tonsillectomy
for children, considered a routine procedure for many years. As confirmed
by a Cochrane review (Burton & Glasziou, 2009), it retains only a marginal
role in practice. The concept that chronic untreated infections anywhere
in the body can lead to serious consequences also had an impact on
psychiatry, and there was even a brief fad for surgical procedures in mental
hospitals, based on the idea that psychosis is due to chronic focal infection
or autointoxication, leading to the removal of teeth and even portions of
the colon (Scull, 2005). Today, such procedures are unthinkable, and any
surgeon wanting to carry them out would lose hospital privileges.
Unfortunately, the problem of determining whether a surgical procedure
is effective or necessary is hard to resolve. Even now, surgical practice
depends much more on clinical experience than on randomised clinical
trials (Balch, 2006). It is much more difficult to carry out research on
surgical procedures than on drug treatment. But without randomised
controlled trials, accompanied by careful and extended follow-ups of
patients, one cannot be sure that any surgical method is superior to a less
invasive alternative, or is not simply a placebo.
The challenge of chronicity
Many medical fads have gone into decline, but new ones continue to appear.
The reason is that so many diseases are incurable, whereas others are
chronic and can only be palliated. Moreover, advances in acute treatment
mean that most of medical practice involves the management of chronic
illness.
When diseases are progressive but remitting, fads are likely to develop.
Multiple sclerosis provides an excellent example. Most patients get
gradually worse and the ultimate outcome is fatal. This has led to a number
of faddish treatments, most recently one that involves an untested form
of vascular surgery (Kolber et al, 2011). None of these therapies has even
been shown to affect the course of the disease. The fluctuating course of
multiple sclerosis, with sudden and surprising periods of improvement,
can fool physicians into thinking that their interventions are responsible
for changes. As we will see, many mental disorders have a similar course,
leading both patients and their physicians to explain any improvement
on the basis of the most recent intervention. This is an example of how
cognitive biases can affect medical judgement.
21
fads and fallacies in psychiatry
Patient advocacy
In the contemporary world, patient advocacy groups, working mainly
through the internet, aim to raise awareness of chronic diseases and attract
funds for research. This is a positive development, and I have been involved
with one group myself (for borderline personality disorder). We live in an
era in which patients are more actively involved in treatment decisions.
That is also a good thing. Many patients are looking up diagnoses online,
which gives them a chance to understand their illness and their treatment in
more detail. The problem is that the internet (and other forms of publicity)
allow uninformed groups of consumers and patients with a strong agenda to
‘flood’ search engines with dubious ideas, sometimes supported by instant
‘experts’ (some of whom are celebrities rather than professionals). This
is what happened recently in the case of the anti-vaccination campaign,
based on a claim by the British physician Andrew Wakefield that measles,
mumps, rubella and pertussis vaccines can cause autism (Taylor et al,
1999; Goldberg, 2010). The story became an international scandal when,
after systematic research, it became clear that no such relationship exists.
Unfortunately, several physicians became involved in this malignant fad.
Moreover, many parents refused vaccination for their children, which led to
an outbreak of several entirely preventable diseases (Flaherty, 2011). Thus,
like so many other things, advocacy can be double-edged. When conducted
with professional support, it offers help to patients and families in need.
When linked to a fad, it can do real harm.
How the pharmaceutical industry promotes fads
The pharmaceutical industry has played an important role in promoting
medical fads (Goldacre, 2013). To understand why, we need to look at the
relationship between industry and the practitioner. Ideally, they should
work in partnership; ultimately, both want to develop drugs to treat
disease, and positive results benefit patients and please physicians. In
such cases, drug companies should make a legitimate and well-deserved
profit. However, this rosy scenario is far from current reality. The main
reason is that the margin of profit for drugs has become too high. This
is why medicine, particularly academic medicine, has suffered from
being too close to industry (Angell, 2004). Pharmaceutical corporations,
which used to be small, are now large and among the most profitable
companies in the world. Although some drugs have benefited people all
over the world, ‘Big Pharma’ is reluctant to invest billions in developing
new agents, preferring to market ‘copycat’ drugs that resemble those
already available. Even if only a single atom is changed in the molecule,
a new agent can be marketed to physicians, supported by an aggressive
campaign. Industry spends large amounts of money on marketing, much
more than on research. Industry also benefits from new diagnoses that are
22
medicine
associated with drug treatment, so that their influence may also extend
into diagnosis.
The dynamic behind the relationship between the pharmaceutical
industry and physicians depends on the way new drugs make money
for companies. Older drugs, particularly when they become generic,
yield little profit. Thus, pharmaceutical representatives have the task of
convincing practitioners to adopt the latest agents. They provide physicians
with small gifts (Wazana, 2000), and recruit medical opinion leaders to
influence prescription practices (Angell, 2004). These academics may
receive ‘consultant fees’ to actively promote a product. Moreover, an army
of pharmaceutical representatives establish personal relationships with
practitioners, sometimes paying for dinners at fine restaurants.
Yet older drugs are often as good as (or better than) newer agents. Some
years ago, a large-scale study (ALLHAT Collaborative Research Group;
Akiskal et al, 2002) showed that the classical diuretic chlorthalidone is more
effective for hypertension than any of the current favourites (ACE inhibitors
or calcium channel blockers). Similarly, acetyl salicylic acid may be as
effective as any current alternative in reducing the risk for cardiovascular
disease (Gaziano et al, 2006). These findings have been published in top
medical journals, but have had little impact on practice. Physicians have an
almost irresistible attraction to ‘the latest thing’ in drug therapy.
Some authors defend a close relationship between industry and academic
medicine on the grounds that it promotes research into the development
of new drugs (Goldberg, 2010). But although effective collaborations do
occur, they are relatively rare. Some academic physicians carry out clinical
trials run by industry, which sets protocols that are most likely to support
their products (Goldacre, 2013). But industry would rather spend its money
on drug promotion than on more research. One result is that practising
physicians are constantly encouraged to embrace the latest diagnosis and
the latest treatment.
This is not to say that every new idea is wrong, but that medicine is
being practised in a climate that inevitably promotes fads. We cannot blame
industry for this problem. It is the result of our own unjustified enthusiasm.
23
Chapter 3
Psychiatry
Psychiatry could be more prone to fads than other specialties in medicine. I
do not have the data to prove whether that is true. It is possible that I only
see things this way because psychiatry is my specialty and I know the field
well. However, the perception has been shared by some noted colleagues
(Frances, 2009; Carlat, 2010), as well as by some well-informed outside
observers (Horwitz, 2002).
If psychiatry is prone to fads, why should that be the case? One
explanation is that mental illness is poorly understood. Although many
other areas of medicine are equally mysterious, disorders of the mind
carry a unique complexity and will take many decades to unravel. Another
possibility is that mental disorders are particularly hard to treat. Objectively,
this may not be so. As shown by Leucht et al (2012), effect sizes in
psychiatry derived from meta-analyses compare favourably with those in
other medical specialties. Nonetheless, not all patients do well, and there
is something unique about mental suffering. This makes mental health
practitioners keen to find remedies.
Finally, even if psychiatrists help a lot of patients, they do not have a
good understanding of how their treatments work (Healy, 2002). If the
mechanisms of mental illnesses are unknown, one cannot know either
aetiology or pathogenesis, and develop logical interventions to break causal
chains. In psychiatry, this makes the field vulnerable to people with bright
ideas. And usually you cannot prove them wrong, at least not at first.
In this light, it should not be surprising that the history of 20th-century
psychiatry was replete with theories and treatments that promised a great
deal, but did not stand up to scrutiny. Each time a diagnostic fad or a
treatment fad died out, a new one appeared. To shed light on the current
state of psychiatry, it is instructive to go back in history to see how fads
developed and disappeared.
I will illustrate this theme through examples drawn from two very
different branches of psychiatry: psychoanalysis and psychosurgery. I
will also discuss an effective treatment (electroconvulsive therapy) that
temporarily morphed into a fad.
24
psychiatry
Psychiatry 100 years ago
To understand the problems facing psychiatry in 2012, let us go back to the
year 1912. In an annual report to the Journal of Mental Science, as the British
Journal of Psychiatry was then known, an American psychiatrist, William
MacDonald (1913), described only one major area of progress. This was the
observation that new testing procedures had identified treponema pallidum
in the brains of many mental hospital patients. Now psychiatrists could more
accurately separate early-stage syphilis from ‘functional’ psychoses, a finding
that later provided a basis for specific treatment. But although this discovery
proved crucial in the age of antibiotics, it did not affect the diagnosis and
treatment of most mental disorders, whose nature remained a mystery.
Psychiatry only became independent from neurology at the end of
the 19th century, when mentally ill patients began to be systematically
segregated from general hospitals into separate asylums (Berrios & Porter,
1995). These settings, originally more humane than older hospitals, quickly
became overcrowded and dysfunctional.
Many practitioners hoped that mental disorders could eventually be
understood as diseases affecting the brain (Shorter, 1997; Wallace & Gach,
2008). Yet research failed to demonstrate biomarkers or lesions specific to
any existing diagnosis. At the beginning of the 20th century, any unbiased
observer would have had to conclude that psychiatry fell outside the
mainstream of modern medicine. William Osler’s (1916) The Principles
and Practice of Medicine included a short chapter on mental illness, mainly
to say how little was known. Therapeutics also suffered from ignorance.
While blood-letting was dying out, Osler still had to campaign against it.
Meanwhile, treatment methods in psychiatry were primitive and mostly
consisted of sedation.
To be fair, although medicine was ahead of psychiatry in its theoretical
understanding of disease, outside of surgical procedures, its practice
was not consistently effective. Yet the 19th century was a time when the
science of medicine was making dramatic progress. By Osler’s time, the
understanding of disease was moving briskly forward. The great advances of
the 20th century would be based on this research. Medicine in 1912 could
take advantage of X-rays, bacteriological culture, and a few biochemical
tests. But since no major mental disorder was associated with biomarkers,
psychiatry could not make use of any of these tools. It was forced to rely on
a tradition of ‘phenomenology’, that is the detailed description of clinical
symptoms (Jaspers, 1913). Like their neurological colleagues, psychiatrists
were better at description than treatment.
At that time, psychiatry was being practised in mental hospitals, built
outside large cities. Patients could spend years on these wards, sometimes
living out their entire life there. Then as now, the main reason for admission
was psychosis. But the classification of severe mental disorders was
confused and undeveloped. Emil Kraepelin (1856–1926) hoped to improve
25
fads and fallacies in psychiatry
diagnosis through systematic clinical observation and follow-up. Then
the world’s leading psychiatrist, Kraepelin wrote standard textbooks that
promoted this perspective. But given the tools at hand, he could only make
limited progress.
In the 19th century, pathologists had learned how to slice and stain
tissues to examine them under the microscope. This method proved
crucial to the understanding of many diseases. But histopathology
failed to account for the aetiology or pathogenesis of mental illness
(Wallace & Gach, 2008). (In those cases where it could, as in syphilis,
the disease moved to another specialty.) Pathologists failed to find any
consistent pattern of lesions or cellular changes in the brain, similar to
those identified in other organs of the body. And whereas psychosis was
understood to be hereditary, too little was known about genetics to be of
practical value. Imaging, confined to skull X-rays, also added little to the
understanding of psychopathology.
In summary, the psychiatry of 1912 lagged behind the mainstream of
medicine. We can feel sorry about the ignorance of our predecessors in
that long-ago time. Yet even today, we still do not know what causes most
forms of mental illness, and cannot identify cellular, genetic or imaging
findings specific to any diagnosis.
Then as now, treatment of psychoses was mainly biological. But the
best drugs available in 1912 were strong sedatives: bromides, chloral
hydrate, and paraldehyde (Shorter, 2009). The introduction of barbiturates
did not add greatly to this armamentarium. All these agents calmed
patients down, but had no direct effect on psychotic symptoms. Thus,
practice was characterised by an acceptance of chronicity and a degree of
therapeutic nihilism. It had little to offer to severely ill patients, other than
institutionalisation while awaiting remission.
Sigmund Freud was the other world-famous psychiatrist in 1912.
(Freud was trained in neurology, but distinctions between these specialties
were not yet defined.) Psychoanalytic theories were treated with cautious
interest by physicians, and even earned a page in Osler’s (1916) textbook
of medicine. Freud (1916) never claimed to have a treatment for psychosis.
His clientele and his interests belonged to another tradition, dating back to
neurological practice conducted in offices. A clinical picture of ‘neurosis’,
namely symptoms that are troubling but not disabling, characterised the
niche for psychoanalysis.
Neurotic patients, if they had the money, paid for private treatment. But
office practice, isolated from the feedback provided by academic institutions
and critical colleagues, was a place where fads could thrive. Since the time
of the Austrian physician Franz Anton Mesmer (1734–1815), charismatic
clinicians have promoted all kinds of therapies for neurotic problems,
including hypnosis, ‘rest cures’ or the harnessing of willpower (Ellenberger,
1970). Freud thought he had something better. But he turned out to be
wrong.
26
psychiatry
Psychoanalysis as a fad
Psychoanalysis was an archetypal treatment fad. Based on an all-embracing
theory of human psychology, it made great claims as a therapeutic method
(Hale, 1971). Developed by a charismatic leader, it was a movement that
attracted followers who actively promoted it to mental health clinicians and
to the educated public. After a period of initial resistance, psychoanalysis
became powerful and influential, forming part of the intellectual climate of
modernity. Since psychoanalysis had implications for the humanities, Freud
was also attractive to intellectuals.
In psychiatry, psychoanalysis had its greatest success in the USA (Hale,
1995), which might be explained by culture. Americans like to change the
world, have a ‘can do’ culture, and may be more readily attracted to fads
than nations who rely on a strong tradition of pragmatism. After several
decades, the analytic movement reached a position of great influence in
academic psychiatry in the USA.
Since early psychoanalytic theories were often fantastical, many leading
psychiatrists rejected Freud’s ideas. Emil Kraepelin (1921, p. 250) wrote:
‘Here we meet everywhere the characteristic fundamental feature of the
Freudian method of investigation, the representation of arbitrary assumptions
and conjectures as assumed facts, which are used without hesitation for the
building up of always new castles in the air, ever towering higher, and the
tendency to generalisations beyond measure from single observations. I must
finally confess that with the best will I am not able to follow the trains of
thought of this “metapsychiatry”, which, like a complex, sucks up the sober
method of clinical observation. As I am accustomed to walk on the sure
foundation of direct experience, my Philistine conscience of natural science
stumbles at every step on objections, considerations, and doubts, over which
the lightly soaring power of imagination of Freud’s disciples carries them
without difficulty.’
This was a prescient critique. Psychoanalysis declined when its theories
failed to fit into mainstream psychology, which demanded psychometric
precision. It also declined when it became obvious that its treatment
methods were both inefficient and ineffective. By the late 1970s and
1980s, analysis had fallen out of favour, to be replaced by a new psychiatry
based on reliable diagnosis, as well as research in neuroscience and
psychopharmacology.
The question is, why psychoanalysis ever gained so much influence?
I have written a book about this subject (Paris, 2005), and interested
readers will find the details of this complex story there. But one of the more
interesting reasons lay in the intellectual appeal of psychoanalysis. Like
Karl Marx, Freud suggested that behind the appearance of phenomena lay a
hidden reality that only the initiated could comprehend. The impenetrability
of analytic theories and methods, like a mystery that required initiation,
was part of its attraction. Arcane procedures – a couch, a silent analyst,
and a high frequency of sessions lasting for years – gave it the aura of a
27
fads and fallacies in psychiatry
religion. Psychoanalysis also created intense public fascination, almost
from the beginning; in part, because so much of it was about sex. Finally,
psychoanalysis, like Marxism, offered a comprehensive world view that
addressed modern alienation. This was a time when organised religion
had fallen into decline. For those who adhered to the movement, it was a
community of believers and a source of hope for the future.
Freud has to be understood in the context of his times. Although
psychoanalysis was based on unproven theoretical assumptions, and
offered treatment methods that were never tested, such problems were not
unusual. The medicine of 100 years ago was far from evidence based. Even
50 years ago, when I was a student, the authority of professors, relying on
clinical experience and personal charisma, took precedence over systematic
investigation.
One of the most faddish aspects of the analytic movement was the
way it explained its failures. Unsuccessful therapy was attributed to the
resistance of the patient, and/or not carrying out treatment properly or
long enough. These are typical features of quack medicine – failures do not
lead to questioning of one’s methods, but prove one was right all along. It
is a classical example of cognitive dissonance and confirmation bias. One is
reminded of Festinger’s observations on what people do when they prepare
for the end of the world, and when the world refuses to end.
The period of hegemony of psychoanalysis in American psychiatry was
1945–1975 (Hale, 1995). I trained in psychiatry towards the end of that
era, and this experience gave me a bird’s-eye view of those salad days.
Many academic chairs had training in psychoanalysis, even if few practised
it. Freudians had clever strategies for creating and maintaining adherence.
Analysts are trained in a way to maximise belief. In addition to course
work and to supervised cases, they have to undergo their own treatment,
usually for 5 years. Once you make that kind of commitment, it is very
difficult to admit that you have wasted years of your life. It is difficult to
turn against a training analyst who has devoted years to your personal
care. It is also difficult to give up strongly held beliefs, and if you disagreed
with the theory, you might be accused of being insufficiently analysed.
These methods parallel those used by religious and political movements
throughout history.
Yet in spite of attempts at brainwashing, some psychoanalysts rebelled
and rejected the movement. Many of the leaders of neo-Kraepelinian
psychiatry (such as Robert Spitzer, the editor of DSM-III), and the
developers of alternative psychotherapies (such as Aaron Beck, the creator
of CBT) were former analysts. They kept the best part of Freud (listening
to people attentively) and dropped the worst part (unproven theories and
methods).
I work in a department where a few psychoanalysts still practise, most of
whom are now well into middle age. Few young psychiatrists are interested
in analytic training these days. Yet many of my students, in spite of the
stronger scientific education now provided in medical school, are still
28
psychiatry
fascinated with psychoanalytic ideas. They want to understand the human
mind in ways biological psychiatry does not address. Moreover, analytic
teachers spend more time with students, and show more personal interest
than other faculty members.
It was much the same in my time. Like many of my contemporaries, I spent
a couple of years lying on an analytic couch. But I was a fellow traveller, not
a party member. I did not make a clean break with psychoanalysis until later,
when I came to question one of its basic paradigms: that adult problems are
rooted in childhood experiences. I had seen too many patients who were
troubled in spite of a normal childhood, and too many who felt well in spite
of a terrible childhood. I began to read developmental psychopathology, and
was deeply influenced by the work of the British child psychiatrist Michael
Rutter, who saw development as complex and responsive to a multitude
of vulnerabilities and life events (Rutter & Rutter, 1993). I wrote a book
on why the theory of childhood determinism is mistaken (Paris, 2000),
and another on the relationship between psychoanalysis and academic
psychiatry (Paris, 2005). Even so, it was difficult to give up concepts that
had guided my work for so long, and that seemed to explain so much.
When you write a critique of Freud and his system, editors often assign
the book review to a psychoanalyst, virtually guaranteeing a negative
response. This happened to me when Jeremy Holmes (2005) reviewed
my book for the British Journal of Psychiatry, and suggested I sounded like
someone who had emerged from a cult. But psychoanalysis was a cult. It
offered a quasi-religious faith that provides an explanation of the human
condition, and a cure for the angst of modernity. These great expectations
could only invite disappointment. Moreover, an expensive and unproven
treatment that goes on for years on end cannot survive in the current
climate.
I have to ask myself why I took psychoanalysis so seriously when I was
young. Although my teachers considered me to be a rebel, I still thought
they were older and wiser than me. It was rather like growing up in a
religious family. Even if I never became a psychoanalyst, I was surrounded
by a powerful climate of opinion supporting these ideas. In short, I fell
victim to a fad, and it took years to see the world differently. But I use
this word with caution, because psychoanalysis did, after all, survive
almost a century. One reason why psychoanalysis lasted for so long was
that there were few alternatives. When I was a student, even if one was
ambivalent about Freud, if one was interested in talking to patients at all,
the only alternative was behaviour therapy. But that approach, at least in its
original form, was intellectually sterile. Behaviourists essentially denied the
existence of the mind, dooming their discipline. It later went into a steep
decline of its own, and was eventually absorbed into CBT. Moreover, once
psychiatrists had effective drugs for mental illness, psychopharmacology
and neuroscience became the exciting leading edge of the discipline.
Although later versions of psychoanalysis generated some new ideas,
most were little better than Freud’s own speculations, and disappeared with
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fads and fallacies in psychiatry
their originators. The most lasting offshoot has been attachment theory,
developed by John Bowlby (1980), a psychiatrist at the Tavistock Clinic in
London. This model of human development, unlike Freud’s, was linked to
academic psychology and empirical research, and attracted a large research
literature (Cassidy & Shaver, 2008). Attachment theory is an admirable
model in many ways, although it often fails to consider interactions
between genes and environment.
Today psychoanalysis is rarely practised, and the only evidence-based
method that it has produced is brief dynamic therapy (Leichsenring et al,
2004), which is not at all the same. As a treatment, classical psychoanalysis
survives today only as a remnant: in enclaves such as the Tavistock and
Menninger clinics (the latter in Houston, USA), and in a few private practice
settings in other large cities.
The decline of traditional psychoanalysis is instructive for another
reason. Psychiatry had to reject Freud unless it was willing to be treated
with contempt by other specialties in medicine, most of whose practitioners
viewed psychoanalysis with dismay. The specialty therefore returned to its
biological and phenomenological roots, adopting a model that has been
called ‘neo-Kraepelinian’ (Klerman, 1986).
Even so, psychoanalysis left a legacy – the importance of empathic
listening. Almost all therapies have made use of this principle. It is no
accident that evidence-based psychotherapies, such as CBT, were developed
by clinicians originally trained as psychoanalysts. Unfortunately, listening
threatens to become a forgotten skill for psychiatrists today.
Biological fads: frontal lobotomy
Let us now move into a completely different world: the application of
psychosurgery to the treatment of refractory psychosis. While one can
hardly compare neurosurgery to asking patients to lie on a couch, some of
the reasons why the fad was adopted, and later rejected, mirror the story
of psychoanalysis.
Egas Moniz (1874–1955), a Portuguese neurologist, is one of the few
physicians involved in the treatment of mental disorders to have won a
Nobel Prize. But the method he promoted, frontal lobotomy, turned out
to be a fad that has since been discredited. Valenstein (1986) documented
this story in detail, and the title of his book, Great and Desperate Cures,
nicely summarises the climate that made lobotomy possible. Later books
(Pressman, 1998; El-Hai, 2007) offer very similar conclusions.
In the 1950s, large numbers of patients with psychosis could only
be managed by confinement to mental hospitals, often for years. This
desperate situation attracted desperate remedies, and almost anything
seemed worth trying. Walter Freeman, an American physician with great
ambitions but weak scientific training, toured the country demonstrating
a method of frontal lobotomy that could be carried out by psychiatrists
30
psychiatry
(El-Hai, 2007). He would operate with an ice-pick, using a transorbital
technique that did not require conventional anaesthesia. Freeman met
plenty of opposition, but claimed good results and gained adherents. Since
lobotomy was offered to patients whose condition was otherwise hopeless,
the surgery became widely used; even the hospitalised sister of President
John F. Kennedy underwent this procedure.
How did psychiatrists, or at least many of them, become convinced
that lobotomy was an effective treatment for psychosis? The lesson lies,
once again, in the absence of scientific procedures that have now become
standard. At that time, one could publish an article in a prominent medical
journal consisting of a ‘case series’, describing a small number of patients
with a given condition who seemed to get better with treatment. This way
of reporting clinical experiences led generations of surgeons to carry out
interventions that later proved quite unnecessary. Even today, surgical
procedures are supported by fewer clinical trials than drugs, which require
approval by government agencies, whereas the responsibility for regulating
surgical treatments lies with hospital physicians themselves. The lesson
is that medical enthusiasm, even under desperate circumstances, needs
to be curbed. Frontal lobotomy never underwent clinical trials. But if
psychiatrists had responded to Freeman’s claims with the now common
retort, ‘show me your data’, it would never have become a fad.
It is interesting to compare this story with another that developed at the
same time: the use of insulin coma to treat psychosis. That intervention
was widespread in the 1940s and 1950s, and I saw it used when I was a
medical student a decade later. Patients were given enough insulin to be
unconscious, and then woken up with intravenous glucose. The procedure
was far from simple, and required intensive nursing to be safe. Then, in
a paper published in The Lancet, Ackner et al (1957) showed that insulin
therapy had no sustained effect whatsoever on schizophrenia. Insulin coma
was little but a very expensive placebo. Once psychiatrists had antipsychotic
drugs, insulin coma disappeared completely. This was also the main reason
for the disappearance of frontal lobotomy.
