Sadness or Depression - International Persp PDF

History, Philosophy and Theory of the Life Sciences
Jerome C. Wakefield
Steeves Demazeux Editors
Sadness or
Depression?
International Perspectives on the
Depression Epidemic and Its Meaning
History, Philosophy and Theory
of the Life Sciences
Volume 15
Editors
Charles T. Wolfe, Ghent University, Ghent, Oost-Vlaanderen Belgium
Philippe Huneman, IHPST (CNRS/Université Paris I Panthéon-Sorbonne), France
Thomas A.C.Reydon, Leibniz Universität, Hannover, Germany
Editorial Board
Marshall Abrams (University of Alabama at Birmingham)
Andre Ariew (Missouri)
Minus van Baalen (UPMC, Paris)
Domenico Bertoloni Meli (Indiana)
Richard Burian (Virginia Tech)
Pietro Corsi (EHESS, Paris)
François Duchesneau (Université de Montréal)
John Dupré (Exeter)
Paul Farber (Oregon State)
Lisa Gannett (Saint Mary’s University, Halifax)
Andy Gardner (Oxford)
Paul Griffiths (Sydney)
Jean Gayon (IHPST, Paris)
Guido Giglioni (Warburg Institute, London)
Thomas Heams (INRA, AgroParisTech, Paris)
James Lennox (Pittsburgh)
Annick Lesne (CNRS, UPMC, Paris)
Tim Lewens (Cambridge)
Edouard Machery (Pittsburgh)
Alexandre Métraux (Archives Poincaré, Nancy)
Hans Metz (Leiden)
Roberta Millstein (Davis)
Staffan Müller-Wille (Exeter)
Dominic Murphy (Sydney)
François Munoz (Université Montpellier 2)
Stuart Newman (New York Medical College)
Frederik Nijhout (Duke)
Samir Okasha (Bristol)
Susan Oyama (CUNY)
Kevin Padian (Berkeley)
David Queller (Washington University, St Louis)
Stéphane Schmitt (SPHERE, CNRS, Paris)
Phillip Sloan (Notre Dame)
Jacqueline Sullivan (Western University, London, ON)
Giuseppe Testa (IFOM-IEA, Milano)
J. Scott Turner (Syracuse)
Denis Walsh (Toronto)
Marcel Weber (Geneva)
More information about this series at https://www.springer.com/series/8916
Jerome C. Wakefield • Steeves Demazeux
Editors
Sadness or Depression?
International Perspectives on the Depression
Epidemic and Its Meaning
Editors
Jerome C. Wakefield Steeves Demazeux
Silver School of Social Work Department of Philosophy, SPH Laboratory
and Department of Psychiatry Université Bordeaux Montaigne
New York University Pessac, France
New York, NY, USA
ISSN 2211-1948 ISSN 2211-1956 (electronic)

History, Philosophy and Theory of the Life Sciences
ISBN 978-94-017-7421-5 ISBN 978-94-017-7423-9 (eBook)
DOI 10.1007/978-94-017-7423-9
Library of Congress Control Number: 2015959694
Springer Dordrecht Heidelberg New York London

© Springer Science+Business Media Dordrecht 2016
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Contents
Introduction: Depression, One and Many .................................................... 1

Jerome C. Wakefield and Steeves Demazeux
The Current Status of the Diagnosis of Depression ..................................... 17
David Goldberg
The Continuum of Depressive States in the Population
and the Differential Diagnosis Between “Normal” Sadness
and Clinical Depression .................................................................................. 29
Mario Maj
Beyond Depression: Personal Equation
from the Guilty to the Capable Individual ................................................... 39
Alain Ehrenberg
Depression as a Problem of Labor: Japanese Debates
About Work, Stress, and a New Therapeutic Ethos..................................... 55
Junko Kitanaka
Darwinian Blues: Evolutionary Psychiatry and Depression ....................... 69
Luc Faucher
Is an Anatomy of Melancholia Possible?
Brain Processes, Depression, and Mood Regulation .................................... 95
Denis Forest
Loss, Bereavement, Mourning, and Melancholia: A Conceptual
Sketch, in Defence of Some Psychoanalytic Views ....................................... 109
Pierre-Henri Castel
Suffering, Meaning and Hope: Shifting
the Focus from Depression in Primary Care ................................................ 121
Christopher Dowrick
v
vi Contents
An Insider View on the Making of the First French