How a good treatment can become a fad
Electroconvulsive therapy (ECT) had been developed in the 1930s to treat
psychosis, but was more effective for depression, for which it became the
primary treatment in the 1940s and 1950s. It is still used today, mainly for
severe depression or melancholia, in which it can be dramatically effective,
but it can also be used for some cases of schizophrenia and bipolar disorder,
and has advantages over drugs in safety for the treatment of depression
among the elderly (Fink, 1999). In some ways, ECT is an ‘anti-fad,’ in that
it is much more effective than most psychiatrists realise. They have been
seduced by the romance of psychopharmacology to favour treatments that
are designed to alter brain chemistry. We still have little idea why ECT works.
31
fads and fallacies in psychiatry
Electroconvulsive therapy became popular when there were no effective
drugs for depression. Once tricyclic antidepressants were introduced, ECT
was less frequently prescribed. However, when it was the only option, ECT
had been used indiscriminately and in the 1950s, patients with depressive
symptoms of any kind might receive this treatment (Shorter, 2009). Thus
ECT was not a fad, but a good treatment that could be used faddishly. This
is also a common problem in psychopharmacology, where good drugs can
be made bad through overuse. Part of the story of psychiatric fads is that
whenever a treatment is effective for some patients, clinicians want to try it
on everyone. Today antipsychotics are being prescribed for a wide range of
patients who are not in the least psychotic, in the hope of benefit, practices
that are not evidence based (Maher et al, 2011).
Electroconvulsive therapy works dramatically when given to patients
who really need it. As a psychiatric trainee, I was deeply impressed with its
effectiveness. Patients who barely spoke a word due to severe depression or
catatonia would ‘come out of it’, sometimes after the very first treatment.
I began to think this was psychiatry’s penicillin. Today, as ECT has been
largely replaced by antidepressants as first-line treatment, it is more likely
to be used when drugs fail. And it continues to suffer from a stigma among
those who fear what psychiatrists can do to the mind.
Electroconvulsive therapy was at the center of a very serious scandal
at my own medical faculty (McGill University in Montreal). McGill is one
of the leading medical schools in Canada, where physicians from William
Osler to Wilder Penfield made their reputation. Some 40 years after the
event, the media was still coming around to ask how such terrible things
could have happened. Several books have been written about the story, but
the best is In the Sleep Room by Anne Collins (2002), which places the scandal
in historical perspective. Collins showed that when few effective treatment
options are available, as was the case before the development of effective
drugs, fads are more likely to take hold.
The man behind this story was D. Ewen Cameron (1901–1967), a
Scottish–American physician who founded the McGill Department of
Psychiatry in 1943. Cameron became one of the world’s most eminent
specialists, serving as President of the American Psychiatric Association
and a founder of the World Psychiatric Association. He was an ambitious
man who wanted to make his mark on his field, aspiring to a Nobel Prize
in medicine.
In the 1950s, Cameron began to treat patients with a method he called
‘de-patterning’. This involved giving massive doses of ECT (up to 100
treatments). Cameron’s idea was to turn a side-effect of ECT (memory loss)
into a therapeutic effect. He thought that doing so could remove memories
and close down dysfunctional brain circuits, to be replaced by new and
healthier patterns of thought and behaviour, created by ‘psychic driving’, a
procedure in which patients were exposed to hours of recorded messages.
Cameron’s therapy was bizarre and unscientific, even by the standards
of his time. At the first World Psychiatric Association meeting in Canada
32
psychiatry
in 1961, visitors were already criticising the ‘Montreal horrors’. Actually,
de-patterning has never been shown to have any long-term effect on the
course of the patients’ lives and illness, other than wasting time and
failing to provide effective therapy (Schwartzman & Termansen, 1967).
But following Cameron’s ‘mad scientist’ procedures, numerous lawsuits
against the hospital were filed, leading to large payouts for compensation.
The story took a more bizarre twist in 1977, 10 years after Cameron’s
death, when it was revealed that some of the funds for the project had been
provided by the Central Intelligence Agency (CIA). Naturally, the media
loved this angle. The American government of the time was concerned
about the possibility that captured soldiers might be ‘brainwashed’ into
revealing secrets, and it was claimed that this had happened to prisoners of
war in Korea. (A fictional treatment of that scenario gained currency in the
film The Manchurian Candidate (1962) by John Frankenheimer and starring
Frank Sinatra.) But since de-patterning did not actually do anything, it
would have been of no use to spies. Nonetheless, the story was kept alive
for decades by litigation, and the media ate up the CIA connection.
When psychiatrists had little to offer many of their patients, depatterning, like frontal lobotomy, proposed a radical cure that aroused
huge expectations. Even in the context of the time, none of this would
have happened if proper scientific procedures had been carried out. After
the Second World War, randomised controlled trials were already being
conducted on medical treatments. But Cameron would confront his critics
by asking ‘Are you saying I don’t know how to do research?’. Actually,
Cameron had no idea how to do proper scientific work. But neither did most
of his colleagues. And he was too powerful to be effectively challenged. The
psychopharmacology pioneer Heinz Lehmann, one of my great teachers,
kept out of Cameron’s way by working at a mental hospital several miles
away.
One of the lessons of this story is the abuse of power. Because Cameron
was a master of medical politics and a psychiatric superstar, he was able
to promote a malignant fad. A final irony is that Cameron, like most of his
contemporaries, believed in the environmental causation of mental illness,
but proposed an aggressive biological intervention to remove maladaptive
behavioural patterns, and replace them with new ones.
Another lesson of the story is the danger of impatience. Cameron
wanted to solve the most serious problems of psychiatry, and do so
rapidly. Ironically, the development of effective psychopharmacology
made his efforts at least partly redundant. Today, drugs, evidence-based
psychotherapies and rehabilitation programmes have greatly improved the
prognosis of even the most serious mental disorders.
Just as other medical fads, de-patterning ended in failure. Cameron’s
hubris met its nemesis, and he himself gave up on the procedure. He left
McGill, and returned to the USA in 1963, where he died 4 years later from
a heart attack. With poetic justice, Cameron collapsed while climbing a
mountain that was higher than he could manage.
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fads and fallacies in psychiatry
Even today, this story continues to be used as a stick to beat psychiatry.
If only we could say we have grown out of falling for simple and dangerous
answers to the problems of mental illness. Unfortunately, we have not.
Past and present fads in psychiatry
Fads continue to afflict contemporary psychiatry. This book discusses
some of them. There are problems affecting aetiology, epidemiology,
diagnosis and prevention. But the most important fads continue to lie
in treatment. Psychiatrists are reluctant to admit that their therapeutic
methods, although sometimes successful, leave much to be desired. We
need to carry out more sophisticated clinical trials of existing treatment
methods. But to find more consistent therapies, we will need to understand
the causes of mental illness.
Psychiatric expertise may not be necessary to treat mild disorders in
which symptoms improve naturalistically over a reasonably short time.
These patients can be sent to other professionals, or followed with watchful
waiting. Another important element in ensuring that these individuals
are treated effectively is the availability of a multidisciplinary team (Paris,
2008a). Yet a specialist is usually required to manage complex and chronic
problems, such as severe depression, bipolar disorder, schizophrenia, eating
disorders, severe personality disorders, and severe substance misuse. These
are the conditions psychiatrists spend most time on today. But to provide
effective treatment for these illnesses, we need much more research.
Unfortunately, treatment research in psychiatry does not always address
the chronicity and relapsing pattern of many mental illnesses. Clinical trials
of drugs are often conducted in a time frame of weeks, not the months or
years required to find out how well they work. Moreover, patients selected
for clinical trials are often atypical and unrepresentative of the populations
psychiatrists are asked to treat. The same problems arise in psychotherapy
research, almost all of which concerns patients with less severe problems
treated for short periods of time. There is, however, an evidence base for
some more lengthy interventions, such as rehabilitation for psychiatric
patients (Pratt et al, 2006).
The reason why research that follows sicker patients for longer periods
is rare is fairly obvious – money. But we should not fool ourselves into
believing that either our drugs or our psychological interventions can be
applied to the real-world and highly complex problems we face every day.
When a new treatment, either the latest drug on the market or the latest
brand of talking therapy, is developed, we should assess it cautiously and
not jump on a bandwagon. Without that degree of caution, we will end
up being just as wrong as Sigmund Freud, Walter Freeman, or D. Ewen
Cameron.
34
Part II. Effects
Chapter 4
Aetiology
Psychiatrists may not like to admit it, but they do not always understand
why their patients are sick. Actually, this problem is not unusual in medicine
at large. Knowledge about the aetiology of disease, especially of chronic
diseases, often lags behind treatment efficacy. Yet although psychiatrists
spend much of their time managing patients with poorly understood
illnesses, they still manage to help most patients who come their way. In
some respects they are ahead of neurologists, who are sometimes seen as
better at pinpointing lesions than doing something about them.
Even so, human nature being what it is, it is difficult to remain in a state
of doubt. Even though fast responses often lead to wrong conclusions,
our minds are programmed for closure (Kahnemann, 2011). Faced with
suffering patients who can be desperate for help, physicians usually prefer
confidence to uncertainty. This cognitive bias encourages pretensions to
unrealistic and unreachable knowledge. We hold on to the illusion that
we already understand the causes of mental illness, even when research is
limited or absent.
Biological reductionism
The more a theory tries to explain everything, the more likely it is to be
wrong. Psychoanalysis was a good example. It had an answer for everything,
but accounted for nothing. Biological psychiatry has done much better,
yet many of its ideas are oversimplistic and fallacious. This is due to the
nature of the relationship between mind and brain. The scientific strategy of
reductionism refers to a process in which complex phenomena are explained
by mechanisms operating at a simpler level (Gold, 2009). Cutting things into
component parts has been an essential and productive method in science and
reductionism has been particularly successful in medicine. Little progress was
made by past practitioners who did not understand how the human body was
structured. While physicians are still taught to think of patients as a whole,
research at the level of organs, tissues and cells is responsible for most of the
progress in medicine over the past century.
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fads and fallacies in psychiatry
However, reductionistic strategies have limitations. Today, with DNA in
mind, many researchers focus on genetic mechanisms that have a link to
abnormal chemistry. However, aberrant molecules account for only a few
rare diseases in medicine. Research finds that most genes account for a very
small percentage of outcome variance, in all but a few classical Mendelian
conditions (Uher & Rutter, 2012). Most illnesses cannot be reduced to
simple biochemical pathways.
The brain is the most complex structure known to science. We are not
looking at an organ such as the liver in which most cells do much the same
thing. Instead, the brain has billions of neurons and trillions of connections,
each of which can be functionally unique. Some psychiatrists (Zorumski
& Rubin, 2011) have suggested that research on neural circuits could help
to solve some of the most important problems in understanding mental
disorders. But that is not a project for a decade, it is a project for a century.
The crucial problem with the reductionistic strategy is that complex
structures have emergent properties that cannot be explained by their
components (Kendler, 2005; Gold, 2009). In other words, the whole is more
than the sum of its parts. That is why medicine is not a branch of chemistry.
Even in the basic sciences, one would not attempt to explain biological or
physical phenomena on the level of quarks or quanta (Kirmayer & Gold,
2011). In psychiatry, researchers need to study thought, emotion and
behaviour at a mental level. Thus, even though the mind is illuminated
by neurochemistry, it cannot be reduced to molecules. Reductionism
remains useful, but we need to put this strategy in perspective. Psychiatry
must study the mind and its disorders at every level, from molecules to
social networks. Unfortunately, it is rare to find practising psychiatrists or
researchers who are knowledgeable enough, or sophisticated enough, to
think this way.
Fallacies in research on neurotransmitters
Neurochemistry aims to explain mental processes and symptoms on a
molecular level. Neurotransmitters are chemical messengers that operate
throughout the brain, and the most important are amino acids (glutamate,
gamma-amino butyric acid (GABA), monoamines (serotonin, dopamine,
norepinephrine), other small molecules (acetylcholine, nitric oxide), and
neuropeptides. Glutamate and GABA mediate transmission at the vast
majority of synapses, but since monoamines modulate activity throughout
the brain psychiatric research has focused on them.
Psychiatric drugs have striking effects on monoamines. Antipsychotics
block dopamine, and antidepressants block the reuptake of serotonin. These
observations have sometimes been used to support aetiological theories.
One is that schizophrenia is caused by abnormal dopamine transmission.
The hypothesis remains controversial, and even if it tells part of the story,
it is almost certainly oversimplistic (Howes et al, 2012). Another is that
38
aetiology
depression is caused by underactivity (or imbalance) of serotonin or
norepinephrine. That hypothesis has even less evidence to support it, and
no one has ever demonstrated monoamine imbalances in patients who have
depression (Moncrieff, 2008).
It is difficult to generalise from mechanisms of drug actions to causes
of disease. For example, acetyl salicylic acid (ASA) is known to block
prostaglandins, but these molecules are not responsible for the symptoms
relieved by ASA. In the same way, although antipsychotics block dopamine,
it does not follow that patients with schizophrenia must have abnormal
dopamine receptors. Although most antidepressants are agonists for
monoamines, no evidence has yet shown that patients with depression have
an imbalance of these transmitters.
Even so, the theory of chemical imbalances has had an almost irresistible
appeal to clinicians. One reason is that neurochemical theories seem
to make the practice of psychiatry more ‘scientific’. On the basis of this
model, practitioners sometimes adjust medication at every visit, rather like
balancing electrolytes in patients on intravenous infusions. Many patients
love the theory, since it makes them victims of chemistry, rather than of bad
life choices that have made them unhappy. Certainly, neurotransmitters do
play a crucial role in many mental disorders. But they are only one link in
a complex chain. Explaining complex phenomena in a simple way tends to
be fallacious. Moreover, the concept of chemical imbalances has been the
basis of major treatment fads, in which antidepressants and antipsychotics
are used to manage abnormal mental states of all kinds. It would be better
if psychiatrists were willing to acknowledge that although their drugs can
be effective, no one really knows how they work.
Fallacies in research on psychiatric genetics
The discovery of DNA, the unravelling of the genetic code, and the Human
Genome Project are among the greatest triumphs in the history of science.
In medicine, great hopes are held for genetics as a way to understand the
causes of disease. Yet progress has been unimpressive thus far. Even in
conditions such as cystic fibrosis, where major genes have been identified,
genetic research has not led to more effective treatment. And for most
illnesses, heritability is only one factor in a complex and interactive set of
risks.
The excitement over DNA has led to a certain naivete about what it
would take to apply genetics to understanding disease. Disappointment
with genetic research has occurred for many diseases in medicine. In
conditions that are strictly Mendelian (such as Tay–Sachs disease), it is
possible to prevent disease by educating carriers. But little progress has
been made in the complex diseases that arise in adulthood. The methods
of genetic association, genetic linkage and genome-wide association are all
promising, but they have not come up with the goods. By and large, they
39
fads and fallacies in psychiatry
yield findings that are non-specific to any illness, and that only explain a
small percentage of outcome variance. One reason is that a large number
of alleles, each with weak effects, influence the risk for mental disorders.
Another derives from the strong environmental influences on every chronic
illness in medicine.
Today, there is more disillusionment than promise about medical
genetics. A standard joke is that no matter how many corners we turn,
breakthroughs are always ‘just around the corner’. That is what happens
when enthusiasm raises unrealistically high hopes. As we will see, this is
a story that can be told about every faddish development in the history of
psychiatry. Although genetic research may still bear fruit, we might have to
wait decades for results that can make a clinical difference.
Scientists have also come to realise that DNA is a code, not a blueprint.
Genetic effects ‘bend the twig’ but do not determine the shape of the tree.
That is the logic behind research on gene–environment interactions (Rutter,
2009). In most diseases, neither genetic nor environmental risks are
sufficient by themselves to be considered aetiological. It is the interaction
between them that is crucial. Yet these relationships remain controversial,
mainly because gene–environment interactions also account for only a small
percentage of variance in outcome.
The latest wrinkle in the story is epigenetics. Gene expression is mediated
by chemical tags (methyl groups and histones) that surround molecules of
DNA. Environmental stressors influence methylation, producing changes
in gene activation that can be passed down to the next generation (Szyf et
al, 2009). This is a fascinating line of research, but its clinical application
remains uncertain. Today high hopes have been raised for epigenetics, as
they have been for so many previous methods. Only time will tell whether
understanding the control of gene expression will provide the breakthrough
psychiatrists have been waiting for.
Fallacies of childhood adversity
While neuroscience currently dominates psychiatric thinking, psychological
theories have had more influence on mental health clinicians who practise
psychotherapy. The idea that adult symptoms are the outcome of early
childhood experiences was central for psychoanalysis, and is still very much
around. This theory is not a complete fallacy, but a half-truth or quartertruth.
On the one hand, a large body of literature demonstrates that childhood
adversity is a risk factor for a range of mental disorders (Rutter &
Rutter, 1993). It is indeed better to have a happy childhood than an
unhappy one. It is also true that child abuse carries a real risk for adult
psychopathology. At the same time, an equally large body of literature
demonstrates that resilience to adversity is ubiquitous (Paris, 2000). Thus,
although psychological risk factors lower thresholds, they do not lead to
40
aetiology
predictable pathological outcomes. People with severe adversities, such as
dysfunctional or abusive families, may have no mental problems as adults.
Conversely, many patients who have experienced no significant adversities
as children may still develop mental disorders.
It makes sense for resilience to be the rule in development. Human life is
replete with trauma and loss. If people were as vulnerable as some psycho­
logical theories suggest, our species would have long since gone extinct.
A psychotherapist who sees only a few hundred patients in a lifetime
may get a different impression. All patients have stories to tell, and many
of them are poignant. It is easy to make links between the past and the
present. Early in my career, I became quite adept at that game, making
facile ‘formulations’ attributing current symptoms to childhood problems.
Experience with many thousands of consultations, supported by research
on resilience, led me to a different conclusion. Once I dropped my cognitive
bias in favour of making links between childhood and adulthood, it became
clear that the connection was weak. This is certainly the case for the longterm effects of childhood sexual abuse, an adversity that has been the focus
of so many research studies (Fergusson & Mullen, 1999). It is true that a
significant minority of individuals are affected by these experiences into
adulthood, but it is equally true that a majority rise above them. That is
the difference between a risk factor and a cause of disorder.
The inconsistent relationship between past and present supports
the need for a broader model. Some people are more vulnerable by
temperament to adversity, whereas others are less vulnerable. This has been
best demonstrated by behavioural genetic research in twin samples. Almost
all mental disorders are heritable, in the range of about 0.40 of outcome
variance (Plomin et al, 2000). But the heritable portion constitutes a risk
factor, not a cause, and the other half of the variance is environmentally
determined. However, the role of the environment in mental disorder is not
accounted for by factors shared by siblings in the same family, but is unique
to individuals, in part reflecting the influence of peer groups and schools.
The results of behaviour genetic studies provide some of the most
important findings in the history of psychology. First, they disprove the idea
that personality and mental illness are directly determined by experiences
in the family. Second, they suggest that the risk for mental illness can be
influenced by social factors – or by sheer luck.
These principles help to explain the somewhat unpredictable effects
of trauma. Adverse events, even if highly traumatic, do not usually lead
to post-traumatic stress disorder (PTSD) or to any mental disorder at
all. Post-traumatic stress disorder emerges from an interaction between
exposure to stressors and vulnerability: high-trait neuroticism, leading to
more intense emotional reactions (McFarlane, 1989; Breslau et al, 1991).
This important finding remains largely unknown to psychotherapists, who
can sometimes be all too quick to attribute a wide range of symptoms to
traumatic experiences and to diagnose patients with PTSD.
41
fads and fallacies in psychiatry
This is a good example of a cognitive error (post hoc, ergo propter hoc).
Psychotherapists listen to and sympathise with patients’ life histories, but
must keep in mind that adverse life events do not cause mental disorders.
This idea remains popular because it is simple, and because, like chemical
imbalances, it places blame outside the patient.
Fallacies of child abuse
We live in a society concerned about the protection of children, and about
the possibility of harm inflicted on the innocent. The worldwide scandal
about child abuse in the Catholic Church was a good example. But we also
live in a society where, in most families, both parents need to work, leaving
their children in the care of others. Tensions about the need for day care may
explain why false accusations of child abuse were common 20 years ago,
and at least for a time, working in day care became a high-risk occupation.
But the blame for that scandal (one of the worst ever to afflict the mental
health field) mainly lay with psychotherapists, including a few prominent
psychiatrists.
The idea that child abuse is very common, and accounts for a large
proportion of mental disorders, was influential in the 1980s and 1990s.
These adversities are indeed more common that previously realised. But
the issue became charged and emotional. If one criticised the assumption
that abuse is a crucial cause of mental disorder, one could be accused of
protecting offenders. These ideas have gone out of favour, but are still
espoused by some psychotherapists.
What the evidence shows is that there is a statistical, but not a predictable,
relationship between childhood experiences and adult outcome. Despite
the fact that reports of abuse can be frequent in some clinical populations,
community studies show that the vast majority of those affected never
develop mental disorders (Fergusson & Mullen, 1999). Also, since child
abuse co-varies with parental neglect and other forms of family dysfunction,
long-term effects are not due to any specific kind of experience, but to
problematic rearing as a whole (Paris, 2000).
A more serious problem arose when it was claimed that even when
patients did not remember child abuse, such experiences could be
‘repressed’, but identified by a characteristic pattern of symptoms (Herman,
1992). This theory did a serious disservice to those who had truly been
victimised as children. It was popularised in a book written by two teachers
that sold a million copies (Bass & Davis, 1988). These ideas are entirely
unscientific. First, repression, a concept proposed by Freud, has little
support from empirical research (Bower, 1990). Adverse experiences may
be put out of mind (suppressed) rather than repressed. Second, severe
traumatic experiences are not repressed, and patients with PTSD cannot
stop thinking about them (McNally, 2009). Finally, the repressed memory
concept assumes, as did Freud, that memory is a kind of video recorder and
42
aetiology
that all life experience is accessible using the proper techniques. That idea
is wrong, since research shows that most events are not kept in memory,
that the memories we do retain are narratives that are ‘rewritten’ after the
fact, and that very little remains in memory from the early years of life
(McNally, 2003).
The repressed memory movement emerged, surged, and then died
out after a few years. But while it lasted, the fad did terrible damage.
Families were shattered by false accusations, and accused day workers
were sent to jail by juries instructed to ‘believe the children’. Patients were
convinced that they must have been sexually abused as children on the
basis of symptoms that are in no way specific to any life event. Only a few
psychiatrists, such as Paul McHugh of the Johns Hopkins University (2008),
stood against the tide. Although the critics were eventually vindicated,
some of the harm associated with the fad was permanent. If ever there was
a case where fallacious thinking damaged patients, this was it.
Fallacies of social risk
Social factors, ranging from the state of the economy to the strength of social
networks, have a profound influence on the development of mental disorder
(U’Ren, 2011). But even psychiatrists who are aware of this research may
not want to think much about these issues. Medical practitioners are not
in the business of promoting social change or advocating for a better world.
Physicians are not trained to prescribe for society as a whole.
The community psychiatry movement of the 1960s, which I am
old enough to remember, raised expectations that could not be met.
Nonetheless, symptoms brought on by social stressors, including the
depression and anxiety that practitioners deal with on a daily basis, cannot
always be treated with the interventions that psychiatrists know best
how to provide. If patients are socially isolated, poor or unemployed, no
antidepressant in the world will make them happy. Although psychiatrists
pay lip service to the biopsychosocial model (Engel, 1980), they prefer to
see problems as nails for which their hammers can be effective.
Social psychiatry has had many follies (Krupinski, 1992). Some
psychiatrists promoted the ‘primary prevention’ of mental illness (Caplan,
1964), and seemed to think they knew how the world should be run.
Such ideas were based on hope, not science. No one has ever shown that
major mental disorders can be prevented. How could they be, if we do not
understand what causes them? It is no doubt true that bad social conditions
are risk factors for psychopathology. But making the necessary changes is a
job for politicians, not for physicians.
In the same way as for biological and psychological theorists,
exaggerated claims for prevention based on social theories led inevitably
to disillusionment. The fad for social psychiatry reflects much about the
1960s, when, under the influence of radicals such as R.D. Laing (1967),
43
fads and fallacies in psychiatry
even individuals with psychosis were seen as victims of society. But while
social risks are important in common mental disorders, in psychoses,
although they can be a risk factor, they are not a primary cause. Thus, the
fad only succeeded in standing in the way of psychiatrists doing what they
are best at. Today, hardly anyone reads Laing, although clinicians interested
in the humanities may retain an interest in the ideas of Michel Foucault
(1961), a French philosopher who knew nothing about psychosis, but
convinced many of his readers that psychiatric patients were misunderstood
rebels stigmatised by society.
Thinking multivariately
In middle age, when I embarked on a second career as a researcher, I needed
to upgrade my knowledge of statistics. I quickly learned that the t-tests and
chi-squares of my undergraduate days were out of date, only used when
samples were small. Most research reports now made use of multivariate
analyses. Multiple and logistic regression, path analysis, model fitting
and hierarchical modelling can measure what proportion of the variance
is uniquely related to any one risk factor. These procedures more closely
correspond to the real world, in which no single risk leads to any predictable
outcome. Also, the relationship between a risk factor and an outcome can
be quantified, rather than treated as an absolute relationship.
We all prefer to think in a linear fashion, but the real world is
multivariate. In other words, many different causes can contribute to
the same outcome, and no outcome can be accounted for a single cause.
Therefore, psychiatrists need to think multivariately when assessing and
treating patients. A wide range of biological variations and adverse life
experiences can increase risk for disorder. Only a combination of all these
factors brings people to a tipping point at which they fall ill. Applying these
models could be a useful antidote to faddish thinking.
44
Chapter 5
Diagnosis
Diagnosis is an essential part of medical practice. Since diagnosis often
guides treatment, it is important to get it right. Classifying disease also
helps physicians to communicate with each other. A category that is easily
recognisable packs a great deal of useful information.
Ideally, diagnostic categories should be valid, that is describe illnesses
that correspond to natural disease entities and that have a specific aetiology,
a likely prognosis, and a predictable response to treatment (Robins & Guze,
1970). Current diagnoses in psychiatry are too inexact to meet such criteria.
The reason is that little is known about their aetiology and pathogenesis.
In medicine, clinical observations can be confirmed using laboratory tests,
genetic testing, imaging or biopsies. Psychiatry lacks any of these tools, and
is not therefore in a position to define true diseases (Uher & Rutter, 2012).
The absence of a gold standard leaves diagnosis open to faddish ideas.
Classification systems
In the past, psychiatrists did not take diagnosis very seriously. Classifications
were developed by the American Psychiatric Association: DSM-I (1952) and
DSM-II (1968), and by the World Health Organization (ICD, 1993). But
these systems were used for record-keeping, not for treatment-planning. In
the 1960s, psychiatry came under attack for negligence about its diagnostic
system. How could anyone consider the field scientific if practitioners
could not agree on what was wrong with most of their patients? Reliability
for even the most important diagnoses was low. It was also found that
the same type of patient could be labelled ‘manic-depressive’ by British
psychiatrists whereas Americans called them ‘schizophrenic’ (Cooper et al,
1972). It later turned out that a mistake of this kind could be even more
serious than was thought at the time. The introduction of lithium, effective
for bipolar disorder but not for schizophrenia, made differential diagnosis
crucial. This was also an example, still unfortunately rare, in which specific
responses to specific treatment methods contributed to the definition of a
major mental disorder.
45
fads and fallacies in psychiatry
Forty years ago, psychiatry was under siege from several directions.
The critique of anti-psychiatrists, although almost entirely invalid (Clare,
1976), was hard to answer if practitioners could not agree about basic
categories. To address this criticism, and to obtain more respect from
medical colleagues who looked down on psychiatric diagnoses, something
had to be done.
The Americans took the lead. The third revision of the Diagnostic and
Statistical Manual, DSM-III (American Psychiatric Association, 1980) was
a serious attempt to create a more reliable classification. Whereas in the
ICD manual diagnosis is based on complex prototypical descriptions, DSMIII’s innovation was to make diagnosis algorithmic. To qualify for a given
category, the patient had to fulfill several of a list of operational criteria or
symptoms. Listing criteria and asking clinicians to count them was also a
user-friendly procedure.
The DSM system became popular all over the world, even in the UK,
where the ICD has remained standard. A category could be reasonably
reliable if clinicians accurately observed symptoms and followed standard
procedures. But validity was another matter. Almost none of the diagnoses
met even minimal criteria to be considered valid.
The DSM system has since gone through multiple editions: DSM-III-R
(1987), DSM-IV (1994), DSM-IV-TR (2000) and DSM-5 (2013). All suffer
from the same problems. First and foremost, categories are based entirely
on clinical observation, not on laboratory findings. Medicine always begins
with signs and symptoms, and diagnosis has benefited from blood tests,
specific imaging findings or genetic markers. Psychiatry on the other hand
lacks all of these, and is in more or less the same position as medicine was
in the 19th century.
Second, DSM categories overlap with each other. That is because they
are defined by common symptoms, so that the more symptoms a patient
has, the more likely they are to meet criteria for more than one disorder.
There are very few criteria in the manual that are absolutely required, or
that rule out alternative diagnoses. Moreover, the more severely ill a patient
is, the more likely they are to meet criteria for more than one disorder. This
has been called ‘comorbidity’ but since patients do not usually have two
separate disorders, it might be better termed ‘co-occurrence’.
Finally, DSM has never produced a definition of mental disorder that
can distinguish psychopathology from normality. (It does have one, but I
defy anyone to make sense out of it.) Instead, categories are ‘fuzzy’, fading
into subclinical (but common) symptoms at the edges. This makes it all
too easy to ‘medicalise’ universal experiences of psychological distress
(Conrad, 2007).
Most of the diagnostic categories that psychiatrists use in practice
are not diseases in the usual sense. In the absence of an aetiological
mechanism, one cannot say whether phenomenological clusters describe
unique pathological processes. They are syndromes – symptoms that tend
to be seen together. Yet while research in psychiatry has been limited by
46
Diagnosis
the use of DSM categories, in the absence of deeper knowledge, this may
be the best we can do for now.
The editors of DSM-III saw their manual as provisional, and thought that
as research progressed, most of these problems could eventually be worked
out. That expectation proved far too optimistic. Thirty years on, in spite
of progress in neuroscience, research has not yet shed light on the causes
of the most important mental disorders, or provided data that can validate
psychiatric diagnoses. That is why DSM-IV only made minor changes to
the system.
DSM-5 initially aimed to be a ‘paradigm shift’ (Kupfer & Regier 2011).
But the revised manual could not develop a new paradigm as long as its
criteria remain dependent on clinical observation. For this reason, both
DSM-5 and ICD-11 (expected in 2015) can only tinker with definitions.
These problems will not be resolved until much more is known about
mental illness. While one could be tempted to offer an alternative, that
will take decades, when research on mental disorders becomes mature. For
now, I recommend following the classifications as written in the manuals,
on the important grounds that clinicians need a common language. But I
also suggest that psychiatrists avoid reifying diagnoses, and accept that they
are provisional constructs that mainly serve as a way of communication.
In summary, although the DSM system was a move in the right direction,
what we call diagnosis in psychiatry is a collection of syndromes whose
origin remains unknown. In some ways, classification has not advanced
greatly since the time of Kraepelin. Some believe that neuroscience will
solve these problems, but we still know too little about the brain, and
this research has not yet shed enough light on mental disorders to guide
their classification (Hyman, 2007). For example, scientists are now able
to measure brain functioning, albeit indirectly, through the use of imaging
methods. Even so, this method raises as many questions as it answers.
While we can identify functional changes in the brain in patients with
psychoses or severe depression, they are not specific and are variable within
the same diagnosis. Moreover, most changes seen on imaging are not
localised but are diffusely spread over many regions. The coloured pictures
emerging from these methods are beautiful, but explain little about the
mechanisms behind psychopathology. As Uher & Rutter (2012) note, a
classification based on science could make use of specific findings related
to neuroimaging, genetics and treatment response, but none of these are
currently supported by data.
Diagnostic classifications have a more practical role. They have been
written to include everything doctors see in clinical practice, whether it
constitutes a disorder or not. No fundamental distinction is made between
categories that describe illness (schizophrenia, bipolar disorder, melancholic
depression) v. those that describe reactions to life circumstances (Horwitz,
2002). The expansion of diagnosis into the vicissitudes of normal life is
one of the main reasons for faddish diagnoses. Not all patients whom
psychiatrists see are ill, but they are labelled as if they were. Overdiagnosis
47
fads and fallacies in psychiatry
does not actually require categories to be created de novo. Instead, existing
disorders are extended into broad spectra that describe normal variations.
Contextual forces have driven this process (Frances & Widiger, 2012).
The DSM system has made psychiatric diagnosis interesting and accessible
to the general public. Some diagnoses became popular because of media
attention rather than systematic research. Second, psychiatrists are
encouraged to diagnose conditions that are common in the general
population, and which may or may not deserve ‘caseness’. At the same time,
many categories seen in adulthood have been extended into childhood, so
that children with similar symptoms can receive diagnoses traditionally
reserved for adults. Although some critics (Frances, 2013) have questioned
whether DSM-5 will yield even more diagnostic inflation, the published
version avoided a number of controversial issues and is not remarkably
different from its predecessors. Thus the problem, which also afflicts ICD,
is not associated with any specific manual, but is systemic.
The pharmaceutical industry effectively promotes diagnostic inflation,
particularly in illnesses for which they have products to sell. With direct-toconsumer advertising (fortunately, not allowed in the UK), their interests
have promoted faddish categories. In the USA, one can hardly avoid seeing
ads that instruct people to think they have depression or bipolar disorder,
and ask their physicians to prescribe for them. Also, patient and family
advocacy groups support the use of categories in which they have an
interest. Although that could be a good idea in principle, it almost always
supports overdiagnosis. Also, the internet encourages and facilitates
diagnostic epidemics, and the media feed off these ideas. Many patients (or
their families) become convinced that a condition is present as the result of
learning about it on television or online. Finally, many people in our culture
believe in the possibility of perfect health, and are intolerant of normal
unhappiness and life’s inevitable hardships (Elliott, 2003).
Psychiatry, neuroscience and social science
Today psychiatrists consider the theoretical foundation of their specialty to
lie in neuroscience. It has become almost a matter of faith to define mental
disorders as brain diseases. This point of view gives legitimacy to a field that
outsiders sometimes have trouble understanding. But it leads practitioners
to favour categories seen as brain diseases.
Although hardly anyone outside of religious circles believes that mind
can exist without brain, biological reductionism presents philosophical
and practical problems (Gold 2009; Kirmayer & Gold, 2011). Mind is an
emergent property of neural activity that cannot be reduced to cellular or
intercellular processes. Moreover, a neuroscience model of disorder usually
gives short shrift to psychosocial stressors, even though they are among
the most important causes of common mental disorders. It is true that
biological predispositions determine how adverse events are processed
48
Diagnosis
(Rutter & Rutter, 1993). Nevertheless, it is well established that life
circumstances increase the risk for a wide range of physical and/or mental
illnesses (Holmes & Rahe, 1967).
It follows that researchers need to collaborate with a wide variety of
allied disciplines, including social scientists. Psychiatrists often work with
psychologists, and may be acquainted with their theoretical perspectives.
But they are less familiar with sociology. One of the founders of that field,
Emil Durkheim (1897), made a seminal contribution to the meaning
of suicide. Some later sociologists (e.g. Scheff, 1975) were hostile to
psychiatry, yet few today question the existence of mental disorders –
only how well distress brought on by life adversities fits a medical model
(Horwitz, 2002). The biopsychosocial theory of mental disorders (Engel,
1980) aimed to integrate neuroscience, psychology and sociology. But
psychiatrists, even though expected to know a good deal about the brain,
are not taught enough about the social sciences, even if much of what they
see reflects more about circumstance than chemistry.
Diagnostic illusions
Psychiatry borrows on the prestige of medicine. Both physicians and
patients seem to believe that diagnoses of mental disorder are as real
as cancer or cardiovascular disease. Many patients I see describe the
diagnoses they have been given, and hold on to them for dear life. Almost
any explanation for suffering can make people feel better (Frank & Frank,
1991). Instead of feeling inadequate and at fault, patients see themselves
as struggling with forces that lie somewhat outside their control.
What patients do not know is that a diagnosis can be little but someone’s
opinion. They would like to think that our categories are as solid as
those supported by a medical test. Some even ask me whether they can
have a blood test or a brain scan. This helps to explain the popularity of
questionnaires used to ‘confirm’ conditions with unclear boundaries, such
as ADHD or bipolar II disorder. But since the gold standard for all such
measures is still the signs and symptoms that are the basis of categories,
these procedures only offer the appearance of science.
The most favoured diagnoses, and the categories most likely to become
fads, are those that lead to a specific treatment intervention. In patients
who are feeling low for any reason, depression may be diagnosed because
practitioners want to prescribe antidepressants. This hammer quite easily
finds its nail. Similarly, in patients who are moody or irritable, bipolar
disorder may be diagnosed with the hope that mood stabilisers will help.
Almost any patient who has problems with attention or concentration may
receive a diagnosis of ADHD, after which stimulants can be prescribed. The
problem is that all of these vague diagnostic labels correspond to clinical
populations that are highly heterogeneous. We have no biological markers
to determine the boundaries of these diagnoses. What looks the same
49
fads and fallacies in psychiatry
need not be the same. Treatment based on appearances is not necessarily
effective.
Another set of diagnostic illusions comes from beliefs about the causes
of mental disorders. The theory that mental disorders are due to ‘chemical
imbalances’ has been very attractive, both to physicians and to patients. It
has been widely promulgated by pharmaceutical companies who are selling
agents that claim to restore these balances. I cannot think of how many
lectures I have attended that show beautiful slides of the synapse, with tiny
balls of neurotransmitters moving across the gap. This is marketing, which
offers the appearance of science without substance.
Neurotransmitters such as serotonin, dopamine and norepinephrine
are important mediators of neural processes. They have been shown to be
related to a wide variety of human behaviours, and to have effects that can
be altered by psychiatric drugs. But that does not prove that an imbalance
of neurotransmitters is the primary cause of mental illness – chemical
changes could be secondary rather than primary. One would have to show
that patients with depression, bipolar disorder and schizophrenia have a
deficit (or abnormal production) of neurotransmitters. No one has ever
come up with that kind of evidence (Valenstein, 1998; Moncrieff, 2008).
Simplistic ideas support fads, but are hard to give up. They offer a safe
haven of certainty in unchartered waters. It could take another hundred
years before psychiatrists understand the causes of mental illness and are
in a position to use that knowledge to develop a valid classification. One
can readily understand, however, why clinicians want answers now.
Two kinds of diagnostic fad
Lack of knowledge about the nature of mental disorders has not prevented
the promulgation of novel diagnoses or the extension of those already in
existence. Fads develop in areas of psychiatry that are inadequately studied,
and are applied to patient groups who do not respond to standard therapy.
Like many errors in medicine, they reflect good intentions gone wrong.
The first kind of fad is very common. It takes an established diagnostic
entity and suggests that it accounts for symptoms in a much broader
spectrum of patients. I will show how this process applies to major
depression, bipolar disorders, post-traumatic stress disorder, attentiondeficit hyperactivity disorder, and autism spectrum disorders.
The second kind of fad is less common, but equally problematic. It takes
a symptom pattern and turns it into a diagnosis. I will discuss a striking
instance: the group of dissociative disorders.
Broadening the diagnostic spectrum
Major depression
Depression lies at the heart of psychiatry. How can it constitute a fad? It
is hard to convince psychiatrists that there is even a problem. Some years
50
Diagnosis
ago, at the annual departmental party, in which residents present ‘skits’
satirising their teachers, I was portrayed as saying, ‘I feel depressed, but
I don’t believe in depression’. Perhaps what did not come across to my
trainees is that I was not questioning the existence of depression itself, but
the diagnosis of a ‘major depressive episode’.
People do feel low and suffer from altered mood. But depression can be
a symptom, a syndrome, or a disease. Melancholia is the form of depression
that best qualifies as a disease (Parker, 2011). These patients have severe
lowering of mood associated with prominent physical symptoms, and can
sometimes be psychotic. These are also the patients who respond best to
antidepressant therapy (Kirsch et al, 2008), and in whom pharmacological
augmentation is most likely to be successful.
In contrast, patients with milder depression may not have a disease, but
can better be described as unhappy. There are many reasons to be unhappy
in life, so feeling low from time to time can be considered as part of the
human condition, rather than something to be ‘medicalised’. Horwitz &
Wakefield (2007) suggest that psychiatry has confused sadness with illness.
The diagnosis of a major depressive episode, a term originally introduced
in DSM-III, describes a very broad concept. The description of depression in
ICD-10 is very similar. In DSM-5, one only needs to meet 5 out of 9 listed
criteria to receive this diagnosis. (It was arbitrarily decided that more than
half was sufficient.) And the length of symptoms required is only 2 weeks.
It is very hard to understand the adoption of this time scale, which is also
found in ICD-10. Almost anyone who is consistently unhappy for a fortnight,
and has other symptoms, such as insomnia and loss of concentration, can
be seen as having a major depressive episode. That makes the prevalence
of the condition very high, up to 50% over a lifetime (Moffitt et al, 2010).
Moreover, diagnosis is not held in reserve if patients become depressed as
a result of adverse life events. DSM-5 has softened exclusions, particularly
the one for grief. The assumption is that any symptoms that last for more
than 2 weeks must reflect an abnormal response to circumstance. Perhaps
the psychiatrists who wrote these criteria have never suffered a severe
loss. Arthur Kleinman (2012), a well-known cultural psychiatrist, took a
very different view in an article describing his own experience with grief,
published in The Lancet.
Psychiatrists also consider depression to be a single disorder, not a group
of disorders. In 1973, in an influential review paper published in Science,
Akiskal & McKinney argued that the traditional distinctions between types
of depression were invalid. They pointed out that patients with melancholia
can have first-degree relatives with milder depression, and that some
patients with mild symptoms have a family history of severe depression.
Akiskal & McKinney also claimed that all types of depression respond to
antidepressants. Their ideas influenced the definition of major depressive
episode that appeared in DSM-III. The symptom picture it described still
applies to all forms of depression in DSM-5, although clinicians are also
invited to code severity.
51
fads and fallacies in psychiatry
Akiskal and McKinney had a point. There is no absolute separation
between melancholia and mild to moderate depression. That does not,
however, prove that they describe points on a smooth continuum. Moreover,
conflating different syndromes has had problematic clinical implications,
in that all patients with ‘major depression’ will be offered antidepressants.
Which is, of course, exactly what is happening.
The unitary theory of depression is rooted in the biases of biological
psychiatry. It also convinced practitioners that milder disorders could be
treated with the same drugs as severe mental illness. As research shows
(Kirsch, 2009), although some patients with mild depression do respond
to antidepressants, efficacy can be unimpressive.
Let us consider the analogy of a cold and pneumonia. Both have a common
vulnerability, so that when people are immunologically compromised, they
can be susceptible to either. And sometimes patients with a cold develop
pneumonia as a complication. However, that does not make them into
the same disease. Similarly, we do not have evidence to conclude that all
depressions are milder or more severe versions of the same illness. There
are very good reasons, particularly treatment efficacy, for separating off
melancholia from milder depression (Parker, 2011).
Another reason my trainees did not get my point about diagnosis of
major depressive episodes is that they are trained to treat all depressions
with antidepressants. Their teachers take it for granted that once you make
that diagnosis, patients absolutely require medical treatment. Some are
even afraid that lawsuits can ensue if they fail to prescribe. This actually
happened in a famous case in the USA (Healy, 1997), however, that patient
was hospitalised for melancholic depression misdiagnosed as a personality
disorder. In fact, the evidence does not support routine prescriptions of
drugs for major depression (Kirsch et al, 2008).
Antidepressants do not always relieve symptoms and even when patients
seem to respond to these agents, one cannot be sure whether this is not a
placebo effect. That could explain why so many patients describe feeling
better after receiving a new prescription, and then finding that effects
mysteriously disappear. This is a cardinal feature of placebo responses
(Benedetti, 2008). Similarly, it helps explain why some patients feel worse
when drugs are stopped, even within 24 hours (often inconsistent with the
half-life of these agents).
Even so, the wish to prescribe drives a rush to diagnosis. And even
though the finding that antidepressants can be powerful placebos (Kirsch,
2009) has been widely publicised, that has not had much effect on practice.
In Canada, antidepressant prescriptions doubled between 1997 and 2002
(Patten et al, 2007). In the USA, a 30% increase between 2001 and 2004
has been documented (Harman et al, 2009). A more recent survey of
prescription rates of antidepressants in the USA (Pratt et al, 2011) found
that 11% of the entire population is taking one of these drugs. Although
these agents are also used for anxiety, the most common reason for their
prescription is major depression. The one factor that has made physicians
52
Diagnosis
hesitate to offer them is the fear that they might increase suicidality,
even though evidence is inconsistent about how serious a problem this is
(Gibbons et al, 2007).
In summary, melancholia is a real disease that requires biological approach
for effective treatment (antidepressants and/or ECT and/or antipsychotics),
whereas depression without melancholia is a heterogeneous syndrome
that may or may not benefit from pharmacotherapy. Calling both by the
same name (and treating them in the same way) is a fallacy that became a
fad. By setting the bar too low, and by diagnosing depression on the basis
of symptoms that last for short periods, or on the basis of criteria that
resemble unhappiness or sadness, psychiatrists are overdiagnosing the
disorder, leading millions to be given ineffective prescriptions. A unitary
theory led to unitary therapy. Until we have biological markers to identify
individuals most likely to respond to pharmacological intervention, this
problem will continue to plague practice.
Bipolar spectrum disorders
I will now examine a diagnosis that is valid in its own right, but has been
stretched to the point of invalidity. Bipolar I disorder is one of the few
conditions in psychiatry that closely resembles a medical illness. There
is nothing faddish or fallacious about this construct. Although we do not
know the aetiology of classical bipolarity, it has, as described by Kraepelin
(1921), a characteristic course and outcome. Diagnosis also points to
a specific response to treatment with mood stabilisers such as lithium
(Goodwin & Jamison, 2007).
Bipolar II disorder, characterised by hypomania rather than full mania, is
more controversial, but when used cautiously it is also well validated, at least
when the requirement for hypomanic episodes is observed (Parker, 2012).
However, bipolar II disorder is currently being faddishly overdiagnosed.
One reason is that the criteria for a hypomanic episode, listed in both DSM
and ICD, are often ignored. I am surprised how many of my colleagues are
unaware that hypomania requires 4 days of consistently abnormal mood.
Although this time scale is arbitrary, one has to draw the line somewhere.
Otherwise, patients who describe mood swings of any kind, including
euphoric episodes lasting for only a few hours, will be given a bipolar II
diagnosis. Also, DSM allows clinicians to give patients with brief mood
swings a diagnosis of ‘bipolar disorder not otherwise specified’. Moreover,
physicians have been primed to consider bipolarity in an all-too-common
scenario – when antidepressants fail to help patients.
The expansion of bipolarity has been justified by the concept of a bipolar
spectrum, which is thought to explain any and all patterns of mood instability
(Akiskal, 2002). The fad has reached the point where some surveys using
the spectrum concept identify over 30% of depressed patients as having a
form of bipolarity (Angst et al, 2011), or that close to half of all psychiatric
patients could meet broadened bipolar criteria (Akiskal et al, 2006). Some
patients with melancholia do ‘convert’ to bipolarity, but the outcome is
53
fads and fallacies in psychiatry
less common in milder depressions (Parker, 2011). The problem is that
when patients fail to respond to antidepressant therapy and are labelled
‘treatment-resistant’, bipolarity is suspected, and patients may be treated
as having bipolar disorder in the absence of any clinical features. Moreover,
patients in the putative bipolar spectrum do not respond to mood stabilisers
in the way that those with classic bipolar disorder do (Paris, 2012).
Claims that a large number of out-patients in psychiatry have occult
bipolarity are based entirely on the presence of ‘soft bipolar’ symptoms,
namely mood instability and irritability. But these features are also very
common in other conditions, such as personality disorders. Common
symptoms that are non-specific cannot be used as a substitute for biological
markers. In the absence of such markers, bipolarity has sometimes been
assessed with self-report measures or standard interviews. But what these
scales measure is not classical bipolar disorder, but ‘soft bipolarity’. For
example, the popular Mood Disorder Questionnaire (Hirschfeld et al,
2000), sometimes used to ‘confirm’ bipolar diagnoses, has been shown to
be more sensitive to personality disorder than to bipolarity (Zimmerman
et al, 2010).
The fad for a bipolar spectrum has spread to child psychiatry, a
development that should arouse concern. Bipolar disorder, long considered
to begin only at or after puberty, is now being diagnosed in young children to
account for severe behavioural symptoms. This fad has been less influential
in the UK than in the USA, where some pre-pubertal children are being
prescribed mood stabilisers and antipsychotics for years. However, children
with irritable and unstable mood do not develop classical bipolar disorder
over time, and do not respond to treatments developed for adult patients
with bipolar disorder (Duffy, 2007). When these children are followed into
adolescence, they do not develop classical bipolar disorder, but continue to
have ‘soft bipolar’ symptoms (Geller et al, 2008).
The bipolar spectrum fad would not be so worrying if it were not for the
fact that making these diagnoses often leads to the prescription of drugs
associated with significant side-effect burdens. The long-term use of mood
stabilisers and antipsychotics for patients who do not have classical forms
of the disorder is a potential tragedy. Of course, these patients do have a
mental disorder of some kind. In adults, rapidly shifting mood often points
to personality disorder (Koenigsberg, 2010). In children, putative bipolar
cases also meet criteria for conduct disorder, oppositional defiant disorder
or ADHD (Geller et al, 2008), and DSM-5 has added a new (non-bipolar)
category of ‘disruptive mood dysregulation disorder’ to account for the
clinical picture. All these diagnoses have their own problems with validity.
But diagnosing all unstable mood as bipolar is misguided and potentially
harmful.