National Information Campaign About Depression .................................... 137
Xavier Briffault
Extrapolation from Animal Model of Depressive
Disorders: What’s Lost in Translation? ........................................................ 157
Maël Lemoine
Psychiatry’s Continuing Expansion of Depressive Disorder....................... 173
Jerome C. Wakefield and Allan V. Horwitz
Index ................................................................................................................. 205

Contributors
Xavier Briffault is a social scientist and epistemologist working on mental health

at the French National Centre for Scientific Research and in one of the main French
social sciences research centre, Cermes3 (Centre de recherche, médecine, sciences,
santé, santé mentale, société). His main research interests are depression, obsessive-
compulsive disorders, psychotherapy and mental health prevention programmes, as
well as public health interventions in those areas. He conducts on these issues a
sociologically and epistemologically informed analysis of the effectiveness of inter-
ventions, particularly in the context of the extension of the evidence-based medicine
paradigm (EBM) to mental medicine. He also operates as an expert for several pub-
lic health institutions.
Pierre-Henri Castel PhD in Philosophy, PhD in Psychology, 52, is French. He is a

senior research fellow at the Centre National de la Recherche Scientifique (CNRS)
at the Ecole des Hautes Etudes en Sciences Sociales (EHESS) in Paris. He has
worked as a clinician for 20 years in various psychiatric hospitals. He also is a psy-
choanalyst in private practice. His scholarly specialty is the history and philosophy
of mental medicine, from psychoanalysis to psychiatric neuroscience. He has writ-
ten nine books, on hysteria and neurology in Charcot’s circle, a detailed analysis of
Freud’s Traumdeutung, a history of transsexualism focusing on personal identity, a
collection of essays on contemporary psychiatry from the point of view of a neo-
Wittgensteinian philosophy of mind and, recently, a two-volume critical history of
obsessions and compulsions from antiquity to present-day neuroscience and CBT:
Âmes scrupuleuses, vies d’angoisse, tristes obsédés. Obsessions et compulsions de
l’Antiquité à Freud (2011) and La Fin des coupables, suivi du cas Paramord.
Obsessions et compulsions de la psychanalyse aux neurosciences (2012). His work
can be seen as a form of philosophical anthropology based on the history of major
mental disorders (along with their cures), but he has also worked extensively to try
to bridge the gap between the main philosophical currents, the analytic and the
‘continental’, underlying many recent developments in the philosophy of psychopa-
thology (personal website: https://pierrehenri.castel.free.fr).
vii
viii Contributors
Steeves Demazeux is an associate professor of philosophy at the Université

Bordeaux Montaigne (France). He received his doctoral degree at Paris Sorbonne
University (IHPST laboratory) and spent 2 years as a postdoctoral fellow at
CERMES Institute (Paris Descartes University). His research interests include his-
tory and philosophy of psychiatry, philosophy of medicine and philosophy of sci-
ence. He is the author of Qu’est-ce que le DSM? Genèse et transformations de la
bible américaine de la psychiatrie (Ithaque 2013); the co-author, with Françoise
Parot and Lionel Fouré, of Psychothérapie, fondements et pratiques (Belin 2011);
and the co-editor, with Patrick Singy, of the collective volume, The DSM-5 in
Perspective. Philosophical Reflections on the Psychiatric Babel (Springer 2015).
Christopher Dowrick, M.D., FRCGP is professor of primary medical care in the

University of Liverpool and a general practitioner in north Liverpool, England. He
is also board advisor for Mersey Care NHS Trust, senior investigator emeritus for
the National Institute for Health Research in England and professorial research fel-
low in the University of Melbourne in Australia. He is a member of the World
Organization of Family Doctors’ working party on mental health and a technical
expert for the World Health Organization’s mhGAP programme.
His research portfolio covers common mental health problems in primary care,
with a focus on depression and medically unexplained symptoms. He critiques con-
temporary emphases on unitary diagnostic categories and medically oriented inter-
ventions and highlights the need for socially oriented perspectives. He is currently
exploring the role of placebo and contextual effects in antidepressant drug prescrib-
ing and investigating ways to reduce inequity of access to primary mental health
care for people from marginalised and disadvantaged communities. He has over 200
academic publications. The second edition of his book Beyond Depression was pub-
lished by Oxford University Press in 2009. With Allen Frances, he has contributed
to the British Medical Journal’s ‘Too Much Medicine’ series on the over-
medicalisation of depression (https://bmj.com/cgi/content/full/bmj.f7140).
Alain Ehrenberg is a sociologist and director of research at the CNRS (Centre