ADHD
Attention-deficit hyperactivity disorder has been the subject of a vast
research literature, and the use of stimulants to treat children with classic
54
Diagnosis
features of ADHD has a strong evidence base (Barkley, 2006). As with
bipolar I, classic cases of ADHD are uncontroversial. However, many
problems remain in the definition, particularly in adults. The disorder
exists in a form in which hyperactivity is prominent, and a second, more
poorly defined form characterised by inattention (Carlson & Mann, 2000).
Treatment is more effective when hyperactivity is predominant (Leung
& Lemay, 2003). But with the promise of a quick fix with a stimulant
prescription, clinicians may give in to the temptation to see every problem
with attention as justifying a diagnosis of ADHD. Worryingly, the diagnosis
can be ‘confirmed’ by psychological testing, even though the results of
these procedures are not in any way specific (Berger, 2011). This provides
good business for psychologists, but test results lack the specificity and
sensitivity physicians expect from blood tests or imaging. And instruments
(e.g. the Conners Rating Scales) that ask parents or teachers to tally up
symptoms described in the manual are even less valid.
Attention-deficit hyperactivity disorder is a syndrome that can respond
to specific treatment, but extension of its boundaries has reached a point
of faddishness. The community prevalence has steadily gone up in many
countries (Faraone et al, 2000), rising to 8% by 2003, and to 9.5% by 2007,
with a particularly striking increase in adolescents (Zuvekas & Vitiello,
2012). Prevalence is highest in the USA, probably because clinicians in
that country have a lower threshold for identifying the disorder. In the
UK, early warnings about overdiagnosis from authorities such as Michael
Rutter (1987), as well as common sense, seem to have made the problem
less severe.
Many children are overly excited and distractable at times, and boys
tend to have trouble sitting quietly for hours in a schoolroom. But when
the diagnosis is expanded, treatment is less effective. Moreover, results are
not as dramatic as many clinicians think. Although the short-term effects
of stimulants are well established, one large-scale multisite study (Molina
et al, 2009) found that when children were followed up over 6 to 8 years,
outcome was no better than with non-pharmacological interventions.
The most striking current fad has been the extension of the ADHD
diagnosis into adult populations. This is not to say there are no such cases;
not all children fully recover from childhood ADHD by adulthood (Weiss
& Hechtman, 1993). However, to diagnose adult ADHD, a definite history
in childhood has to be established. That may require a careful review of
school records. Unfortunately, clinicians evaluating adults often ignore
this requirement. What too often happens is that ADHD is identified by
problems with attention, whatever the cause. The National Comorbidity
Survey in the USA found a community prevalence of 4.4% for adult ADHD
(Kessler et al, 2006). That is a very high number for a disorder rarely
diagnosed 20 years ago. Epidemiologists should not be swallowing the
DSM criteria whole.
It used to be thought that one could diagnose ADHD by a good response
to stimulants. But it turns out that even healthy people have better
55
fads and fallacies in psychiatry
attention, at least in the short-term, when they take these drugs (Rapoport
et al, 1978); it has been reported that some students use stimulants to
improve their performance on examinations. Helping people to be more
focused through drugs might be called ‘cosmetic psychopharmacology’
(Kramer, 1993), a practice in which people take drugs to perform better
than normal.
Once patients become attached to an ADHD diagnosis, they can be
tempted to explain all their problems on that basis. This is part of a much
vaster trend: the medicalisation of all kinds of life problems. Today one
sees university students who are offered extra time to write examinations
because they have an intellectual disability’. The case is ‘proven’ by
psychological testing procedures that can identify a profile of strengths
and weaknesses in anyone. If you do poorly in school or at work, it is not
because you need to try harder. It is because your brain is malfunctioning.
Autism spectrum disorders
Autism has been long recognised by psychiatrists, and Asperger syndrome
has been viewed as a milder variant. In DSM-5, both syndromes are folded
into a broader autism spectrum. Once again, valid diagnoses are being
stretched to account for phenomena that may or may not be at all related.
Other conditions can produce cognitive impairments similar to those
seen in the autism spectrum, and there is no gold standard for separating
Asperger from social anxiety and introversion. The overdiagnosis of autism
spectrum disorders is a fad in which even people outside of medicine are
calling everyone with eccentricity and social awkwardness as falling within
its boundaries. Yet without biological markers, how can we be sure? The
diagnosis of autism has become imperial, crossing the boundaries of
normality and conquering them.
Children are different in temperament, and trait profiles vary because
each can be adaptive under the right circumstances (Beck et al, 2004). Thus,
while extravert and impulsive children can have problems in modern urban
society, in another setting, they could react rapidly in a more positive way –
some might grow up, for example, to be soldiers. Similarly, introverted and
socially awkward children can use their traits in positive ways, for example,
by going into computer science. But if every nerdy child is diagnosed with
an autism spectrum disorder, many will be stigmatised. Autism and related
conditions used to be considered rare. More recently, they have been
diagnosed more and more frequently, even in adults. The recent survey in
South Korea (Kim et al, 2011), which garnered much attention from the
media, found spectrum diagnoses in over 3% of the general population.
Clearly, something has happened to the definition of autism, which has
been greatly broadened, creating a worrisome fad.
PTSD
Post-traumatic stress disorder is an attractive diagnosis because it suggests
an aetiology. That is illusory. Most people who are exposed to traumatic
56
Diagnosis
events never develop PTSD. Patients with PTSD react to trauma in a unique
way, in accord with their temperament.
The Epidemiological Catchment Area study, based on the DSM-IV
definition, found a community prevalence of 7.8% for PTSD (Kessler et
al, 2005a). The DSM-5 definition of PTSD makes it even more likely that
this diagnosis will be made. Exposure to trauma now includes events that
are not life-threatening and that do not even threaten serious injury. The
definition can be extended to witnessing traumatic events, or only hearing
about them. This leads to overdiagnosis, and by failing to focus on the
impact of severe trauma, weakens the concept (McNally, 2009). Again, this
fad may be less common in other countries than in the USA, where the
culture promotes a sense of victimisation (Sykes, 1992). What I observe
in consultations is that clinicians move all too quickly from a history of
traumatic exposure to a diagnosis of PTSD, a good example of availability
bias. Physicians do not always take the time to determine whether the
characteristic symptoms of the disorder are present (hyperarousal, intrusive
memories, avoidance of stimuli that re-evoke the response). Psychiatrists
and family doctors are in step with popular fads that affect the way ordinary
people talk about life and its vicissitudes. Everyone who is moody is
‘bipolar’, everyone who fails to pay attention has ADHD, and anyone who
has an adverse reaction to life events has PTSD. A history of trauma, no
matter how remote in the patient’s life history, can be seen as associated
with a clinical problem and converted into a diagnosis. This is fallacious
and faddish thinking.
The symptoms of PTSD are not very specific, and have a major overlap
with depression (Bodkin et al, 2007). Most people are resilient to trauma,
but PTSD is most likely to emerge in individuals with high neuroticism
(McFarlane, 1989; Breslau et al, 1991). The diagnosis can be useful
when applied cautiously, but becomes a fad through misapplication. It
oversimplifies clinical reality by pretending, but failing, to provide an
aetiological explanation. The effect of this diagnostic fad is to slot patients
into a diagnosis that does not explain symptoms, and can lead to the wrong
treatment (trauma-focused psychotherapy and/or antidepressants).
Turning symptoms into a diagnosis
Dissociative disorders
Dissociative disorders are rare disorders – so rare that they may not even
exist. Admittedly, some of the symptoms are real enough. Depersonalisation
and derealisation are common in anxiety disorders, mood disorders or
personality disorders, and in a few cases can present as a separate syndrome
(Simeon & Abugel, 2006). The problem lies with the clinical picture of
‘multiple personality disorder’ (now called dissociative identity disorder),
in which separate personalities coexist. Dissociative identity disorder is
worse than a fad, it is a fraud. It reflects an interaction between enthusiastic
therapists who promoted dissociation, and patients who enjoyed the
57
fads and fallacies in psychiatry
attention their condition brought them (Piper & Merskey, 2004). It may
be the only diagnosis in psychiatry promoted by a best-selling popular
book (Schrieber, 1973). The subject of that volume, a patient called ‘Sibyl’,
claimed to have a large number of personalities, which her psychiatrist
thought was due to a history of child abuse. Actually, the traumatic events
described by Sibyl were never documented and confirmed, and a recent
book showed that she had a perfectly normal childhood (Nathan, 2011).
Sibyl also admitted that she only produced alternative personalities when
her therapist asked for them (Rieber, 2006; Nathan, 2011). Although
the story was fraudulent, it appealed greatly to the public (and to some
professionals) because of its drama.
The fad for dissociative disorders did great damage to patients and
families, because it led to expensive and arduous treatment methods (years
of hospital-based psychotherapy), and because it was often associated
with false memories of child abuse. It also supported the fad for ‘recovered
memories’ that plagued clinical practice for years (Paris, 1996a,b). The
diagnostic fad for dissociative identity disorder peaked in the 1990s, and
then declined. But it lasted long enough to do damage. In a social climate
where both parents work, and worry about the quality of care their children
receive, it became dangerous to work in a day care centre, and a few day
centre workers went to prison on false charges. The fad was most prominent
in the USA, and although it had less impact in the UK, treatment guidelines
for these fictional disorders have recently been considered by NICE.
Diagnostic fads and fallacies
Psychiatrists are faced with complex symptoms that are difficult to
understand and difficult to classify in a meaningful way. It is tempting to
fall back on diagnostic fads that make complexity simple. For each of the
faddish diagnoses described in this chapter, a therapy can be attached.
Unfortunately, many of these treatments are unproven, ineffective or
harmful.
On the whole, the more severe the mental disorder, the better the system
works. There can be little doubt about diagnosis when a patient presents
with a classical picture of schizophrenia, melancholia or bipolar disorder.
Psychiatrists today spend more time than ever on these patients. The
main problems lie with the common mental disorders, conditions that are
particularly difficult to classify. Many patients seen by psychiatrists do not
fit neatly into any category. The danger, as pointed out by Batstra & Frances
(2012), is that diagnostic inflation identifies people with normal problems
as having a mental disorder. In the milder ranges, they might be better
described as distressed, whereas we are shoehorning them into illness. The
overdiagnosis of mental disorders does a disservice both to patients and to
psychiatry as a whole.
58
Chapter 6
Epidemiology
Epidemiology, the study of factors governing the frequency of disease in
the community, can be the first step in understanding why people fall ill.
Clinical samples are unrepresentative of what illnesses look like in the
community, whereas community surveys tell one how frequent disorders
are and examine their correlates in detail.
In psychiatric epidemiology, many large and expensive studies have been
conducted over the past 25 years, particularly in the USA. Research began
with the Epidemiological Catchment Area Study (Robins & Regier, 1991),
expanded in the National Comorbidity Studies (Kessler et al, 2005a,b),
and was augmented by large-scale studies of substance misuse (Grant
et al, 2004). Yet many of the conclusions that have been drawn by these
studies remain doubtful. Some of the methodological problems include
an almost complete reliance on self-report, the use of cross-sectional
assessments without follow-up, and the use of partially trained research
assistants (Newson et al, 2010). But the most worrying issue is that so
much of psychiatric epidemiology has depended on diagnosis as defined
by our current classification systems. No one knows whether diagnoses,
such as those derived from the DSM or the ICD, are valid in the same way
as medical conditions. When research has moved beyond these diagnoses,
it has had to assess the frequency of symptoms considered to be their
subclinical manifestations (e.g. Merikangas et al, 2007). In the absence of
any gold standard for determining the boundary between normality and
pathology, this approach leads to a consistent inflation in estimates of
prevalence.
Inflated prevalence
Grant reviewers have to read a large number of submissions and easily get
tired. That is why researchers learn to write the first paragraph of their
applications to grab the reader’s attention. The most common strategy
is to support the importance of research by describing the prevalence of
the condition under study and its impact on public health. For example,
59
fads and fallacies in psychiatry
if the grant concerns alcoholism, reviewers can be told that this condition
affects 10% of all men (Robins & Regier, 1991). If the research concerns
major depression, reviewers can be informed that surveys find that 13%
of all men and 21% of all women will meet criteria sometime during their
lifetime (Kessler et al, 1993). The question is whether these numbers are
credible. Many people drink too much, and almost everyone gets depressed
from time to time. High-prevalence disorders of this kind are not easy to
separate from life’s problems.
Depression is particularly ubiquitous. If one accepts the definitions
in diagnostic manuals, the high prevalence found in surveys is actually
an underestimation. The reason is that reported numbers depend on
recollection of past episodes, which can be forgotten. In a prospective
longitudinal study (Moffitt et al, 2010), the rates of common mental
disorders were twice as high as in community surveys, and major depression
attained a lifetime prevalence of 41%. Prospective research actually suggests
that almost half of the general population meets criteria for a mental
disorder at some time during a lifetime (Moffitt et al, 2010). Allowing for
inaccuracies of memory, prevalence, at least based on current definitions,
could be much higher.
This finding could be considered either alarming or reassuring. On the
one hand, mental disorders, or at least the symptoms of disorder that DSM
cobbles together into categories, are part of the human condition. On the
other hand, if 50% of us go through life without experiencing a mental
disorder, that is more than can be said about physical illness. One might
argue that if half the population never experiences mental disorder, that
is very good news. Perhaps doubts about the prevalence of mental illness
only reflect the continuing stigma attached to any psychiatric diagnosis.
But what if the mental disorders studied by epidemiologists describe life
problems that are fuzzily defined and overidentified as diagnostic entities?
Most community surveys have focused on diagnoses defined by the DSM
system. There is little doubt that some of these categories qualify as medical
illnesses: schizophrenia, bipolar disorder, melancholic depression, and
one might also include severe forms of substance misuse and personality
disorder. But others are disorders or syndromes, not diseases in the same
sense as tuberculosis or epilepsy, even if they describe problems that
clinicians see. The best examples are milder forms of anxiety (Horwitz &
Wakefield, 2012) and mild to moderate depression (Horwitz & Wakefield,
2007), both associated with discontent. Even though these feelings can
be a reason for consulting a mental health professional, and despite the
fact that most psychiatric symptoms (even hallucinations) can occur from
time to time in healthy people, there is a qualitative difference between
unhappiness and mental illness.
Psychiatrists do not have a way to define the concept of ‘mental disorder’,
or to separate it from vicissitudes of the human condition (Frances &
Widiger, 2012). Everyone (with the exception of anti-psychiatry radicals)
agrees that schizophrenia and bipolar disorder are diseases in the sense
60
epidemiology
that medicine has always recognised. But do milder disorders qualify for
the same status?
Consider the diagnosis of major depression. It only requires 2 weeks of
symptoms, often following exposure to psychosocial stressors. Most people
recover from these episodes without treatment, and mild depression may be
better understood as a reaction to circumstance than as an illness (Horwitz
& Wakefield, 2007). Most of these ‘depressions’ remit spontaneously after
a few weeks (Patten, 2008). That is because they are temporary reactions
to circumstance, even if they easily meet current criteria. The bar for major
depression is so low (5 out of 9 symptoms over only 2 weeks in the DSM
system) that anyone who is acutely or chronically unhappy can receive a
diagnosis.
I am not saying that these patients should be turned away because
they are not sick enough. Although most psychiatrists concentrate on
more serious cases, unhappy people need to be evaluated. But they do
not necessarily require the same kind of specialised help provided to
patients with severe illness. Physicians sometimes manage the common
cold, but ‘normal’ conditions are distinguished from serious illnesses
such as pneumonia. The tendency to see all psychopathology as lying on
a continuum is the source of the trouble. If there is no boundary between
normality and pathology, everyone has a mental disorder, making the whole
concept meaningless.
These distinctions are also important because diagnostic categories are
heterogeneous, and treatment indications can be different for different
patients. In depression, mild cases do not benefit from antidepressants
to the same extent as severe cases do (Kirsch et al, 2008; Parker, 2011).
Similarly, in anxiety disorders, clinicians need to distinguish normal
reactions to life stressors from crippling dysfunction (Horwitz & Wakefield,
2012).
Psychiatric diagnosis has become imperial in its scope. Patients with
normal or near-normal problems can receive both diagnosis and treatment.
This may not be a new problem, but it is getting worse. High rates of
symptoms in the population have been found in all studies based on the
DSM system, including the Epidemiological Catchment Area study (Robins
& Regier, 1991) and the National Comorbidity Surveys (Kessler et al, 1994,
2005a).
Depression, anxiety and alcoholism are examples of high-prevalence
disorders, but many of the same problems arise when less common
disorders are broadly defined as part of a spectrum. Some epidemiologists
have claimed a high rate for bipolar disorders (Merikangas et al, 2007),
prevalence of which has dramatically gone up (from 1 to 4%). The
category of attention-deficit hyperactivity disorder, which cannot be reliably
separated from other behavioural disorders, has been estimated to affect
10% of all boys in school (Barkley, 2006). Autism spectrum disorders, long
considered rare, have gone up even more dramatically as they have been
re-defined as a broader spectrum (Fombonne, 2003). In Korea, Kim et al
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fads and fallacies in psychiatry
(2011) found a community prevalence of 3%, a result that was so surprising
it was highlighted in media all over the world. This kind of diagnostic
inflation seems to be a fad. But community surveys are used to support the
claim that disorders are much more prevalent than previously thought. The
implication is that psychiatrists have been missing something important,
and need to lower their diagnostic bar.
In every case, it is simply assumed that the diagnoses based on criteria
or prototypes listed in the manual are valid. But that cannot be taken
for granted. In a previous era, when researchers took classification less
seriously, the preferred method was to measure symptoms or levels of
functioning, instead of illness categories. Classical research from 50 years
ago, such as the Midtown Manhattan Study (Srole, 1980) and the Stirling
County Study (Leighton et al, 1963), both conducted before the publication
of DSM-III, measured distress or dysfunction. Even so, the same problems
emerged, in that at least a third of the general population scored as mentally
ill. At the time, many were shocked at such a claim. Today few would even
blink.
What is a mental disorder?
Epidemiological research measures the frequency of psychological
symptoms. But everyone experiences periods of anxiety and depression,
as well as periods of moodiness, inattentiveness, or use of substances.
This raises the question of whether there is any valid way of separating
psychopathology from normality (McNally, 2011; Kagan, 2012).
These issues have been debated for at least a hundred years. Kraepelin
(1921), who worked in mental hospitals, wanted psychiatry to focus on
severely ill patients whose symptoms would not overlap with normality. On
the other hand, Freud (1916), who conducted an office practice, took the
view that everyone was a little ill, and that differences between patients and
non-patients were a matter of degree. Ironically, this concept, overthrown
by DSM-III and the neo-Kraepelinian movement, is being revived by the
neuroscience model.
If subclinical symptoms of mental disorders are points on a smooth
continuum between disorder and normality, mental illness would blend
into normal trait variation. This view is shared by the editors of DSM-5
(Regier et al, 2011), and by researchers at the US National Institute of
Mental Health (NIMH; Insel et al, 2010). At one end of the continuum,
symptoms would be sufficiently severe that few would contest that an
illness is present. At the other end are people who have only transient
distress, and who almost everyone would agree do not have a disorder.
The problem lies with the group in the middle, who may have ‘subclinical’
symptoms. Some epidemiologists have argued that subclinical symptoms
are, on a statistical basis, risk factors for serious disorders (Kessler et al,
2003). Most people with minor symptoms either recover or continue to
62
epidemiology
have subclinical distress. Classifying them as ill would lead to an enormous
number of false positive diagnoses.
Every academic discipline is ambitious, and wants to expand its
boundaries. That goes some way to explaining why some psychiatrists see
everyone as somewhat disordered. Meanwhile, the boundaries of diagnosis
grow broader with time, with each edition of the DSM manual thicker than
the last. But most disorders, as defined by current criteria, are syndromes –
collections of symptoms, not true diseases. Admittedly, patients come with
a wide range of problems that psychiatrists are asked to deal with, so we
need to have a way of classifying them. But that does not justify making
medical diagnoses, or using the skills of highly trained specialists to help
people deal with the normal life stressors.
Finally, one might ask whether psychiatric diagnoses are culturally
relative. Severe mental disorders such as schizophrenia and bipolar I
disorder are universal, and common mental disorders can be observed in
other parts of the world (Kessler et al, 2009). But some conditions are highly
cultural – one does not, for example, see eating disorders in countries where
people are starving.
In summary, mental disorders have a high prevalence because it is
impossible to separate psychopathology from life. Current diagnoses
are provisional formulations that may or may not stand the test of time.
Thus, as long as prevalence is based on an imprecise classification system,
epidemiological findings in psychiatry have to be taken with a grain of salt.
The prevalence of major depression
Let us now focus on major depressive disorder, a paradigmatic example
of the problems of psychiatric epidemiology and of psychiatric diagnosis.
Younger clinicians may not realise that this category is relatively new,
introduced by DSM-III in 1980 (Shorter, 2009). In DSM-II, psychiatrists
distinguished between ‘endogenous’ and ‘reactive’ depression. The
endogenous type was equivalent to melancholia, a severe and sometimes
life-threatening illness that tends to come ‘out of the blue’ (Parker, 2005). In
contrast, reactive depressions are brought on by stressors, and remit when
circumstances change for the better. It has been said that no one should
diagnose depression if symptoms remit when a patient finds a new lover or
becomes unexpectedly wealthy.
The reason why lifetime prevalence for major depression is 50% is that
depression is not always that ‘major’. Most patients with mild depressive
symptoms never present to physicians, and can usually be expected to
recover spontaneously (Patten, 2008). Hence current prevalence estimates
reflect a low bar for diagnosis of depression (Horwitz, 2002), and do not
distinguish between disabling disease and brief episodes of lowered mood,
particularly when associated with sadness or grief (Horwitz & Wakefield,
2007). This is not to say that patients who do seek help for less severe
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fads and fallacies in psychiatry
symptoms do not have a problem; however, they need not be classified as
having a disease.
Inflated prevalence creates a problem both for clinical practice and
mental health policy. Epidemiology is used to guide the way resources
are allocated. Even though mental illnesses are highly prevalent, only a
minority of potential patients will seek treatment (Kessler et al, 2005b).
Yet high prevalence is not necessarily a cause for concern. We need to be
respectful of people who choose to solve problems on their own. We should
also do better to make it easier for severely ill people to seek treatment,
rather than focusing on people with milder symptoms who may not actually
benefit from our services (Patten, 2008). That is why depression screening
programmes have a weak rationale, and are a poor use of scarce resources
(Thombs et al, 2012). They identify people who are unhappy enough to
meet criteria for major depression, but have symptoms that are mild and
transient. If psychiatry were to conduct useful screening, it should be
looking for untreated cases of melancholic depression.
Mental disorders in the clinic and in the community
Some researchers conducting surveys that identify subclinical symptoms
problems have expressed deep concern that so few individuals seek therapy.
For example, Merikangas et al (2007) noted with alarm that most people in
the community who experience mood swings (but do not meet criteria for a
hypomanic episode) are not in medical treatment. This may only show that
participants in community surveys are wiser than epidemiologists. Nobody
has ever shown that drugs are effective for simple moodiness (Patten &
Paris, 2008). This normal variation does not require medical intervention.
Moreover, increased emotional reactivity can be adaptive under some
circumstances (Beck et al, 2004).
Psychiatrists have more than enough to do without looking for more
business. With support from public and/or private insurance, most mental
health practitioners have more patients than they can manage. In any case,
psychiatrists are highly trained specialists who should be focusing their
efforts on the sickest patients. Little will be accomplished if screening
programmes based on epidemiological surveys bring large numbers of
patients with mild symptoms into the busy world of primary care. In the
end, people are wiser than we give them credit for. They are perfectly right
not to go to psychiatrists or other mental health professionals for minor
problems. Nor should epidemiology be used to encourage even more people
to take psychotropic medication. Nobody ever said life had to be happy.
64
chapter 7
Psychopharmacology
The triumph and tragedy of psychopharmacology
The successful treatment of mental illness with drugs that began in the
1950s was a landmark in the history of medicine, and as an undergraduate
student, I had the luck to see it happen. In 1958, I joined a group that spent
weekends visiting a nearby 4000-bed mental hospital. The physicians there
were just beginning to use antipsychotics. The condition of many patients
was desperate. Yet, a few years later, by the time I entered medical school,
effective treatment was widely available. Although relapses were still
common, patients who had psychoses no longer spent months, or years,
languishing in hospitals. There can be no doubt that antipsychotic drugs
are among the most effective drugs in all of medicine.
Other breakthroughs followed. Antidepressants (mainly tricyclics) were
also introduced in the late 1950s, proved effective for patients with severe
depression, and turned ECT from a standard treatment to a back-up. By
1970, lithium was available for the management and prevention of manic
episodes. I saw patients with bipolar disorder who had been admitted to
hospital 25 times or more recover and return to their lives. This was an
inspiring time to study psychiatry.