National de la Recherche Scientifique). He has developed research programmes and
research units on mental health issues. His main books are about transformations of
individualism and autonomy, mainly through the area of mental health: Le Culte de
la performance (Calmann-Lévy 1991), L’Individu incertain (Calmann-Lévy 1995),
La Fatigue d’être soi (Odile Jacob 1998, translated into six languages including in
English: The Weariness of the Self. Diagnosing the History of Depression in the
Contemporary Age, McGill UP, 2010, with an original foreword) and La Société du
Malaise (translated in German and Italian).
Luc Faucher is full professor in philosophy at the Université du Québec à Montréal

(UQAM, Canada). After a PhD in Montréal, he has been postdoctoral fellow at
Rutgers University under the direction of Stephen Stich. His research interests cover
philosophy of cognitive sciences, philosophy of race, philosophy of emotions and
philosophy of psychiatry. He is the co-editor (with Christine Tappolet) of The
Contributors ix
Modularity of Emotions (2008) and the editor of Philosophie et psychopathologies

(2006). He published papers in Philosophy of Science, Philosophy of the Social
Sciences, Emotion Review, Journal of Social Philosophy, Synthese and The Monist.
A former student of the Ecole Normale Supérieure, Paris.
Denis Forest is professor of philosophy at the University Paris Ouest Nanterre and
an associate member of the Institut d’Histoire et de Philosophie des sciences et des
techniques (IHPST, Paris). His main areas of research are philosophy of neurosci-
ence and philosophy of mind. He has recently collaborated to the volume Brain
Theory: Essays in Critical Neurophilosophy edited by Charles Wolfe (Palgrave
Macmillan 2014). His second book, Neuroscepticisme: les sciences du cerveau sous
le scalpel de l’épistémologue, has been published by Ithaque (Paris 2014).
David Goldberg has devoted his professional life to improving the teaching of
psychological skills to doctors of all kinds and to improving the quality of services
for those with severe mental illnesses. He has advised the Department of Health
over the years about service developments and has been extensively used by the
World Health Organization as a mental health consultant. He completed his psychi-
atric training at the Maudsley Hospital. He went to Manchester, where for over
20 years he was head of the Department of Psychiatry and Behavioural Science. In
1993 he returned to Maudsley as professor of psychiatry and director of research
and development. His interests are in vulnerability factors which predispose people
to develop depression and in teaching general practitioners to give a better service
to psychologically distressed patients. His research over many years has been con-
centrated on the details of communication between GPs and their patients, and he
has applied these principles to his teaching of mental health workers in developing
countries. He has a major interest in the best way primary care and specialist mental
health services should relate to one another. For the past 25 years, his interests have
extended away from doctors to the people who are in states of distress with particu-
lar attention to the factors that make people vulnerable to stressful life events. His
first book on this subject dealt with both GPs and their patients (Mental Illness in
the Community, the Pathway to Psychiatric Care with Peter Huxley), and his most
recent book takes a thorough, developmental look at the determinants of this vulner-
ability (The Course and Origin of Common Mental Disorders with Ian Goodyer).
He has been chairman of two NICE Guideline Development Groups, the first for
depression and more recently for the guideline for depression among those with
physical illnesses. He is a fellow of Hertford College, Oxford; King’s College,
London; and the Academy of Medical Sciences. He retired in 1999 and now works
part time at the institute. He is currently chairman of the Psychiatry Research Trust
at the Institute Of Psychiatry, London.
Allan V. Horwitz is board of governors professor in the Department of Sociology