Like most psychiatrists of my generation, I was deeply impressed with
these new drugs, and had no hesitation in prescribing them. Moreover,
psychopharmacology was a scientifically based field, with a theory built
on research in neuroscience and a practice rooted in systematic clinical
trials. Yet several decades later, I find myself a critic of the field, at least
as it is currently practised. I am puzzled, and sometimes appalled, by the
way drugs are being prescribed, and find myself fighting a tidal wave of
overprescription. Although today’s drugs are no better than what was
available 40 years ago (Healy, 2012), they are given to almost every patient
who comes to a physician with psychiatric symptoms.
To understand these problems better, I wrote a book (Paris, 2010a) about
what the research literature in psychopharmacology actually shows. I was
stunned to discover how large the gap is between what we know and what
practitioners actually do. Many practices that are taken for granted, and
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supported by government agencies and/or treatment guidelines, turn out
to be backed up by only two or three studies (some of which are dubious
on close inspection). The power of hope drives the prescription of drugs, or
multiple drugs, for almost every problem known to psychiatry.
I have learned that a discipline based on empirical data is not immune to
fads. The problem is that practitioners need results too badly. Psychiatrists
and family physicians who treat patients with mental disorders want them
to get well, and do not always accept the limitations of their tools. With
the encouragement of academic physicians who promote the wider use of
current agents, they prescribe drugs to treat problems for which they were
never intended. Once again, the hammer finds its nail.
Some of the problems of psychopharmacology derive from our inadequate
diagnostic system. Mental illnesses cannot yet be scientifically classified,
and much of the time, we do not really know what we are treating. Even so,
physicians cannot resist throwing drugs at symptoms. This leads to faddish
treatments that have invaded the mainstream of psychiatry. Since most
disorders listed in DSM-5 and ICD-10 are not true diseases but syndromes,
it is not surprising that treatment is rarely specific to diagnosis. Psychiatric
drugs target symptoms. That may not be a problem when the target of
treatment is clear. But as we will see, that is often not the case.
How psychopharmacology is practised
Today’s psychiatry looks more like a medical specialty than it did when I
was in training. Since most practitioners agree that clinical practice should
apply neuroscience, psychopharmacology is the dominant force in modern
psychiatry. This paradigm shift was driven by the wish of psychiatrists
to practise just as other physicians do, to make diagnoses and write
prescriptions. ‘Just talking’ to patients became seen as old-fashioned and
not very effective. There are also practical reasons for the decline of talking
therapy. Where psychiatrists are paid on a fee-for-service basis, they can
make more money by seeing four patients within an hour for medication
instead of one patient for psychotherapy. Moreover, not all academic centres
provide trainees with sufficient experience in psychotherapy, or in the
management of psychosocial problems.
The American psychiatrist Daniel Carlat (2010) published an eloquent
book examining the consequences of such an approach, affecting the way
psychiatry is being practised. Carlat describes the dispiriting picture of
current clinics – most patients seen for 10–15 minutes, asked about current
symptoms, after which their medications may be ‘adjusted’. This is a
travesty of how mental health services should be provided. While surveys
(Mojtabai & Olfson, 2010) show that psychiatrists do talk with patients,
this is mostly chatting, not any recognisable form of evidence-based
psychotherapy. The prescription pad comes out well before taking the time
to find out what is going on in a person’s life.
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When the only focus of the clinical encounter is symptoms, prescription
rates are bound to go up. Yet even the most commonly used drugs are not
as consistently effective as many physicians think. Meta-analyses (Kirsch
et al, 2008; Fournier et al, 2010) suggest that antidepressants are not much
better than placebo for mild to moderate depression. In other words,
initial severity is the strongest predictor of response (Khan et al, 2011),
so that sicker patients respond better than those with mild symptoms,
whereas patients with the mildest symptoms are more likely to show a
placebo response. Admittedly, other studies maintain that antidepressants
can be more broadly effective (Gibbons et al, 2012), but these effects are
not consistent. Given that measures of treatment outcome in psychiatry
are rough (Isacsson & Adler, 2012), it seems safe to conclude that some
patients with milder depression respond, but we do not know how to
identify them in advance. The bottom line is that antidepressants do work,
but not predictably (Thase, 2011). And when they are prescribed to people
who are mostly unhappy, they may not work at all. To be fair, psychiatrists
sometimes think that other physicians have more effective treatments, but
they should be less envious. Although effect sizes (which measure change
in standard deviation units) are modest in psychiatry, so are they for most
drugs in medical practice (Seumuller et al, 2012; Leucht et al, 2012). Let us
not idealise the rest of medicine just because psychiatrists sometimes feel
they are poking around in the dark.
The limits of antidepressant therapy
What should clinicians do when drugs do not work? This is an increasingly
common scenario as antidepressants are routinely prescribed for lessthan-convincing reasons. Sometimes it seems sufficient for patients to
report misery, or to cry in the doctor’s office to be offered a drug. In
less severe cases, psychiatrists should consider watchful waiting or nonpharmacological evidence-based alternatives, as recommended by NICE
(National Institute for Health and Clinical Excellence, 2009). However,
the current climate of opinion focuses on trying another drug (‘switching’),
or adding another drug (‘augmenting’). These procedures can sometimes
be effective, but, as shown by large-scale effectiveness studies such as
the Sequenced Treatment Alternatives to Relieve Depression (STAR*D;
Valenstein, 2006), they do not work consistently. The evidence base for
augmentation and switching is much weaker than most clinicians think
(Rush, 2007). STAR*D showed that some patients who fail to respond to
the first drug benefit from a course of a second drug, but after that, a law of
diminishing returns sets in. Nevertheless, that has not prevented attempts
at augmentation and switching from becoming almost routine in practice.
Consultants only see treatment failures, and it is possible that some of the
people I will never be asked to see have benefited from these pharmacological
interventions. (It is also possible that many patients stopped taking their
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medication.) But I often consult on patients who have been tried on
four or five antidepressants, sometimes in combination, ‘augmented’ by
antipsychotics (and/or mood stabilisers). I am not impressed with this kind
of practice, which is based on the idea that any patient can be helped if the
physician can just find the right cocktail of drugs for them.
One of the main reasons (but not generally recognised) for the uncertain
effects of antidepressants derives from problems in defining the target.
Major depression is not a disease, but a heterogeneous syndrome (Parker,
2005). Most of the patients sent from primary care for consultation do
not have classical features of melancholia, and would be better described
as unhappy. They have life problems that are unlikely to respond to drug
therapy alone and that need to be addressed in other ways. A patient who
is chronically unemployed and socially isolated should not be expected to
receive dramatic benefits from psychopharmacology. Often, all that can
be expected is a better night’s sleep, and even that can come at a price of
side-effects.
Even so, physicians continue to prescribe drugs for unhappiness, which
they simply redefine as ‘major depression’ (Horwitz & Wakefield, 2007;
Mojtabai & Olfson, 2011). This is why 11% of all Americans over the age
of 12 are currently taking an antidepressant (Pratt et al, 2011), numbers
that include almost a quarter of all women aged 40–59. This pattern of
overprescription could be one of the greatest psychiatric fads of all time.
The power of the placebo
It is hard to know whether prescribed drugs are working. Patients get
better, but can we establish cause and effect? People also get better for other
reasons – their life situation can change, or symptoms spontaneously remit.
Yet psychiatrists, and their patients, like to explain everything on the basis
of the last prescription. That is why medications are endlessly ‘adjusted’
to no purpose.
We tend not to see the obvious explanation for why patients get better
after taking a drug. The elephant in that room is the placebo effect.
Physicians are taught about placebos, but do not always understand their
power (Benedetti, 2008). By and large, the sickest and most acutely ill
patients tend to show a weak placebo response. That turns out to be true for
depression: placebos have little effect on severe cases (Kirsch et al, 2008). In
contrast, placebo effects are greater in chronic illnesses, in conditions with
an intermittent course, and in conditions that overlap with normality. The
mild to moderate episodes of low mood which so many people experience
from time to time show placebo effects that can be as high as 40%. This
is fairly close to the results (about 50%) we get from the prescription of
antidepressant drugs. Also, placebo responses tend to be more temporary
than drug effects, leading to the otherwise mysterious scenario in which
drugs stop working after a few months. Some of my colleagues tell me they
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still prescribe antidepressants in such cases, but with low expectations of
response. I sometimes suggest this option to consultees, but prefer not to
recommend drugs if the reason for prescribing them depends more on hope
than on evidence.
What concerns me is that industry pressure, and overly optimistic
advice from academic opinion leaders, have convinced physicians (and their
patients) that finding the right cocktail is only a matter of trial and error.
I am also concerned that clinicians seem irresistibly drawn to seeing every
change in mood in the light of the latest prescription. Once again: post hoc,
ergo propter hoc.
None of these problems mean that antidepressants do not work at all.
Findings about strong placebo effects in depression were discussed in
almost every newspaper in the world in 2008, and made Irving Kirsch, the
psychology professor who led the meta-analysis, famous. His data seemed
to contradict years of clinical trials, but took into account unpublished
negative findings (which researchers supported by drug companies never
published). Unfortunately, Kirsch fell victim to his own renown, publishing
a book claiming that antidepressant therapy is a ‘myth’ (Kirsch, 2009). But
that is not what his data showed – drugs were definitely better than placebo
when depression is severe. It is arguable that even if only a minority of
patients respond to antidepressants, and even if we cannot predict which
ones they will be, it is worth trying them out. However, it does not follow
that drugs should be the only treatment, or that patients should be tried
on every agent on the market until something pans out. Another twist in
the story is that clinical trials of antidepressants show effects in anxiety
disorders and obsessive–compulsive disorder (OCD) (Casacalenda &
Boulenger, 1998) that may be more consistent than in depression. This
broad spectrum of action suggests that antidepressants are misnamed,
and should not be thought of as specific to one constellation of symptoms.
Since major depression is a high-prevalence condition, the market for
treatment could almost be unlimited. That is why industry is more closely
involved with psychiatry than with other specialties, and why it promotes
antidepressants for everyone. The story goes back decades, to the days
of tricyclics. These drugs still remain valuable (Shorter, 2009), but nonpsychiatric physicians were concerned with their side-effect profile. In the
1990s, when tricylics gave way to selective serotonin reuptake inhibitors
(SSRIs), the diagnosis of major depression became much more common,
and more patients began to receive prescriptions.
I remember beginning to prescribe fluoxetine for depression in the
1980s. At first, so many patients came in feeling so much better, sometimes
just a week later, that I thought I was seeing miraculous changes. What I
forgot was that interviewing patients, taking a careful history and showing
empathy for their distress is also therapeutic. Many depressed patients
feel better after a thorough consultation without taking any drug at all.
Fluoxetine may have also had greater placebo effects because it was
generally well tolerated.
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Patients who experience no benefit from antidepressants will stop taking
them. Others do well and stay well. A large literature supports maintenance
treatment in relapsing individuals (Geddes et al, 2003). The puzzle is that
some patients describe a temporary benefit that disappears after a few
weeks to months. It has been sometimes suggested (Fava, 2003) that this
reflects a long-term tolerance to the drug. I find that hard to believe. It
seems more likely that the initial response was a placebo effect, which could
only be expected to decline with time.
Context has a powerful influence on placebo effects (Benedetti, 2008).
A patient who has already read about a drug, or who has (in the USA) been
exposed to direct-to-consumer advertising, may have positive expectations
even before consulting a physician. If a clinician is enthusiastic about the
drug, these effects will be even stronger. But that is no guarantee that
benefits will last.
Placebo effects may therefore be particularly common when drugs are
new. It has sometimes been suggested, rather wryly, that physicians should
prescribe new agents before they stop working. I know a few colleagues
who always prefer the latest drugs on the market over the most established
ones. I take the opposite view, favouring drugs that have been around for
years, and whose therapeutic effects (and side-effects) are better known.
Old drugs are often just as good, if not better, than new ones. They are also
much cheaper. But the wish to be up to date influences physicians to use
newer, more expensive, but potentially less effective agents.
The pharmaceutical industry
One would think that inexpensive drugs would be a boon to mental health
practice. Actually, the prescription of any drug goes down sharply the day
after it becomes generic (Avorn, 2004). One recent study found that the
prescription of brand-name antidepressants decreases when patents run out,
and that many physicians prefer the latest (more expensive) agents (Bolton
et al, 2012). These observations demonstrate how strongly pharmaceutical
marketing influences practice. Physicians, impressed by the latest option, or
curious to try it out, do not want go on using yesterday’s agent.
Industry knows about these attitudes, and takes good advantage of them.
Drug companies naturally try to extend their patents as long as they can.
But even when patents eventually run out, Big Pharma has a few tricks up its
sleeve (Goldacre, 2013). A favourite is to market an ‘extended release’ form
of the same drug, which can then be sold at the old price. Some physicians,
and many patients, are fooled by this ploy. A capsule that releases a dose
slowly over the course of the day might be useful in a few clinical situations.
Yet by and large, there is no evidence that extended release makes any
difference for psychiatric drugs, almost all of which can be taken once a day
with no loss in effectiveness. No data support the superiority of extendedrelease formats over standard forms of antidepressants, or show any effects
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different than taking drugs once a day at bedtime (when patients are most
likely to remember to do so and therefore be ‘adherent’). Another trick is to
re-market the same drug in isomeric form. While this ploy extends patent
protection, it does little to help patients.
Drug companies spend most of their budgets on programmes to get
physicians to prescribe products that remain under patent. The multibillion
profits of industry show how effective these strategies are. The simplest
way to market a drug is by advertising. But although glossy ads in medical
journals promote half-truths, their scientific limitations have not made
them disappear. I edit a psychiatry journal, and we do not subject our
advertising to peer review. Without advertisements, we would have to shut
down our operation completely, so all I can do is to hope that our readers
ignore them. About 20 years ago, JAMA learned the hard way about the
power of the pharmaceutical industry. After publishing articles criticising
the information provided in drug ads, several large companies stopped
advertising in JAMA entirely, nearly bringing the publication down, and
forcing the editorial board to resign en masse (Angell, 2004).
Industry has other effective strategies to influence physicians. The main
one is a small army of pharmaceutical representatives, hired for charm and
good looks. Small gifts such as calendars and pens are common, and some
of my colleagues go to expensive dinners with ‘drug talks’ at the company’s
expense. But personal contact is more important. Representatives drop
by physicians’ offices and encourage them to try the latest drugs. Often,
free samples are provided to get things started. That is why I see indigent
patients coming for consultation who have already been prescribed the
most recently developed and expensive agents.
It has been sometimes claimed that pharmaceutical companies should
be less strictly regulated, since industry needs to invest in developing new
drugs (Goldberg, 2010). But that is not how drug companies spend their
money. Developing a new agent can cost many millions, and investments
can be completely lost if the drug fails to deliver. The high risk of drug
development is the reason why the pharmaceutical industry prefers to
market the drugs it already has, or to develop variants of existing agents.
While some truly new drugs for cancer have been developed in recent years,
in psychiatry, almost every new agent has been a ‘copycat’ product that
resembles those that have long been on the market.
We are in need of better drugs. Yet there have been no notable
improvements over the past 20 years – not even in side-effect profiles.
Most of the great advances in psychopharmacology occurred 40 years ago.
Psychiatrists could practise quite effectively only using agents available
in the 1970s. Atypical antipsychotics are no more effective than typicals
(Lewis & Lieberman, 2008). Second-generation antidepressants are no
more effective than tricyclics, and there is little reason to believe that any
one of them is better than any other (Cipriani et al, 2009; Gartlehner et al,
2008). Anticonvulsant mood stabilisers are no better than (and usually
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inferior to) lithium (The BALANCE Investigators and Collaborators, 2010).
If psychiatrists could practise perfectly well with a 1975 pharmacopeia, the
glory days of psychopharmacology may be behind us. This is unfortunate.
Everyone knows that antidepressants that worked faster and more
consistently would be a great advance. But no one knows how to develop
them, and industry is not seriously trying.
Another way that Big Pharma markets new drugs and gets physicians
to adopt them is by paying for the services of prominent academics, often
called ‘key opinion leaders’. This does not mean that these experts run
clinical trials, as these studies are run by industry using their own protocols.
Instead, companies provide large sums of money to university-based experts
for giving ‘drug talks’. These lectures are infomercials masquerading as
‘continuing medical education’ (Carlat, 2010). A common tactic in an
industry-sponsored drug talk, for example, is not to praise the sponsor’s
product, for that would be too obvious, but to say something critical about
all of the sponsor’s competitors.
Thus if you are a researcher with a high reputation, you do not have to
make do on your salary, but can earn millions from ‘consultant fees’ and
paid speaking tours. Top academics are also funded for ‘consultations’ that
take place at luxury resorts. I am ashamed to acknowledge that psychiatrists
take more money from industry than any other specialty in medicine
(Angell, 2004; Carlat, 2010). That could be because psychiatric drugs are
used so widely, making us more likely to be solicited.
Interestingly, hardly any academic who earns a large income from industry
thinks he or she is doing anything wrong. It is easy to fool yourself that
you are ‘just providing information’, and that your relationship with drug
companies is a partnership that benefits patients. Carlat (2010) described
from his own experience how easy it was to be corrupted by industry
money. He eventually declined to speak on behalf of any drug, and started
a report on the internet that critically appraises all the latest developments
in psychopharmacology. Unfortunately, Carlat is an exception. Others never
seem to get the point.
Antipsychotic fads
Antipsychotic drugs are very effective for the purpose for which they were
developed – the management of psychotic symptoms. We need better agents
that could also relieve the negative symptoms of schizophrenia. But that is
not the most serious current problem in psychopharmacology.
Antipsychotics are being used for a wide variety of indications in patients
who do not have psychosis, in spite of serious side-effects. The prescription
of atypical antipsychotics as augmenting agents for major depression
without melancholia is particularly popular. This option can be effective in
patients with melancholia (Parker, 2005), but is only weakly supported in
mild to moderate depression (Nelson et al, 2008). Although the US Food
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and Drug Administration (FDA) has approved indications for some of
these agents, they are based on the minimum requirement of two positive
clinical trials, which are, needless to say, conducted by the manufacturers
(Paris, 2010a).
Of even greater concern, atypical antipsychotics are being used for some
of the same indications traditionally reserved for benzodiazepines: the
management of anxiety and insomnia (Comer et al, 2011). This practice
is not entirely new. When I was in training, there was a heavy advertising
campaign for Etrafon-D, a combination of the tricyclic amitryptiline and the
typical antipsychotic perphenazine. Today, adding atypical antipsychotics
to a cocktail has been made to seem less risky by the perception that they
are perfectly safe.
How did antipsychotic drugs, originally developed to treat schizophrenia
and mania, become the ‘new Valium’ of clinical practice? Quetiapine in
particular is being prescribed almost as a cure-all. Typical antipsychotics
were known to create serious problems, and I once saw a patient who had
developed symptoms of tardive dyskinesia after being prescribed Etrafon-D
for less than a year. Physicians have been made aware that atypicals,
although they do not have as many short-term side-effects, can create serious
long-term problems, such as large weight gain and metabolic syndrome.
This suggests that these agents should only be prescribed when absolutely
necessary, but that is not what is happening in the world or practice.
The pharmaceutical industry has successfully promoted the wider use of
these agents, while downplaying all the problems. Off-label prescriptions
in mild to moderate depression, as shown by a large-scale meta-analysis
(Maher et al, 2011) and a Cochrane review (Depping et al, 2010), are
not evidence based. Even so, antipsychotics are being widely prescribed
(Mojtabai & Olfson, 2011), and are particularly popular for anxiety
symptoms, another practice not supported by clinical trials (Comer et al,
2011). The practice of adding an antipsychotic to a treatment regime when
patients fail to respond to antidepressants contributes little to outcome
(Fullerton et al, 2011), except in melancholic depression (Shekelle et al,
2007). Nor is there good evidence for using antipsychotics as a primary
treatment for depression, as I sometimes see done in patients coming for
consultation. The real reason for this practice is that patients often do
not respond to antidepressants. In such cases augmentation may be more
attractive than psychosocial interventions.
Today antipsychotics are prescribed for all kinds of symptoms. But this
particular hammer makes many things look like nails. Their routine use
for insomnia is another fad, even though other, much less risky options are
available, such as benzodiazepines or sedating tricyclics. Antipsychotics
may also be offered to patients with borderline personality disorder, even
though their effects are marginal and consist mostly of sedation (Stoffers et
al, 2010). These drugs are considered to be contraindicated in dementia, in
which they increase mortality (Lee et al, 2004; Schneider et al, 2006), but old
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age psychiatrists still use them for lack of a better alternative. In summary,
the widespread prescription of antipsychotics to patients who do not have
psychosis shows insufficient concern about efficacy and safety. Long-term
side-effects could eventually lead physicians to regret these choices.
This fad also demonstrates the power of marketing. For example,
olanzapine was aggressively promoted, leading to record profits for
its manufacturer. The even greater success of quetiapine, an atypical
antipsychotic that differs little from its older competitors, can also be
explained by a massive marketing campaign supporting its prescription.
Recently, for similar reasons, aripiprazole has had a great deal of success,
in spite of lower potency and a thinner evidence base.
I was trained to respect antipsychotics, which means I recognise their
power but fear them. I am amazed at how few physicians think twice about
writing these prescriptions. And the doses can be almost as amazing. It is
no longer surprising for me to receive for consultations patients who are
on 500 mg of quetiapine, a dose usually reserved for psychosis, given when
lower levels failed to control anxiety and depression. If even those higher
doses failed, patients were sent for consultation.
Of all the psychiatric fads current today, the overprescription of
antipsychotics is probably the most harmful. At least psychoanalysis only
wasted people’s time. Giving powerful drugs to almost every patient in
psychiatry is not even a mistake. It is foolish.
Antidepressant fads
Antidepressants are effective when used properly. As we have seen, the more
the clinical picture approximates melancholia, the better they work. Some
patients with severe depression will need augmentation with antipsy­chotics
or lithium (Parker, 2005). But these effects are unimpressive in patients who
fall within an overly broad definition of major depression, and are rarely
effective in people who are unhappy about adverse life circumstances.
Surveys show that antidepressants are often prescribed in the absence
of a diagnosis of depression (Mojtabai & Olfson, 2011). Sometimes these
agents are given in the context of a life crisis. Then, when the patient
got better, which might also have happened with no prescription, the
improvement is attributed to pharmacotherapy (post hoc, ergo propter hoc).
Often, patients are kept on these drugs for years because of fear of a relapse.
And patients themselves are so afraid of a relapse that they sometimes claim
to fall apart after missing a single dose.
In my work as a consultant for physicians in primary care, most patients
I see are already on antidepressants (unless they refuse to take them). The
individuals sent to a specialist are those who fail to respond, sometimes to
multiple agents. That is why about half of my consultations concern what is
misleadingly called ‘treatment resistance’ (misleading because one cannot
speak of resistance when one does not know what one is treating). The
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search for the ‘right’ antidepressant for patients ‘resistant’ to treatment can
be futile, given evidence that almost all of these agents are equally effective
(Cipriani et al, 2009).
I understand why antidepressants are overprescribed by busy
practitioners, who lack the time or the skills to fully explore their patients’
life circumstances. Moreover, since response is so variable from one patient
to another, if there is little else to offer a patient, and if antidepressants have
not been tried (or have only been given in subtherapeutic doses), they may
be worth a trial. But I advise consultees not to be overly aggressive. If more
than one agent has already been tried, I do not usually suggest going to
another, since effectiveness studies suggest that a law of diminishing returns
kicks in after two tries (Rush et al, 2006). I rarely recommend pursuing
augmentation strategies with antipsychotics, which have not been shown
to be consistently effective in effectiveness studies (Valenstein, 2006; Fava
& Rush, 2006). The usefulness of multiple antidepressants is also unproven
(Rush et al, 2011), although there has been a successful, albeit not evidence
based, industry-promoted fad for adding bupropion to prescriptions for
serotonin uptake inhibitors. In summary, you can keep trying a new drug
or a new combination of drugs, but at some point you have to stop chasing
the illusion of finding the right mix. I advise my consultees to rethink these
clinical problems, and to ask why their patients feel low.
The vast majority of depressed patients I see face life adversities that
give them reasons for being unhappy. For example, on a recent (and not
atypical) day, I was asked to consult on medication regimes for a woman
whose husband unexpectedly abandoned her after a long marriage, on a
woman whose husband was dying of cancer, and on a man whose brother
had fired him from the family business. As far as I could tell, none of these
circumstances had been examined in any detail before prescribing drugs.
And not surprisingly, all these patients were ‘treatment resistant’, in spite
of aggressive psychopharmacological interventions.
I am not saying that circumstances provide a complete explanation for
mood symptoms. I agree that clinical depression is an exaggerated response
to stressors that do not consistently cause illness in everyone. In the
past, psychiatrists emphasised psychosocial factors to the point of being
‘brainless’, only later becoming ‘mindless’ (Eisenberg, 1984). However,
to treat depression after a life adversity as a purely medical problem,
and to be surprised when that strategy proves insufficient, is irrational.
Unfortunately, the climate of modern psychiatry leads physicians to ask
the wrong questions. Instead of reframing problems on a human level, they
only want to know whether they need to be prescribing a different drug.
Mood stabiliser fads
Patients are often overdiagnosed with bipolar spectrum disorders. If one
assumes that mood swings are pathogonomic of bipolarity, anyone who is
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moody – adult, adolescent or child – can be diagnosed. And while many more
patients are being given lithium or anticonvulsant mood stabilisers, clinical
trials do not support this expansion of drug treatment (Patten & Paris, 2008).
I specialise in personality disorders. (These patients take me away from
consultation into the challenging world of treating severe psychopathology.)
These days most of my patients have been diagnosed with bipolar
disorder at some point, and given mood stabilisers, often accompanied by
antipsychotics. The NICE guidelines (Kendall et al, 2009) do not support
the use of these drugs in borderline personality disorder, but if a psychiatrist
thinks that these patients have bipolar disorder, they will treat them in that
way. Many physicians seem irresistibly attracted to this fad. Since mood
stabilisers are sedatives, some patients feel a little calmer on these agents,
but effects are in no way specific. After all, even the most powerful drugs
can act as placebos.
I have written a book about why these practices are wrong (Paris, 2012).
Mood swings are a key symptom of borderline personality disorder. Unlike
hypomania, which emerges spontaneously, mood shifts are environmentally
responsive, change by the hour rather than by the week, and do not respond
to treatment with mood stabilisers. Nonetheless, some patients become
attached to the medications they have been given and continue to believe
they have a disorder with a specific pharmacological remedy. If they knew
that bipolar disorder has a much more serious prognosis than personality
disorder, they might feel differently. Personality disorders are difficult
clinical problems, and I feel a responsibility to advocate on the behalf of
these patients. They were mistreated when I was young, and still are. The
difference is that instead of being offered 5 years of psychoanalysis they
could not afford, they are prescribed five drugs they do not need.
Adjusting medication
One of the more problematic aspects of current psychiatric practice is the
use of medication ‘adjustments’. When patients see a physician for a checkup they are asked about their current symptoms. If they are feeling better
or about the same, then the current prescription will be renewed. But if
they do not feel better, then the regime is likely to be changed, either by an
increased dose or a new agent. These procedures treat mental disorder as if
it were a chemical imbalance susceptible to titration. Such procedures make
sense in the management of diabetes, but are not evidence-based practice
for mental disorders.
When a physician starts new medications, they have to make adjustments.
Generally one increases the dose until a clear response is apparent. If sideeffects are problematic, the dose may have to be decreased. In severe cases,
there can be indications for adding a second medication for augmentation.
A second drug can also be prescribed to target other symptoms (such
as insomnia). But once a response is obtained, there are few reasons to
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change the prescription. In depression, patients often stay on the same
treatment for 6 months to a year, after which one can try stopping it. This
means that some patients can eventually be taken off drugs, but those who
experience a relapse have to be managed on the same regime for years to
come (Hansen et al, 2008). Unfortunately, many physicians are reluctant to
stop antidepressants, so they never find out whether maintenance therapy
was actually required. Also, since in many patients medication shows only
partial results, frequent changes in medication are common. I have seen
quite a few patients who become attached to having their medications
adjusted, which makes them feel attended to and cared for.
Medication adjustments are based on the assumption that changes in
symptoms are a reflection of innate instability. In this view, brain chemistry
has a nasty way of getting out of joint, and a chemical imbalance can be
corrected by adjusting a drug cocktail. But there are many other reasons
why people feel better or worse at any particular time. Obviously, life
circumstances can and do change. A psychiatrist will not find out if all they
do is ask about symptoms.
Second, practitioners make the cognitive error post hoc, ergo propter hoc.
The tendency to explain everything that happens to patients on the basis
of the last treatment intervention is not unique to psychiatry, but manages
to confuse both physicians and patients. Clinicians often fail to recognise
placebo effects, and relapse may be due to life circumstances rather than
fluctuations in neurotransmitters.
The cult of medication adjustment reflects the theoretical orientation of
psychiatry and the training of its practitioners. When leaders in the field focus
almost exclusively on neural networks and neurochemistry, one can hardly
expect practitioners to see things differently. A new breed of psychiatrist
has emerged, a specialist knowledgeable in psychopharmacology, but at a
loss when asked to talk to people about their lives.
Prescriptions without end
It is estimated that 11% of the adult population in the USA is now taking
antidepressants, which represents a 400% increase over the past two decades
(Pratt et al, 2011). Some patients are on these drugs for life. Although it
is well established that depression can be chronic, and that patients may
need maintenance treatment (Geddes et al, 2003), it is not always obvious
who requires maintenance. It can be an evidence-based practice for patients
with recurrent and severe unipolar depression, but it is not necessary for
all patients who meet criteria for major depression at some point in their
lifetime. Fortunately, the long-term side-effects of antidepressants are fairly
benign. Yet that is just what makes it tempting for physicians and patients
to take the path of least resistance and prescribe for the long term. And if
patients who do not have psychosis are on maintenance treatment drugs
with antipsychotics, the practice is more worrisome.
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Patients are often given multiple drugs, as much out of frustration as out
of an evidence-based therapeutic plan. Polypharmacy, which means patients
take four or five drugs for years, develops gradually (Zanarini et al, 2001).
When patients do not respond to initial therapy (with an antidepressant
or an atypical antipsychotic), they may be given a drug from another major
group, and this ‘augmentation’ procedure continues, even when the revised
regime does not help much.
Psychiatrists often prescribe drugs off-label, with or without
encouragement from pharmaceutical representatives. This is part of a larger
trend in which most patients are managed with polypharmacy (Mojtabai
& Olfson, 2010). One of the more striking features of modern practice
is that no matter what the diagnosis, patients can receive a cocktail that
includes at least one antidepressant, an antipsychotic, a mood stabiliser,
and a benzodiazepine. Polypharmacy has never undergone systematic
clinical trials (Mojtabai & Olfson, 2010). One sometimes hears multiple
prescriptions defended on the grounds that mental disorders are complex
problems that require complex solutions (Ghaemi, 2002). But in the
absence of research, they may simply reflect a fad.
The prescription of drugs should be cautious and supported by systematic
clinical trials. Moreover, these trials need to be fair, and not ‘fixed’ to obtain
a predetermined outcome (Healy, 2012). New drugs are regulated by
government bodies, and are only supposed to be approved when empirical
data are sufficient. But that is the ideal. Drugs are often allowed on the
market on the basis of two or three studies, which do not provide enough
data to justify a meta-analysis (Brooke et al, 2005; Paris, 2010a). And in
practice, physicians can do much as they please.
Psychopharmacology, which should be, and often is, scientific can
sometimes reflect fashion more than science. This need not happen. A
more conservative and more effective practice would be to prescribe drugs
sparingly with more specific targets and goals.
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Chapter 8
Psychotherapy
I was trained at a time when psychotherapy, particularly psychodynamic
therapy, was a central focus for psychiatry in the USA. Today, these
methods play a more marginal role in practice, and CBT, now the favoured
approach, is usually farmed out to other professionals. Talking therapy
requires expensive human resources. Although psychiatrists report carrying
out psychotherapy in practice (Mojtabai & Olfson, 2008), these are not
necessarily formal or systematic interventions.
This field has also suffered from its share of fads and fallacies.
Psychotherapy is an evidence-based treatment; however, it is not always
effective and can sometimes be harmful (Paris, 2013a). Ironically,
psychiatrists receive more consistent training in psychotherapy than
psychologists and social workers (Weissman et al, 2006), who provide most
of the services.
From the creation of psychotherapy in the late 19th century, many
professionals have been puzzled about how ‘just talking’ helps people with
mental disorders. Patients often ask the same question. Yet in common
mental disorders, talking therapies give drugs a run for their money. In a
landmark meta-analysis, Smith and colleagues (1980, p. 10) concluded:
‘psychotherapy benefits people of all ages as reliably as school educates
them, medicine cures them, or business turns a profit’. But of course
medicine does not always cure, business does not necessarily make a profit,
and psychotherapy does not always work. Even so, talking therapies work
often enough to be an important option, particularly when pharmacological
interventions are not particularly effective.
Still, there are serious problems with the current practice of psychotherapy.
Goals are often unclear and treatment often goes on for too long, sometimes
interminably. I was taught to see patients once or twice a week for several
years, and practised in that way for some time. Eventually, I realised this
kind of treatment is neither effective nor cost-effective. It can go on forever,
in endless circles of ‘cyclotherapy’. At one point, I took a sabbatical from
practising therapy and concentrated on reading the research literature. I
learned that most of what I had been taught was wrong. Although the main
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founder of psychotherapy, Sigmund Freud, had many ideas that remain
useful, he was the source of many of the problems that continue to bedevil
the field.
Psychoanalysis had all the features of a fad. It sprang from one person’s
bright idea, was unsupported by evidence, but spread like wildfire. Ever
since, faddish methods and fallacious reasoning have infected all other
forms of psychotherapy. Ever since Freud, therapists have been keen to
define their methods as unique, and to give them brand names.
Research suggests that psychological treatment is not a specific
technical intervention, but a healing relationship. Its most essential
elements: attentive, open-ended listening, empathy, and the provision of
an explanatory narrative, can be found in virtually every method (Frank &
Frank, 1991). These are the ‘common factors’ that best predict outcome
(Wampold, 2001). Yet even when provided, they do not guarantee a good
result and more specific methods may still be needed to manage specific
problems.
Psychotherapy research
Psychotherapy needs to be based on research in much the same way as
psychopharmacology. It must be rooted in science, not authority or rhetoric.
Outcomes can and should be held to the same standard as drug therapy,
and treatments should not be prescribed unless supported by clinical trials.
Clinicians should never accept anecdotes as proof, but demand that talking
therapies be tested systematically for efficacy.
Psychotherapy is not a benign procedure. It needs to be regulated,
in the same way as drugs are. But no government agency is asked to
approve any method, so that oversight of what goes on in practice,
or who offers treatment, is very loose. Up to recently, almost anyone
could claim to be a therapist or a ‘counsellor’ without challenge. Even
when a master’s or a doctoral degree is required, nobody checks up on
the product delivered to patients. Unfortunately, treatment sometimes
consists of little but sympathetic listening. Patients have no assurance that
they are receiving evidence-based interventions. Moreover, psychotherapy
usually costs money, something that most patients lack. In the UK,
psychological therapy is funded by the National Health Service (NHS), but
treatment by well-qualified psychologists is difficult to access, whereas to
receive psychotherapy in the USA, a person needs to either be financially
comfortable or have generous insurance coverage.
The first clinical trials of psychotherapy were conducted about 50
years ago, about a decade after these methods were applied to medicine.
Within a few years, the research literature became voluminous, leading to
the publication of a Handbook of Psychotherapy and Behavior Change (Bergin
& Garfield, 1978) that summarised thousands of studies. This standard
textbook has now reached a sixth edition (Lambert, 2013).
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One of the main findings of research is that psychotherapy is useful for
a variety of psychological problems, and equals medication in effectiveness
for common mental disorders (Wampold, 2007). The second crucial finding
is that most psychotherapies work in much the same way, and produce
about the same results. The literature does not support the existence of
the hundreds of methods that are now available. The mechanisms behind
these ‘common factors’ have been known for decades (Frank & Frank,
1991). Patients benefit from treatment if they are motivated, if they
work well with the therapist, if they can talk freely about their deepest
feelings, and if they explore practical alternatives to deal with current
problems. Thus, the proliferation of so many therapies with different
names is a marketing phenomenon that is contrary to existing data, with
no evidence for the superiority of any approach, or even for a matching of
symptoms and methods. It is reminiscent of the claims for the superiority
of one antidepressant over another. The failure to find differences between
methods in head-to-head comparisons has been called a ‘dodo bird effect’
(Wampold, 2001), a reference to a scene in Alice in Wonderland, in which the
bird informs participants in a race that all have won and all shall have prizes.
If psychotherapy works in much the same way in all effective methods,
then therapists should focus more on common factors and less on specific
methods. There could only be one form of psychotherapy, making use of
the best ideas from all sources. A movement for ‘psychotherapy integration’
(Norcross & Goldfried, 2005) has been around for some time, but in a
competitive environment has thus far failed to gain adequate traction.
Does the importance of common factors mean that psychotherapy works
as a placebo? Yes and no. Yes, in the sense that any process that promotes
hope promotes healing. But no, in the sense that well-structured treatments
are generally more effective than watchful waiting, monitoring or chatting.
There is also strong evidence that some therapists are much better than
others (Wampold, 2001).
What distinguishes formal psychotherapy, which is expensive, from lowcost interventions by non-professionals? ‘Befriending’, the provision of a
sympathetic ear by unpaid volunteers, can be effective for mild depression
(Mead et al, 2010). But that kind of case is not typical of psychotherapy
practice. By and large, the more severe the problem, the more patients need
specific methods. For example, in borderline personality disorder, clinical
trials consistently find that structured methods designed for these unusually
challenging patients are better than ‘treatment as usual’ (Paris, 2010b).
As a consultant, I see many people who tried psychotherapy but failed
to benefit from it. That makes me wonder about the quality of the product
they received. Quite a few patients describe a course of treatment in which
a therapist listened but offered little feedback. This can be a distorted view
of what happened, but all too often, much of what passes for professional
intervention is little but ‘hand-holding’. Support may be enough for
transient symptoms, but not for chronic and more severe problems. One
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gets the impression that some therapists consider it sufficient to listen
and sympathise with patients as they report the details of their week. That
creates an endless cycle leading nowhere. Being totally non-specific turns
therapy into mush.
Even in the best hands, psychotherapy can fail. Outcome depends partly
on patient characteristics (Lambert, 2013). By and large, patients with
better functioning get more out of therapy, so that the rich get richer and
the poor get poorer. Therapist skill also plays a role, although this factor
tends to be exaggerated by those who embrace brand names.
When psychotherapy does not work, it needs a rethink. All too often,
psychotherapists try for too much, and continue treatment for too long.
This can lead to endless therapy, assuming the patient, or the insurer, can
afford it. Crucially, there is no evidence that long-term therapy is effective.
Some researchers (Leichsenring & Rabung, 2008) have claimed evidential
support for the efficacy of long-term therapies. But the evidence for these
conclusions is very weak. Their meta-analyses were based on studies with
small samples with small effect sizes, describing treatment for a very wide
range of problems.
Almost all the research supporting psychological treatment has examined
short-term interventions lasting a few months. The mean length of therapy
that is effective is usually about 20 sessions (Norcross & Goldfried,
2005). Thus, continuing psychotherapy for years on end is not evidencebased. Unfortunately, the practice is all too common. It is not specific to
psychoanalysis, but can affect therapists of every theoretical persuasion.
In common mental disorders (anxiety and depression), patients can be
offered a choice between medication and a brief course of therapy. Some
will prefer to talk, whereas others will prefer to take a pill. But in practice,
patients are not necessarily given these options. Psychiatrists and family
physicians may have their prescription pads open from the early stage of
an interview.
The decline of formal psychotherapy in psychiatry is well documented in
the USA (Mojtabai & Olfson, 2008), and the situation is not that different
in the UK. The NHS is working to make it more available, and there is a
formal initiative for improving access to psychological therapies (the IAPT
programme; Turpin et al, 2006). However, the human resources to make
this work are not always available.
A prominent British psychiatrist (Craddock et al, 2008) has objected
to any diversion of resources by the NHS to psychology, on the grounds
that talking therapies are more appropriate for mild problems in primary
care than for the severe disorders seen by psychiatrists, and that medical
treatment should take priority. There is a grain of truth in this critique.
Common mental disorders, often reactions to adverse life circumstances
(U’Ren, 2011), do not necessarily require medical management. Yet
when patients go to psychiatrists or family physicians with depressive or
anxious symptoms, drugs may be routinely prescribed, whereas appropriate
referrals for psychotherapy may not even be considered.
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Evidence-based psychotherapy
All psychotherapies are more or less equal, but some are more equal than
others. Let us try to separate methods that are evidence-based from those
that are not.
Formal psychoanalysis was not based on evidence. That is the reason it
has been dying out. Freud’s approach has been refined into psychodynamic
therapy, a kind of ‘psychoanalysis lite’ in which patients are seen once or
twice a week for a few years, yet even with this modification, treatment is
not evidence based. The only version of psychodynamic therapy that can
be considered firmly evidence based involves interventions lasting a few
months (Leichsenring et al, 2004). No research supports the use of any
therapy for more than a year. It is possible that some patients do require
more time, but we need data to support that practice. Otherwise therapy
can become little more than an extended form of befriending.
Cognitive–behavioural therapy has the strongest evidence base of any
form of psychotherapy (Beck, 1986, 2008), but was specifically designed to
last for a few months. It is now the best-known (and most asked-for) method.
Even so, it cannot claim to be uniquely effective. Head-to-head comparisons
with other well-structured methods have not shown its superiority, either
in depression (Elkin et al, 1989), or in personality disorders (McMain et
al, 2009). Where CBT therapists have been most creative is in developing
toolkits for almost every symptom seen in psychiatric practice.
Cognitive–behavioural therapy also capitalises on the common factors
that make talking therapy effective. Like any well-structured treatment, it is
better than placebo or ‘treatment as usual’ (i.e. the unstructured and messy
reality of clinical practice). Its only real competitor, interpersonal therapy
(Klerman & Weissman, 1993), is not that different, since it also focuses
on solving current problems. Despite claims of improvements on CBT, one
of these methods, acceptance and commitment therapy (ACT; Hayes et al,
2006), is little but a variant of concepts that Beck developed decades ago,
packaged with a new three-letter acronym. If a single, evidence-based form
of psychotherapy emerges in the future, it will probably look a lot like CBT.
How effective are psychological interventions for the severe mental
disorders that psychiatrists concentrate on? Cognitive–behavioural
therapists have developed interventions to reduce the effects of delusions
in schizophrenia (Turkington et al, 2006) and similar methods have been
applied to bipolar disorder (Jones, 2004). Clinical trials show these
interventions, often linked to family psychoeducation, to be efficacious
(Garety et al, 2008).
Personality disorders can also be severe in their effects on longterm functioning. In borderline personality disorder pharmacological
interventions are not very effective but psychotherapy often is (Paris,
2008b). (That is why I remain active as a therapist, working in specialised
clinics.) But that does not mean that any unstructured therapy can help
these highly troubled patients.
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The proliferation of psychotherapies
There are now hundreds of ‘brands’ of psychotherapy, each claiming to
be useful for a wide variety of problems. Yet only a few have undergone
systematic clinical testing. The existence of so many brands of treatment
suggests that the history of the field could be a story of one fad after another.
Why cannot therapists agree on one method and stick to it?
The reason is that psychotherapy is a crowded and competitive market.
There is real money to be made by developing a new approach. That is
why each brand of therapy is presented as unique, even if almost all are
variants on a theme. For marketing purposes, three-letter acronyms give
an impression of scientific support. (Some wags have suggested that four
or five letters would yield even better results.)
The proliferation of therapies is a reflection of the way that psychological
treatments are marketed to mental health professionals. Marketing works
because psychotherapists are poorly trained in science (Dawes, 1994).
Freud, indifferent to research, established a tradition that encouraged
speculation, not data collection. Anecdotes were treated as conclusive
evidence. Everyone who followed Freud did much the same thing, writing
books based on clinical experience, not on clinical trials.
Practitioners of psychotherapy may not read the scientific literature on
their craft, or pay attention to what it shows. Many have a doctoral degree,
but few make much use of it. This is particularly likely for therapists
working outside of academic centres or the NHS. Unlike physicians who
prescribe drugs, no industry representatives come to offices to encourage
psychologists to adopt a brand of psychotherapy. They read about a new
method, or hear about it, and try it out. The doubt that characterises
scientific thought does not fit well with the enthusiasm that sometimes
drives clinical practice.
The ‘guru’ tradition in psychotherapy means that ideas may be more
associated with a person than with data. Therapists with an idea can create
a niche through articles, books and workshops, and make a financial profit.
I know of some experts who spend much time travelling, and who expect
a first-class ticket, a hefty fee, and a book-signing opportunity. Like key
opinion leaders in psychopharmacology, they fall victim to the appeal of
money and fame. Moreover, the rise of psychotherapy gurus, with apostles
and acolytes to spread their ideas, has affected every single method,
including CBT. Even though CBT is the therapy most committed to clinical
trials, it does not always work, which can lead its practitioners to go on
seeing patients for years, just like psychoanalysts.
Psychotherapy is a complex procedure that no one can fully master. A
gap also remains between what evidence-based treatments can do and what
patients need, as many problems have never been addressed by empirical
research. But practitioners who belong to the psychotherapy culture are
looking for answers, not questions.
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psychotherapy
Psychotherapy fads: benign and malignant
Benign fads
Psychotherapy fads can be benign, when they are little but variants of
already available and evidence-based methods. Or they can be malignant,
introducing procedures that have not been tested and that can do real
damage.
Eye movement desensitisation and reprocessing (EMDR; Shapiro, 1995)
is an example of a benign fad. It is as good as (but no better than) existing
methods and has been associated with another fad, the overdiagnosis of
PTSD. The method was developed by an American psychologist, Francine
Shapiro, who also skilfully marketed it. It has long been known that
cognitive reprocessing of traumatic events helps people with PTSD (Bisson
et al, 2007). In EMDR, patients are asked to carry out eye movements while
remembering traumatic experiences. In an EMDR session that I watched,
the therapist waved a wand back and forth in front of the patient. I was
reminded of the 18th-century physician Franz Anton Mesmer, and his
famous method of ‘animal magnetism’.
Careful comparisons show that EMDR is no better than standard
methods, and that eye movements are not a necessary element (Seidler &
Wagner, 2006). Yet EMDR has become a business, producing a product with
brand recognition. It may help some people, but its wide adoption is a fad.
This story is typical for psychotherapy. Standard methods often work. There
is no need to get excited about the latest therapy or the latest acronym.
Malignant fads
Malignant fads are different. These methods do not draw on common
factors but depend more on drama: patients screaming in rage, or past
events emerging into consciousness as in a movie. They take the worst
aspects of psychoanalysis and turn them into a caricature.
Recovered memory therapy is the best example. In the course of the
1990s, this idea had a great vogue (McHugh, 2008). Building on Freud’s
idea that adult problems are rooted in childhood experiences, and that
memories of these events can be ‘repressed’, it proposed to exorcise these
devils. It often used hypnosis, a highly suggestive technique, to convince
people that false memories are true. These methods are rarely used today,
but they have not entirely died out, and are a classic illustration of the
danger of fads.
Freud was totally wrong about memory. Most life events are not
permanently recorded in the brain, and those that are will be modified by
later experiences (Schacter, 1996; McNally, 2003). Moreover, false memories
are common (Loftus & Davis, 2006). So why did the idea that patients can
‘recover’ memories gain popularity among therapists, patients and the
educated public? Largely because remembering a traumatic experience, a
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phenomenon beloved by the cinema, was highly dramatic. These methods
sometimes created ‘multiple personalities’. And the consequences went
beyond the consulting room, as some began to imagine that day-care
centres were hotbeds of child abuse.
The self-esteem fad
Psychotherapy has been susceptible to fuzzy concepts and buzzwords that
claim to explain what it does. In the time of psychoanalytic dominance, the
paramount idea was that understanding the unconscious and the past was
the ‘royal road’ to a cure. For CBT therapists, modifying cognitive schemas
was the crucial element. In recent years, one of the most pervasive, albeit
empty, fads is the idea that therapy should promote ‘self-esteem’.
People like to feel good about themselves, but they have to do something
to deserve it. The cult of self-esteem is a quick-fix fad, promoted by media
personalities and infecting the practice of psychotherapy (Furedi, 2003).
I cannot count the number of patients who attribute their troubles to a
deficit of this elusive faculty. What the idea fails to take into account is that
self-esteem is a result of achievement – a person should value themselves
if they have contributed something to the world.
Twenge (2006) describes the cult of self-esteem as a cultural fad derived
from psychotherapy that has also come to influence parenting styles. The
belief that having a good opinion of oneself is a necessary condition for
success in life gets things backwards. Some of the people with the highest
opinion of themselves are narcissists and psychopaths (Baumeister et al,
1996). The rest of us are (quite rightly) more self-critical. Therapists who
promote pap about self-esteem are doing a disservice to clients. While some
people do have irrationally low opinion of themselves, self-esteem need not
be a direct goal, but an indirect by-product of better functioning.
Psychotherapy: treatment or cultural phenomenon?
In the modern age, people value individuality. If they seek therapy, they may
be attracted to self-exploration, promulgated as a positive value. We live in
a culture where people can actually be proud to be ‘in therapy’, proclaiming
the value of searching for meaning within their own psyche. Unfortunately,
the original purpose of psychotherapy, which was to relieve symptoms,
can be lost. Some patients become therapy addicts, spending many hours
looking for answers in the psyche, instead of in the world they live in.
Perhaps one need not complain too vigorously, but psychotherapy has
come to constitute a secular religion, and patients may embark on it as a
spiritual journey (Epstein, 2006). As long as no public money supports
such ventures, taxpayers are not being cheated. Yet there is still a price to
be paid. Some talented psychiatrists turn away from the care of severely
mentally ill patients to ‘treat’ individuals who may not in fact need their
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psychotherapy
help that much. One can sympathise with a wish to focus one’s career on
the treatment of people whose problems are milder and more tractable. But
that does not make doing so an ethical choice.
The good news is that psychiatrists now spend most of their time
doing what they are trained for, caring for patients with severe mental
illness. The bad news is that the division of the mental health professions
into biological and psychological camps, already described almost 60
years ago (Hollingshead & Redlich, 1958), undermines the prescription
of psychotherapy. The absence of an integrative perspective may also
discourage therapists from taking neuroscience into account. The continuing
split within the mental health professions has failed to give psychotherapy
its due.
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Chapter 9
Prevention
Primary prevention
Vaccines have saved more lives than antibiotics. It would be better to nip
mental disorders in the bud than to wait for them to develop and so it has
often been suggested that psychiatrists redirect some of their energies to
prevention (Bhui & Dinos, 2011). But how do you prevent something you
do not understand? The biological causes of severe mental disorders remain
largely unknown. Thomas Insel (2009), director of NIMH in the USA, has
suggested that whole genome scans could be used to identify vulnerability
markers. However, 10 years after the introduction of that technology, too
little has been learned and most of the studies using it have been fishing
expeditions.
One can accept that severe mental disorders are rooted in neurobiology
(Insel & Wang, 2010). Yet the devil lies in the detail. No single gene explains
more than a small percentage of variance, and there are no data showing
that even a few major genes can predict mental illness with any accuracy.
Moreover, most neuroscience models fail to consider interactions with the
environment, or to consider seriously the implications of epigenetics. The
idea that physicians can accurately predict risk for any individual remains
a pious hope.
Prevention of psychological adversities is also dubious. Life is full of
negative events of all kinds. And if you think that families are to blame for
some forms of mental disorders, just try regulating parenting. Although
some studies support the use of parental education to reduce the incidence
of behavioural disorders in children (Hutchings et al, 2007), it would
be premature at this point to generalise from samples in randomised
controlled trials to broader clinical populations.
Preventive psychiatry has emphasised social interventions that might
affect the prevalence of mental disorders (Paykel & Jenkins, 1994). There is
certainly evidence that social stressors (such as poverty and powerlessness)
are risk factors (Scheid & Brown, 2010; U’Ren, 2011). These findings may
have importance for global mental health (Patel & Prince, 2010). But we do
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Prevention
not always know how to make society better, and psychiatrists are hardly
the ones to make such changes.
At this point, primary prevention lacks a strong evidence base. Its
principles may be sound, but we are not yet in a position to use them. To
prevent mental illness, we need to know what causes it. By and large, we
do not.
Fifty years ago, some psychiatrists thought they knew – the patient’s
family was probably at fault. That is why prevention programmes of that
era focused on early child education and intervention (Caplan, 1964).
These proposals were grandiose and never implemented. Applying them
would have been expensive, and there was no consistent evidence that they
would have worked. In spite of promoting public education, mental health
professionals do not know any more than the average person about how to
raise children. And rates of mental illness are as high today as they were in
the recent past (Kessler et al, 2005b).
Another theory about mental illness, popular when I was a young
psychiatrist, was that society is to blame. This idea fit into a left-wing
political perspective, in which capitalism is blamed for everything. What
impressed me about social psychiatry was the passion of its advocates.
Preventive psychiatry crossed over from medicine to politics, and was not
committed to a cautious, evidence-based perspective. Today it is clear that
social change cannot be medicalised, and that psychiatry has its hands full
looking after people with severe mental illness.
Even so, social activism is not quite dead. It is still promoted by writers
such as the psychiatrist Joanna Moncrieff (2008) and the psychologist
Richard Bentall (2010). I agree with Moncrieff and Bentall that a psychiatry
based entirely on neuroscience is overly reductive. But then so is social
psychiatry, particularly when based on naive Marxism. Even if social forces
are risk factors, there is no evidence that making everyone wealthier or
more comfortable would reduce the prevalence of severe mental illness.
These disorders affect rich and poor, and are part and parcel of the human
condition. They can be traced back to every period of history, and are found
in every society (Shorter, 1997).
Secondary prevention
Secondary prevention refers to early identification of illness, even in
childhood, allowing for interventions to prevent its progress. A good
example concerns the early roots of criminal behaviour, classified by
psychiatry as antisocial personality disorder (Black, 2013). This condition
begins in childhood, sometimes in the pre-school years, as conduct disorder.
Since conduct disorder is one of the few diagnoses in psychiatry found in
behavioural genetic studies to be strongly shaped by the environment
(Cadoret et al, 1995), it has attracted attention of those interested in
preventing it.
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The Canadian psychologist Richard Tremblay has devoted his career
to this problem. His research team has produced some of the largest and
most important longitudinal studies of children followed into adulthood
(Tremblay, 2010). I have been fortunate to collaborate with him on a few
of these studies, but antisocial behaviour cannot easily be prevented.
Some studies from Tremblay’s group (Côté et al, 2007) have thus far
yielded unimpressive results. Problems tend to start very early, usually
with high levels of physical aggression. Adult outcomes are predictable
from observations at age 3 (Caspi et al, 1996), but no one knows how to
treat such children. One famous study claimed that antisocial behaviour
results from an interaction of a genetic variant (affecting mono-amine
oxidase activity) with maltreatment (Caspi et al, 2002), a finding that
has been replicated (Fergusson et al, 2011). But this relationship is more
statistical than consistent, and it is not clear how it can be used to guide
prevention. Tremblay (2010) has expressed hope that applying the findings
of epigenetic research could lead to useful interventions. At this point, a
Scottish verdict of ‘not proven’ must be invoked.
Another example of secondary prevention is the currently influential
movement to identify adolescents at risk of psychosis so as to treat them
early (McGorry et al, 2008). In psychiatry, most of the major disorders
tend to begin in adolescence, sometimes before their characteristic clinical
picture develops. However, there is no consistent evidence that early
diagnosis makes a difference in outcome, or that interventions are more
effective when instituted earlier.
A recent controversy centred on the concept of ‘risk psychosis’, or
what DSM-5 proposed to call ‘attenuated psychosis syndrome’. Patients
who eventually develop first-episode psychosis often have prodromal
symptoms, and it has been suggested that treating them before more severe
symptoms emerge might prevent sequelae from developing (Addington et
al, 2008). In Australia, under the influence of the well-known psychiatrist
Patrick McGorry, a national programme was put into place for the early
identification and treatment of such cases. Yet in spite of much research,
there is no proof that early treatment makes a difference for prognosis.
Two-thirds of those who have the attenuated picture never convert to
psychosis, leading to a large number of false positives (Cannon et al, 2008).
Thus, many patients would be treated unnecessarily. This is why the DSM5 manual did not include this diagnosis. This example also underlines
some of the pitfalls of secondary prevention. Identifying early markers for
psychopathology need not mean that there is a treatment that can change
the course of an illness.
Fallacies of suicide prevention
Of all the clinical dilemmas that psychiatrists face, the most troubling
concerns patients who kill themselves. Most of us have lost a few patients
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in this way. Suicide is also a leading cause of death in many countries
around the world (Hawton & van Heeringen, 2009), and it would be good
if we knew how to prevent it. Furthermore, if we were able to determine
which patients were most at risk, we could use this information to save
them. Yet at this point we do not know how to usefully predict or prevent
suicide (Paris, 2006).
Psychiatric trainees are taught to assess suicidal risk in specific ways.
They are instructed to ask questions, such as whether a patient has a
suicidal plan, has attempted suicide before, or has a family member who
died by suicide. Positive answers to these questions are supposed to point to
an increased risk. Yet carrying out such enquiries is not a tested algorithm,
or an evidence-based procedure. There are just too many false positives.
Even if frequent intervention could prevent a few suicides, we would have
to treat thousands with unnecessary hospitalisations to achieve such a goal,
hardly a cost-effective strategy.
Let us examine the research. Suicide is an uncommon outcome. When
one is trying to predict a rare event, even when risks have a statistical
relationship to outcome, most people with the risk will not have the
outcome, and most people with the outcome will not have the risk.
Identifying a population with an elevated risk for suicide completion is not
clinically useful because there are always too many false positives.
For example, although individuals who have made repeated attempts
are more at risk, most never carry out a suicide (Hawton & van Heeringen,
2009). Precisely the same conclusion applies to all other risk factors that
trainees are taught to assess: impulsivity, psychosis, serious medical
problems, high stress, poor functioning, lack of social supports, and a family
history of suicide. Most who carry any or all of these risks will not die by
suicide, and most of those who attempt suicide eventually stop (Maris,
1981; Paris, 2006). There can also be false negatives, in that patients who
kill themselves can lack any of these risk factors. Clinicians usually see
patients who are ambivalent about suicide. But most completed suicides
occur in people (usually men) who make a first attempt, and use guns
or ropes to ‘make sure’ (Beautrais, 2001). We cannot predict events that
entirely fail to come to clinical attention.
Although psychiatrists can identify statistical risks for suicide that
apply to groups, they cannot predict whether or not suicide will occur in
any single case. Large-scale studies that attempted to predict suicide in
very large populations of patients after admission to hospital found that
completion could not be predicted (Pokorny, 1983; Goldstein et al, 1991).
Even though some factors were associated with suicide, algorithms failed
to predict any individual outcome. That is why most psychiatric evaluations
for suicide are useless. They are driven by fear of litigation, not by research
findings.
If suicide cannot be predicted, it cannot be prevented. There is little
evidence that any specific intervention stops people from dying by suicide.
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Some experts take a more hopeful view (Mann et al, 2005), but when
it comes to suicide, good intentions are not good enough. In spite of a
dramatic growth in the numbers of mental health professionals and in the
prescription of antidepressants, suicide rates, although variable over time,
have not showed long-term change (Maris et al, 2000). Nor has there been
any reduction in the frequency of ideation, gestures or attempts (Kessler
et al, 2005c).
There is also little evidence that drugs reduce suicide rates. The most
convincing data come from studies of bipolar disorder (Cipriani et al, 2005),
showing that patients who take lithium have a lower rate of completed
suicide than those who do not. Some data also suggest that patients
with schizophrenia who take clozapine (but not any other antipsychotic)
have a reduced rate of suicide (Meltzer & Okayli, 1995). The case for
antidepressants is unproven (van Praag, 2003), with only suggestive and
indirect evidence from long-term follow-up (Leon et al, 2011). All these
studies have a problem in establishing causality. One possible explanation
is that patients who adhere to pharmacological regimes may be less likely
to die by suicide than those who do not adhere.
The best evidence that suicide can be prevented comes from primary
prevention using population health principles, by reducing access to fatal
means. A famous example was the lowering of rates that occurred when
Britain changed the content of natural gas provided to homes to reduce
the content of toxic fumes (Clarke & Lester, 1989). If society wants to stop
people from killing themselves, it could focus on that kind of intervention,
and not depend on psychiatrists making assessments of suicidality in clinics
and emergency rooms. It may be possible to do a better job of prediction
in the future, but for now we discredit ourselves by claiming to do the
impossible.
Hospitalising suicidal patients can be a fallacy. Doing so makes sense
in melancholic or psychotic depressions, in which treatment can rapidly
reverse the course of the illness. But for most clinical scenarios, it has never
been shown that patients are likely to die by suicide if sent home from
an emergency room, or that they will not do so if admitted to a hospital
ward. Predicting suicide from the presence of ideation or a history of past
attempts is not practical.
Moreover, in what way is a hospital environment ‘safe’? There is no
such thing as a safe place for patients who are intent on suicide. In order
to physically prevent suicide on a hospital ward, nursing procedures have
to be extreme. Patients may be put on a suicide watch, with someone hired
to sit with them 24 hours a day. Even so, and in spite of all precautions,
suicides do occur. The hospital environment is not helpful for those who
have made recurrent attempts, and it may even be harmful (Paris, 2006).
These patients belong to a different population from those who die by
suicide (Beautrais, 2001). Many have personality disorders. Chronically
suicidal patients may be admitted for suicidal threats, minor overdoses, and
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self-mutilation, but no specific treatment is offered on a ward that cannot be
provided in another setting. Often, the patient simply sits there while being
monitored and observed. This is not treatment. The longer a patient stays
in hospital, the more reinforcement they receive for being ‘suicidal’. I have
been asked to consult on patients who have spent up to 5 years on wards
because psychiatrists were afraid they would kill themselves if let out.
It has long been known that suicide rates vary over history and social
context (Durkheim, 1897). But there has never been a time or a society
in which suicide was absent. The aim of prevention is laudable, but the
thinking behind it is fallacious. This is not to say that psychiatrists never
do anything that might prevent suicide, but in the aggregate, the effects
are not striking. Psychiatrists might be best advised to focus on what they
know and to treat illness.
The future of prevention
When we learn what causes mental illness, we will have a better idea how to
prevent it. It is true that smallpox vaccination worked before anyone knew
about viruses or immunology. But that was a lucky break. Most advances
in prevention require precise knowledge. And when an outcome is rare, it
may not be cost-effective to attempt prevention.
Moreover, understanding the aetiology of a disease cannot always be
directly applied to treatment or prevention. A good example is cystic
fibrosis, in which a genetic flaw is well known, but in which therapy still
remains dependent on physiotherapy or lung transplant. Consider as well
the large-scale resources devoted in recent years to developing a malaria
vaccine. We are still working on that one.
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Part III. Antidotes
Chapter 10
Evidence-based psychiatry
The experience of being the editor of the Canadian Journal of Psychiatry taught
me a great deal about what to believe or what not to believe about medical
research. We do not accept articles based mostly on opinion, and routinely
turn down submissions which draw conclusions from small samples or lack
a control group. I suspect some of our readers find our standards too high,
and the prose of the articles we publish a little dry. But raising the bar is
one way of encouraging the practice of psychiatry on the basis of evidence.
Evidence-based medicine is a movement in its own right, and it has
greatly influenced the way medicine is practised (Evidence-Based Medicine
Working Group, 1992). It has been closely associated with two universities,
Oxford University in the UK and McMaster University in Canada. The
concept of evidence-based medicine was originated by a pioneering
British physician, Archibald Cochrane, whose name lives on in a series of
authoritative (and famously sceptical) ‘Cochrane reports’ on the efficacy of
medical treatments. Those of us who follow Cochrane are often surprised
to see just how little medical science knows.
Evidence-based medicine rests on a simple but powerful idea. An
editorial in the BMJ (Sackett et al, 1996) described it as ‘the conscientious,
explicit, and judicious use of current best evidence in making decisions
about the care of individual patients. The practice of evidence-based
medicine means integrating individual clinical expertise with the best
available external clinical evidence from systematic research.’
These principles can be applied to mental health practice. In a major
cultural shift, evidence-based psychiatry has become a force to reckon with
(Geddes & Carney, 2001). The influence of evidence-based medicine is
apparent in the changed content of all psychiatric journals. It is sobering
to read their contents from 40 years ago. Even the top journals were full of
case reports, case series and unsupported clinical opinions. Such articles
are now rarely, if ever, published. Instead, the pages of medical journals are
filled with quantitative studies that test hypotheses, as well as systematic
reviews and/or meta-analyses. It is no longer sufficient to have clinical
experience. You have to present empirical data.
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The gold standard in medicine is the randomised controlled trial (RCT),
designed to measure the efficacy of a treatment, that is whether it is
superior to placebo or to an alternative intervention. These observations
can be supplemented by effectiveness studies that examine how well the
treatment works in the messy reality of clinical practice.
Largely because of evidence-based medicine, the practice of psychiatry is
now expected to follow clinical guidelines, such as those published by NICE
and the American Psychiatric Association. These organisations publish
systematic reviews with conclusions based on the best existing empirical
evidence on treatment effectiveness. Although guidelines can be wrong
(and often are), it is better to have them than not to have them. At the very
least they provide a brake that discourages faddish treatment. By and large,
NICE guidelines and Cochrane reports represent the state of the art. But
since there is often not enough data to reach firm conclusions, they should
be viewed as a work in progress.
Some have criticised the application of evidence-based medicine to
psychiatry, and certain limitations are inevitable. Westen (2006) and
Ghaemi (2009) underlined problems with the generalisability of RCTs.
These studies tend to attract unrepresentative samples, i.e., patients with
less severe disorders, lower levels of comorbidity, and higher adherence.
Many individuals participate only after answering an advertisement. These
limitations make it difficult to generalise, even in the best studies, from
RCTs to practice. That is why I advise my trainees never to rely on single
studies, but to wait for replications and meta-analyses. No one should
change the way they treat patients on the basis of a single study.
Even meta-analyses can be flawed, particularly if they depend on data
drawn from unrepresentative RCTs. Also, given the judgement calls
required to decide what studies should be entered in meta-analyses, it is
not uncommon for two to offer different answers to the same question.
But that is the nature of science. Conclusions always depend on what is
accepted as good evidence.
This is also why most clinical practice guidelines lack high-quality data to
support their recommendations. When experts are forced to say something,
they will say more than they should. While NICE guidelines can usually be
counted on to be cautious, the American Psychiatric Association guidelines
often overstep the evidence. This problem can even affect Cochrane reports,
famous for their conservatism.
The lesson is that you have to remain critical, even of guidelines written
by academic leaders. Some of their recommendations reflect strong biases,
supported by cherry-picking the literature. One would like to believe that
experts are dispassionate, but most have strongly held points of view.
One cannot always trust researchers who have invested years in their own
research to be fair to opposing ideas.
While the basic principles of evidence-based medicine remain valid, it
can take many decades to collect the data clinicians need to make evidencebased decisions. Moreover, there is little information that can be used to
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guide most of the questions faced by physicians. Some of my colleagues do
not like evidence-based medicine because it does not tell them how to talk
to people, or how to be empathic and caring. But evidence-based practice
is not about communication, it is about facts. It need not be associated
with mindless empiricism or cold decision-making, or lead to algorithmic
diagnoses followed by routine prescriptions. The parlous state of modern
psychiatry cannot be blamed on science, which actually supports spending
more time with patients. The problem runs much deeper than that.
For some years, I have been in charge of an evidence-based medicine
seminar for psychiatric residents. I ask trainees to bring in clinical questions
arising from their work and to explore the literature for answers. Almost
without exception we find that research is insufficient to reach any
conclusion, and that many clinical principles that everyone knows to be
‘true’ have never been empirically tested. Some trainees find this exercise
discouraging, since they want answers to help their practice, and may view
Cochrane reports as depressingly conservative. But others find its cautious,
measured perspective a breath of fresh air.
The rise of evidence-based medicine reflects a change in the authority
of physicians and their relationship with patients. Patients are no longer
passive consumers of services. Many, quite rightly, expect to be informed
about their treatment, and to be a part of any decision-making process.
Some even arrive with printouts downloaded from the internet. This
makes clinical practice a little more challenging. Physicians used to be
expected to know the answers to any and all questions. Psychiatrists have
been particularly guilty of speaking from a position of authority, even on
issues outside their own area of expertise. Now physicians can sit down
with patients in front of a computer and look up answers together. Patients
can also be encouraged to go home and read about their diagnosis on a
reputable site. Medical practice has become much more of a collaboration.
In summary, the practice of evidence-based medicine promotes doubt,
not certainty. That is a good thing, mainly because doctors know much less
than they think they do. A few years ago I was explaining evidence-based
medicine to a humanities professor. Looking at me with dismay, he asked,
‘Do you mean to say that doctors haven’t always been practising on the
basis of evidence?’ The public has an absolute right to expect physicians to
base clinical decisions on scientific data.
Yet at this point, evidence-based medicine remains more of an ideal
than a reality. Many decisions in practice must still be based on clinical
experience. For example, choices as basic as deciding whether to hospitalise
patients are almost always made without data. But the percentage of nonevidence-based decisions will shrink gradually over time.
Conservatism, patience and evidence-based medicine
Fads are a poison, and the antidote is evidence-based psychiatry.
Nevertheless, psychiatrists still need to be critical about the quality of
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evidence. They can easily be fooled by a single study, most of which are
never replicated (Ioannidis, 2005). Agencies that approve drugs, for
example the Food and Drug Administration in the USA, set the bar much
too low, allowing agents to be put on the market after only two clinical
trials. That is why I never prescribe any drug that is new on the market and
this is also why established psychotherapies are better choices than newly
developed methods. To change one’s practice, one needs a large number
of trials in clinically representative samples, sufficient for meta-analysis
and pointing in the same direction. It is better to stick with tried-and-true
therapies until the weight of evidence supports something better. Following
these principles leads to a much more conservative approach to the practice
of psychiatry. That is just as it should be.
If even Cochrane reports can get things wrong, how can busy clinicians
make informed decisions? Moreover, clinical trials, however rigorous, are
not conducted in real-world samples. They point the way, but cannot guide
practice in any detail. That is why efficacy studies have to be supplemented
by effectiveness studies, in which researchers do not select patients, or
enroll a control group, but make systematic observations on what happens
naturalistically in a real clinical setting.
One of the most famous and most influential effectiveness studies in
this history of psychiatry was the STAR*D study, which drew on a large and
representative sample from clinics around the USA (Valenstein 2006; Rush,
2007). The most important findings were that: (a) major depression can
be chronic, severe and associated with substantial comorbidity; (b) many
patients drop out of treatment; (c) initial response to antidepressants is often
slow; (d) remission is less frequent than partial improvement; (e) some, but
not most, patients do better if switched to a different antidepressant; (f) a
minority of patients benefit from augmentation; (g) a minority can benefit
from adding cognitive therapy. Welcome to the real world of clinical practice,
and leave the artificial world of clinical trials behind!
But what did this massive and expensive project actually tell us about
how to treat depression? Those who already favour aggressive therapy can
take heart from the results, but the effects of augmentation and switching
were not actually impressive. And while two-thirds of patients eventually
recovered, many took a year to do so. We know that depression has a natural
course, and that many individuals recover within a year, as happened even
prior to the era of modern psychopharmacology (Shorter, 2009). Last but
not least, without a control group, we cannot know whether any of the
medications worked, or only acted as placebos. Thus, it can be said that
STAR*D raised as many questions as it provided answers. If it is hard
to interpret multimillion-dollar projects sponsored by NIMH, it is even
more difficult to draw conclusions from the smaller studies that appear in
journals. Again, the best counsel is patience.
Even so, patience is hard on my students. They are learning a new set of
skills, and want answers. I may not gain popularity for doing so, but I tell
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them not to believe what their teachers say unless they check out the data
themselves, something that turned me into a first-class sceptic. I also tell
them to doubt what they hear from expert lecturers with an axe to grind.
Finally, I suggest they need to be particularly dubious about what they
read in textbooks, which are usually written with a superficial unjustifiable
certainty. I remind my students that medical science only slowly increases
knowledge, and that the process can take decades.
This being said, the limitations of evidence-based medicine reflect an
early stage in its development. We are talking about a method that is only
70 years old, and that has only slowly come to become a paradigm for
medicine. I am confident about its future.
Evidence-based consultation
The work environment of psychiatrists influences how they think. These
days, practitioners are less likely to work in offices outside institutions,
isolated from their protective umbrella. That model was suitable for
the exclusive practice of psychotherapy, but makes little sense for the
management of severely or chronically ill patients, who need services from
a professional team that provides skills that medical specialists lack. Today,
psychiatrists are less likely to provide direct care to patients with conditions
of mild to moderate severity, who can be just as effectively managed by
others. This is not say that psychiatrists have stopped treating patients,
but that they concentrate on the sickest individuals that absolutely require
the skills of a specialist.
The growth of primary care allows psychiatrists to pass on their expertise
to a much larger community of providers. Often, family physicians provide
medication while psychologists provide therapy, and psychiatrists back
them up. More and more, patients are benefiting from treatment by
multidisciplinary teams. Psychiatrists serve as consultants on the most
difficult cases. In some respects, this may be the future of the profession.
To make consultation evidence based, one has to resist the temptation
to recommend something new for every patient who has not responded
to standard therapy. If a patient has not yet been offered a fair trial of
medication, and if there is a reasonable indication for making the attempt,
one should recommend pharmacotherapy. But in many cases, several agents
have already been tried without result. Consultants may provide consultees
and patients with better service by pointing to a different perspective.
Once patients are on pharmacological treatment, they sometimes stay
on it indefinitely, much like interminable psychotherapies. Physicians
are afraid to stop drugs for fear of a relapse. Since some of the agents we
use, particularly antipsychotics, have serious long-term side-effects, if the
patient does not have psychosis, I often recommend that they be stopped.
However, people get used to drugs, and after years of use cannot cope
without them. So I am reluctant to give advice that may not be followed. The
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long-term use of antidepressants is much less dangerous, but most clinical
guidelines recommend that they be given for 6 months, and then tapered
to see whether there is a problem with stopping. Maintenance therapy is
generally reserved for those who have had multiple episodes of depression.
But that is not necessarily what happens in practice. Once an antidepressant
is prescribed, it may be renewed indefinitely unless the patient insists on
getting off. And needless to say, the same problems emerge with the longterm use of mood stabilisers (in patients who do not have bipolar disorder)
and to the long-term use of stimulants (in patients whose ADHD diagnosis
is doubtful).
My consultations often suggest approaching treatment from a more
psychosocial angle. However, following this advice may require resources
that are not readily available, particularly if a multidisciplinary team is
not in place. In cases in which nothing further can be done, I provide a
reassuring (and factually correct) message by saying that all bases have
been covered, and that there is little to do but follow the patient for chronic
illness. Such consultations may disappoint those who receive them, given
their cautious conclusions, but they are realistic.
Evidence-based psychiatry may be more useful for preventing bad
practices than for proving good practices effective. Once you understand
these problems, you are less easily enticed by fads. Journal articles are
written in that way. They never speak of ‘proof ’ but say ‘the evidence
suggests…’ If correlations are interpreted as causation, peer reviewers
will bring them up short. Unfortunately, critical views of this nature are
uncommon in clinical settings where hope sometimes trumps experience.
Scientific progress in medicine is gradual, but physicians do not always
avoid being carried away by enthusiasm.
Evidence-based medicine: the antidote to fads
I consider myself a ‘born-again’ follower of evidence-based medicine. Its
principles inspired me and helped me emerge from the inevitable funks
that affect the practice of medicine over several decades. It has taught
me to be conservative and patient in the way I manage patients, and in
the recommendations I give to other professionals. It has taught me to
accept the limitations of my craft, and to value what I can do for patients
in spite of these limitations. It has made me a different kind of teacher,
even if some trainees prefer a little less criticism of the literature and more
encouragement to try ‘the latest thing’. Evidence-based medicine has also
informed my own research. But practitioners should keep in mind that
another century could pass before some of the most important questions
are resolved. Patience and caution are called for. We already have the tools
to help most patients we see, even if we cannot always provide a cure.
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Chapter 11
Overview
In the 50 years that have passed since I entered medical school, psychiatry
has made great progress. It has developed effective drugs, and practical
forms of psychotherapy. Slowly but surely, research is illuminating the
causes of mental illness. While we can be frustrated about a slow rate
of progress, many psychiatric treatments have been shown to be both
efficacious (supported by clinical trials) and effective (working in the real
world of practice).
Yet when not enough is known, we can fall victim to hubris. Psychiatry
has sometimes embraced premature closure and easy answers. The 21st
century began with great expectations for breakthroughs in both theory and
treatment. Following ‘the decade of the brain’ in the 1990s, we prepared for
a brave new world of specific biomarkers and bedside functional magnetic
resonance imaging. One of the latest hopes is for personalised treatment
based on genome analysis (Roberts et al, 2012). None of these things has
come to pass, and one can only be sceptical that they lie just over the
horizon. Psychiatry faces a long journey, and few of us will live to see it
arrive at its destination.
In the meantime, the standard of mental healthcare offers grounds for
both hope and concern. On the plus side, psychiatrists do a good job of
caring for patients with severe illnesses. In the psychoses, clinical guidelines
are evidence based and followed almost everywhere. But as soon as one
moves into the realm of common mental disorders, patients can no longer
be sure of receiving predictable treatment. The absence of a well-established
standard of care leaves mental health practice open to faddishness.
A portrait of modern mental health services
Fewer patients today go directly to specialists. Those with common
mental disorders usually pass through a gateway of primary care. But the
treatments offered in that setting are also determined by the culture of
contemporary psychiatry.
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fads and fallacies in psychiatry
Patients who see a family physician for mood or anxiety disorders of mild
to moderate severity today are usually prescribed an antidepressant. If that
does not work, they may also receive ‘augmentation’, either with a second
antidepressant or with an antipsychotic. These practices are intended to
maximise response to treatment. But as we have seen, antidepressants,
whether single or multiple, are not consistently effective. Fortunately, these
drugs do relatively little harm. In contrast, the off-label use of antipsychotics
is associated with a long list of side-effects. The cost–benefit is doubtful,
and in depression, adding them provides more sedation than augmentation.
And for this very reason, antipsychotics are now being prescribed for
insomnia of any kind, whereas quetiapine has become the ‘new Valium’.
Unfortunately, psychiatric consultants may support these practices. (I
often disappoint my consultees by not suggesting aggressive treatment.) If
a patient has not responded to an antidepressant, most psychiatrists will
recommend trying another one. That is reasonable. But it is not reasonable
to try four or five. These practices are based on the belief that depression
is a disease caused by a chemical imbalance, and that one only has to find
the right drug to manage ‘treatment-resistant’ cases. There is little evidence
to support that approach. And there is little reason to prescribe the latest
agents, which are probably no better and have less well known side-effect
profiles. (Fortunately, at least some regulators, for example the National
Health Service in the UK, mandate the prescription of generic drugs.)
The other serious problem afflicting modern psychiatry is that insufficient
time is spent on obtaining a life history to determine past and present
psychosocial stressors. Psychiatrists are trained to ask screening questions
so they do not miss any important symptoms. In principle, there is nothing
wrong with such procedures, but current training for specialists does not
always prepare practitioners to understand life course or the impact of recent
events. That requires more than the quarter-hour devoted to a ‘medication
check’ in many clinics. Moreover, even when a need for psychotherapy
is recognised, treatment may not be easily accessible, particularly for
specialised and evidence-based methods. Finally, if patients do manage
to find a psychologist, they too often receive a bland and generic set of
interventions that psychotherapy researchers describe (without deliberate
irony) as ‘treatment as usual’. While all practitioners are encouraged to
follow the literature and conduct evidence-based treatment, they can fall
short in practice.
I am painting a bleak picture, and do not want to be unfair. But I aim
to challenge the complacency that afflicts current practice. Mental health
professionals do not always follow guidelines, and have been oversold on
inconsistently effective treatment methods.
A good analogy for psychiatry is the management of chronic pain. Like
depression and anxiety, pain is ubiquitous, but those who suffer from it
demand relief. While short-term interventions for chronic pain can be
successful, long-term management is often problematic. This has led to
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overview
the widespread prescription of opioids, whose effects are transient and
which carry a risk of addiction (Trescot et al, 2008). This problem illustrates
how physicians feel impelled to do something for their suffering patients.
Clinicians may find it difficult to accept that they are doing the best they
can, and to accept therapeutic limitations. When practice is driven by what
physicians want to believe, it is more open to fads.
The practice of psychiatry, both in specialty and in primary care, is
influenced by what physicians hear from experts and opinion leaders. And
what they often hear is that symptoms should almost always be manageable,
and that treatment resistance reflects a failure to prescribe the right drugs.
They are not told the truth – which is that we spend much of our time
treating chronic diseases, and are usually doing the best we can. A ‘can-do’
ideology is reinforced by highly effective publicity from the pharmaceutical
industry. Sometimes, experience with patients seems to support such
practices. But physicians can misinterpret temporary improvements after
prescriptions as a response, and fail to recognise placebo effects. Finally, in
a climate of limited funding, guidelines and protocols may be used more to
contain costs than to provide cost-effective treatments.
I have seen some of my most intelligent and idealistic colleagues and
former students fall victim to the fads in contemporary psychiatry. Their
intentions are good, but most, even those who work in teaching hospitals,
do not live in an academic culture. Few are guided by clinical trials, and
those who think they are may misinterpret studies (or clinical guidelines)
to do what they want to do anyway. Most follow the literature, but do not
examine it in critical detail, and are influenced more by medical culture than
by data. (When colleagues argue for the superiority of the latest drug, and
I ask them to quote evidence supporting this belief, I may draw a blank.)
As a career educator, I would like to believe that the next generation of
psychiatrists, trained in academic centres, will have a better perspective.
But most students listen to what they are taught, even if what they hear
are half-truths. The leaders of psychiatry today tend to be researchers in
psychopharmacology, who, like all subspecialists, favour active use of their
tools. My students also go to conferences where they are told about ‘the
latest thing’ in drug therapy. In such settings, there is hardly any mention
of whether the newest drugs have been supported by multiple clinical
trials. (They almost always have not.) One of my trainees surprised me
by informing me that he had never prescribed a generic drug, because his
teachers always recommended the newest agents on the market.
I was chatting a few years ago with a distinguished American professor
who informed me that he routinely sends patients to consultants for
intensive pharmacological treatment. When I asked, ‘Why should you trust
their opinion?’, his answer was, ‘These are experienced people who know
what they are doing’. I felt sadly reminded of the undeserved adulation
of psychoanalysts in my younger days, who were all too often considered
founts of wisdom.
105
fads and fallacies in psychiatry
The ideology of psychiatry
Psychiatry has a history of going to extremes. Fifty years ago, it promoted
fantastic psychological theories. Then, craving the prestige of other
specialties, it fell madly in love with neuroscience. Moreover, medicine
tends to attract people who prefer action to reflection. Students who
go into psychiatry often have to face great scepticism about their choice
of career, both from peers and from teachers. Trainees therefore have
something to prove, making them reluctant to accept the limitations of
their craft.
We are working with a diagnostic system that is at best provisional.
Epidemiological data are tainted by this rather limited method of
classification. Treatments in psychiatry, whether pharmacological or
psychological, lack consistent efficacy. And needless to say, we have little
idea of how to prevent mental illness. Psychiatrists are doing the best they
can with limited knowledge, but need to be humble in the face of massive
ignorance. A hundred years from now, our successors will view our field in
much the same way we see the psychiatry of the early 20th century. One
can only hope for their compassion.
The best hope for rational practice is to change the culture of psychiatry
to acknowledge our limitations and to depend more on evidence. Most
psychiatrists spend little time reading journals or books, and few read
clinical guidelines. They go to expert lectures, and are influenced by expert
opinion, but most of all they are influenced by what their colleagues think.
If the culture of academic psychiatry did a better job at communicating
what we know and what we do not know, the word might eventually get
around that clinical practice needs to more cautious. That is also why the
antidote to fads lies in evidence-based medicine.
Avoiding fads and fallacies
This has been a critical book, and quite deliberately so. I have raised many
questions for which there is currently no clear answer. But psychiatrists
can benefit from humility, even as they do a fair amount of good for their
patients. We need not feel badly about the slow progress of our field. Our
services remain in high demand, because we have the skills to manage some
of the most troubling and terrifying illnesses in all of medicine.
We are all susceptible to fads, at least from time to time. Most of us
are also susceptible to the fallacious and faddish thinking that leads to
incorrect conclusions. To avoid making these mistakes, I suggest ten general
principles to follow:
1 Do not jump to conclusions without good evidence.
2 Be comfortable with how much you do not know.
3 Accept that you are treating disorders whose causes you do not
understand.
106
overview
4 Keep in mind that all diagnoses are provisional, and do not consider
DSM or ICD to be a ‘bible’.
5 Read the literature, especially high-quality reviews such as Cochrane
reports and NICE guidelines.
6 As much as possible, practise on the basis of evidence.
7 If you hear an expert give a talk, remain sceptical, no matter how
charismatic and convincing the presentation.
8 If a treatment claims to be appropriate for too wide a range of patients,
be suspicious.
9 Do not believe anything you hear from a pharmaceutical representative.
10 Remember that medical science moves slowly, and that well-established
treatments may be better than new ones.
I acknowledge that following all these guidelines is easier said than done.
But no one ever said that practising medicine was simple. We owe it to our
patients to do better.
107
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Index
Compiled by Liza Furnival
acceptance and commitment therapy (ACT)
83
acetyl salicylic acid (ASA) 23, 39
ADHD see attention-deficit hyperactivity
disorder
adjusting medication 76–77
adverse life experiences
childhood 40–42
diagnostic aspects 47, 48–49, 51, 56, 57
pharmacotherapy 68, 74, 75, 82
prevention 88
advertising
direct-to-consumer 48, 70
in medical journals 71
advocacy, patient 22
aetiology, disease 37–44
Akiskal, H.S. 51
ALLHAT Collaborative Research Group 23
American Psychiatric Association 5, 32,
45, 98
antidepressants 74–75
augmenting 6, 67, 68, 72–73, 74
efficacy 6, 65, 67–68, 71, 74
extended-release forms 70–71
long-term use 77
mechanism of action 39
placebo effect 52, 68–70
prescribing practices 52–53, 103–104
resistance to 74–75, 104
stopping 77, 102
suicide prevention 92
switching 6, 67, 75, 104
anti-psychiatry 46
antipsychotic drugs
atypical 72–73, 74
augmenting antidepressants 72–73, 74,
75
benefits 65
bipolar disorders 54
120
mechanism of action 38, 39
overprescription 32, 72–74, 104
stopping 101
antisocial personality disorder 89–90
anxiety disorders 60
pharmacotherapy 5–6, 69, 73
psychotherapy 82
aripiprazole 74
Asperger syndrome 56
asylums 25
attachment theory 30
attention-deficit hyperactivity disorder
(ADHD)
diagnosis 49, 54–56
prevalence 61
attenuated psychosis syndrome 90
atypical antipsychotics 72–73, 74
augmentation, antidepressants 6, 67, 68,
72–73, 74
autism
diagnosis 56
prevalence 61–62
vaccination and 17, 22
autism spectrum disorders 56
availability heuristic (or bias) 13, 57
barbiturates 26
Beck, Aaron 28
befriending 81, 83
behaviour therapy 29
behavioural economics 12
behavioural genetics 41
Bentall, Richard 89
benzodiazepines 73
Best, Joel 11
biological psychiatry 4–5, 37
biopsychosocial theory 49
bipolar disorders
diagnosis 49, 53–54, 60–61
index
pharmacotherapy 65, 75–76
prevalence 61
psychotherapy 83
suicide prevention 92
bipolar I disorder 53, 63
bipolar II disorder 53–54
bipolar spectrum disorders 53–54
bleeding 18
borderline personality disorder
pharmacotherapy 73, 76
psychotherapy 81, 83
Bowlby, John 30
brain
disorders 4, 48
functional imaging 47
brand-name drug prescribing 70–71
breast cancer 20–21
brief dynamic therapy 30, 83
British Journal of Psychiatry 25, 29
British Medical Journal (BMJ) 97
bromides 26
bupropion 75
Cameron, D. Ewen 32–33
Canadian Journal of Psychiatry 97
Carlat, Daniel 66, 72
case reports 16
case series 16–17, 31
cause and effect, establishing 14–15
CBT see cognitive–behavioural therapy
Central Intelligence Agency (CIA) 33
chemical imbalance theories 6, 38–39, 50
child abuse 40, 42–43, 58
childhood adversity 40–42
childhood determinism, theory of 29
childhood sexual abuse 41, 43
children
ADHD 54–56
bipolar disorder 54
preventive psychiatry 89–90
chloral hydrate 26
chlorthalidone 23
chronic fatigue syndrome 15, 19
chronic illness 21, 105
chronic pain 19–20, 104–105
classification systems 5, 45–48
clinical experience 2–3
clinical guidelines 17, 98, 103
clinical trials 34, 98, 100
see also evidence-based practice
clozapine 92
Cochrane, Archibald 7, 97
Cochrane reports 97, 98, 99
cognitive dissonance 12
cognitive errors 12–14, 18, 42, 77
cognitive–behavioural therapy (CBT) 4, 29,
30, 83, 84
Collins, Anne 32
community psychiatry 43
comorbidity 46
conduct disorder 54, 89–90
confirmation bias 7, 12–13
conservatism 99–101
consultation, evidence-based 101–102
cosmetic psychopharmacology 56
Craddock, N. 82
criminal behaviour 89
cults, semi-religious 86
cultural aspects 63, 86–87
Dawkins, Richard 12
day care 42, 58
dementia 73
de-patterning therapy 32–33
depression
aetiology 39
bipolarity within 53–54
diagnosis 49, 50–53, 61
drug treatment 5–6, 52–53, 65, 67–70,
72–73
electroconvulsive therapy 31–32
endogenous 6 3
evidence-based practice 100
major see major depression
mild to moderate 51–52, 60, 61
prevalence 60, 63–64
psychotherapy 82, 83
reactive 63
screening programmes 64
suicide prevention 92
treatment resistant 74–75, 104
see also antidepressants
developmental psychopathology 29
diagnosis 45–58
broadening the spectrum 50–57
classification systems 5, 45–48
epidemiological studies 59, 60–63
fads in medicine 19–20
fads in psychiatry 50–58
historical aspects 25–26
illusions 49–50
normal variation as disease 47–48, 58
turning symptoms into a 57–58
Diagnostic and Statistical Manual of Mental
Disorders (DSM) 5, 45–48
bipolar disorders 53
depression 51
PTSD 57
dianetics 86
diets 19
121
index
dissociative disorders 57–58
DNA 39, 40
‘dodo bird effect’ 81
dopamine 38, 50
drug treatment see pharmacotherapy
DSM see Diagnostic and Statistical Manual of
Mental Disorders
Durkheim, Emil 49, 93
effectiveness studies 100
Eisenberg, Leon 6
electroconvulsive therapy (ECT) 31–34
environmental influences 40, 41
Epidemiologic Catchment Area study 57,
59, 61
epidemiology 59–64
epigenetics 15, 40
Etrafon-D 73
evidence-based practice 7, 97–102
conservatism and patience 99–101
consultations 101–102
failure to follow 105
medical journals 16, 97
psychotherapy 83
expert consensus 17, 105
extended-release drug forms 70–71
Extraordinary Popular Delusions and the Madness
of Crowds (Mackay) 11
eye movement desensitisation and
reprocessing (EMDR) 85
Fads and Fallacies in the Name of Science
(Gardner) 1, 11–12
family physicians 101, 103–104
fatigue, chronic 15, 19
Feinstein, A.R. 17
Festinger, L. 12, 28
fibromyalgia 19–20
fluoxetine 69
Food and Drug Administration (FDA)
72–73, 100
food fads 19
Foucault, Michel 44
Freeman, Walter 30–31
Freud, Sigmund 26, 27–30, 62, 79–80, 84,
85
frontal lobotomy 30–31
GABA (gamma-aminobutyric acid) 38
Gardner, Martin 11–12
gene–environment interactions 40
generic drugs 70, 105
genetics 15, 38, 39–40, 88
glutamate 38
122
good intentions 15–16
Great and Desperate Cures (Valenstein) 30
grief 51, 63
groupthink 18
guidelines, clinical 17, 98, 103
gurus, psychotherapy 84
Halsted, William Stewart 20–21
Handbook of Psychotherapy and Behavior Change
(Bergin & Garfield) 80
heritability of mental disorders 41
Holmes, Jeremy 29
Holmes, Oliver Wendell 18
hope, importance of 15
hospital admission, suicidal patients 92–93
Hubbard, L. Ron 86
Huxley, Thomas 13
hypnosis 26
hypomania 53
imaging, functional 47
In the Sleep Room (Collins) 32
Insel, Thomas 88
insomnia 73, 104
insulin coma therapy 31
insurance, health 6
International Classification of Diseases (ICD) 5,
45, 46, 47, 51
internet 22, 99
interpersonal therapy 83
Ioannidis, John 17
Journal of Mental Science 25
Journal of the American Medical Association
(JAMA) 71
journals, medical 15, 16–17
drug advertising 71
evidence-based practice 16, 97
key opinion leaders 72
Kirsch, Irving 69
Kleinman, Arthur 51
Kraepelin, Emil 25–26, 27, 53, 62
Laing, R.D. 43–44
The Lancet 31, 51
Lehmann, Heinz 33
life experiences, adverse see adverse life
experiences
life history, obtaining a 104
listening, empathetic 4, 30, 81–82
lithium 45, 53, 65, 92
lobotomy, frontal 30–31
index
Mackay, Charles 11
major depression
diagnosis 5 0–53, 61
pharmacotherapy 52–53, 68, 69, 74
prevalence 60, 63–64
marketing
pharmaceuticals 22–23, 70–71, 72
psychotherapies 84, 85
mastectomy, radical 20–21
McDonald, William 25
McGill University, Montreal 32–34
McGorry, Patrick 90
McHugh, Paul 43
McKinney, W.T. 51
media, mass 17, 32, 33
medication see pharmacotherapy
medicine 11–23
melancholia 51–52, 53, 63
see also major depression
meme 12
memories
false 85–86
recovered 58, 85–86
repressed 42–43
Menninger Clinic, Houston, USA 30
mental disorders, defining 60–61, 62–63
mental health services 103–105
Mesmer, Franz Anton 26, 85
meta-analyses 98
Midtown Manhattan Study 62
Moncrieff, Joanna 89
Moniz, Egas 30
monoamines 38–39
Mood Disorder Questionnaire 54
mood stabilisers 53, 54, 71–72, 75–76, 102
mood swings 53, 75–76
multidisciplinary teams 101, 102
multiple personality disorder 57–58
multiple sclerosis 21
multivariate analysis 15, 44
myalgic encephalopathy 19
National Comorbidity Surveys 59, 61
National Health Service (NHS) 80, 82
National Institute for Health and Care
Excellence (NICE) 17, 58, 67, 98
neo-Kraepelinian psychiatry 28, 30
neural circuits 6, 38
neuroscience 4–5, 48–49, 88
neurosis 26
neurotransmitters 38–39, 50
new drugs
introduction 78
need for better 71–72
preferences for prescribing 7 0, 105
NICE see National Institute for Health and
Care Excellence
noradrenaline 38, 39, 50
normal variation
boundary with mental disorder 62–63
diagnosis as disease 47–48, 58
obsessive–compulsive disorder (OCD) 69
off-label prescribing 73, 78, 104
olanzapine 74
Osler, William 18, 25, 26
pain, chronic 19–20, 104–105
paraldehyde 26
patience 100
patient advocacy 22
peer review 13, 16, 17
personality disorders 76, 83
see also antisocial personality disorder;
borderline personality disorder
pharmaceutical industry 22–23, 48, 70–72
pharmacotherapy 4–5, 65–78
adjusting medication 76–77
benefits 65
in clinical practice 66–67
diagnostic labels and 49
historical background 18, 26
need for better 71–72
overuse 5–6, 65–66
problems of clinical trials 34
role of drug companies 22–23, 70–72
suicide prevention 92
phenomenology 25
physicians
good intentions 15–16
preferences for new drugs 70
relationships with drug companies
22–23, 71, 72
placebo effects 52, 68–70, 81
polypharmacy 78
post-traumatic stress disorder (PTSD)
56–57
aetiology 41
psychotherapy 85
prevalence
inflated 59–62
major depression 63–64
prevention 88–93
primary 43, 88–89
secondary 89–90
suicide 90–93
primary care 101, 103–104
The Principles and Practice of Medicine (Osler)
18, 25, 26
123
index
psychiatry 3–6, 24–34
100 years ago 25–26
psychoanalysis 3–4, 26, 27–30, 37, 80, 83
psychodynamic therapy 83
psychopharmacology 4, 65–78
see also pharmacotherapy
psychosis
aetiology 26
efficacy of treatment 4, 65, 103
frontal lobotomy 30–31
secondary prevention 90
see also schizophrenia
psychosurgery 30–31
psychotherapy 79–87
availability 82, 104
benign fads 85
duration 82
efficacy 79, 80–82
evidence-based 83, 101–102
malignant fads 85–86
psychoanalytic 4, 83
quality concerns 81–82
research 34, 80–82
underuse 5–6, 66
variety of types 84
PTSD see post-traumatic stress disorder
purging 18
suicide prevention 92
see also psychosis
science, and medicine 16–17
Science 51
screening programmes 64
selective serotonin reuptake inhibitors
(SSRIs) 69
self-esteem 86
serotonin 38, 39, 50
sexual abuse, childhood 41, 43
Shapiro, Francine 85
Sibyl (a patient) 58
social interventions 88–89
social psychiatry 43–44, 89
social science 48–49
Spitzer, Robert 28
STAR*D (Sequenced Treatment Alternatives
to Relieve Depression) 67, 100
statistical analysis 15, 44
stimulants 55–56, 102
Stirling County Study 62
subclinical psychological symptoms 62, 64
suicide prevention 90–93
surgical fads 20–21, 30–31
switching, antidepressants 6, 67, 75, 104
syndromes, psychological 46–47, 63
syphilis 25
quetiapine 73, 74, 104
talking therapy see psychotherapy
tardive dyskinesia 73
Tavistock Clinic, London 30
tonsillectomy 21
trauma 41, 57
Tremblay, Richard 90
treponema pallidum 25
tricyclic antidepressants 69
Twenge, J.M. 86
randomised controlled trials (RCTs) 98
recovered memories 58, 85–86
reductionism, biological 15, 37–38
repressed memory concept 42–43
resilience to adversity 40, 41
rest cures 26
risk factors
mental illness 40–41, 88–89
suicide 91
risk psychosis 90
Rush, Benjamin 18
Rutter, Michael 29, 55
sadness 51, 53, 63
samples, unrepresentative 16–17, 98
schizophrenia
aetiology 38, 39
diagnosis 60–61, 63
insulin coma therapy 31
psychotherapy 83
124
unhappiness
diagnostic issues 51, 53
pharmacotherapy 68, 74, 75
vaccines 17, 22
Valenstein, E.S. 30
Wakefield, Andrew 22
willpower 26
World Health Organization (WHO) 5, 45
World Psychiatric Association 32–33
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