and interim director of the Institute for Health, Health Care Policy and Aging
Research at Rutgers University. He has published over 100 articles and chapters
about various aspects of mental health and illness and eight books including
x Contributors
Creating Mental Illness (University of Chicago Press 2002), The Loss of Sadness:
How Psychiatry Transformed Normal Misery into Depressive Disorder (Oxford
University Press 2007 with Jerome Wakefield), All We Have to Fear (Oxford
University Press 2012 with Jerome Wakefield) and A Short History of Anxiety
(Johns Hopkins University Press 2013). He was also the co-editor, with Teresa
Scheid, of A Handbook for the Study of Mental Health: Social Contexts, Theories,
and Systems (Cambridge University Press 1999). He also served as dean of social
and behavioral sciences at Rutgers. Since 1980 he has been the co-director (with
David Mechanic) of the NIMH-funded Rutgers’ Postdoctoral Program in Mental
Health. Professor Horwitz is the current chair of the Medical Sociology Section of
the American Sociological Association and is a past chair of the Mental Health
Section of the ASA. In 2006 he received the Leonard Pearlin Award for Distinguished
Lifetime Contributions to the Sociology of Mental Health. He has been a fellow-in-
residence at the Netherlands Institute for Advanced Study (2007–2008) and at the
Center for Advanced Study in the Behavioral Sciences at Stanford (2012–2013).
Junko Kitanaka, Ph.D. is a medical anthropologist and associate professor in the

Department of Human Sciences, Keio University, Tokyo. For her McGill University
doctoral dissertation on depression, she received a number of awards including the
2007 Dissertation Award from the American Anthropological Association’s Society
for Medical Anthropology. This has since been published by Princeton University
Press as a book titled Depression in Japan: Psychiatric Cures for a Society in
Distress, which won the American Anthropological Association’s Francis Hsu Prize
for Best Book in East Asian Anthropology in 2013. The book has been translated by
Dr. Pierre-Henri Castel at Paris Descartes University and published by Ithaque as
De la mort volontaire au suicide au travail: Histoire et anthropologie de la depres-
sion au Japon (2014). She is currently working on a new project on dementia, old
age and the psychiatrisation of the life cycle.
Maël Lemoine is an associate professor in the philosophy of biomedical science in

Tours (France) and at the Institut d’Histoire des Sciences et des Techniques (Paris).
In 2011, he published a book on explanations in medicine. He has since been work-
ing on the ‘naturalisation’ of mental disorders, on model organisms in biomedicine
and on the concept of disease. He published half a dozen papers in English on these
questions. He is currently preparing a book entitled The Naturalization of
Depression.
Mario Maj is professor of psychiatry and chairman at the University of Naples

SUN, Naples, Italy, and director of the Italian WHO Collaborating Center for
Research and Training in Mental Health. He has been president of the World
Psychiatric Association, the European Psychiatric Association and the Italian
Psychiatric Association. He is editor of World Psychiatry, official journal of the
World Psychiatric Association (impact factor 2014: 12.896).
He is member of the advisory board for the Chapter on Mental and Behavioural
Disorders of the ICD-11 and chairperson of the Work Group on Mood and Anxiety
Contributors xi
Disorders for that chapter. He has been member of the Work Group for Mood
Disorders of the DSM-5.
He is honorary fellow of the Royal College of Psychiatrists, UK, and the
American College of Psychiatrists and doctor honoris causa at the University of
Craiova.
He has been active as a researcher and an educator on behalf of the WHO in sub-
Saharan Africa, South East Asia and Latin America. He has been chairman of the
Section on Neuropsychiatry of the Global Programme on AIDS at the WHO
Headquarters in Geneva.
He is member of the editorial board of several international journals. He has been
author of more than 450 scientific papers indexed in Scopus, mostly in the area of
mood, psychotic and eating disorders. His H-index is 50.
Jerome C. Wakefield is university professor, professor of social work and professor

of the conceptual foundations of psychiatry at New York University. He is also an
affiliate faculty in bioethics and an honorary faculty member of the Institute for
Psychoanalytic Education at NYU. He holds a PhD in philosophy, a DSW in clini-
cal social work and an MA in mathematics (logic and methodology of science), all
from the University of California, Berkeley. After post-doctoral fellowships in
women’s studies (Brown University), cognitive science (University of California,
Berkeley) and mental health services research (Rutgers University), he held faculty
positions at the University of Chicago, Columbia University and Rutgers University,
before coming to NYU in 2003. He has published over 250 scholarly articles on the
conceptual foundations of diagnosis and clinical theory, with recent publications
focusing on controversies over proposed changes to DSM-5, especially issues con-
cerning the relationship between depression and grief and the boundary between
normal distress and mental disorder. He is the co-author (with Allan Horwitz) of
The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive
Disorder (Oxford 2007), named the best psychology book of 2007 by the Association
of Professional and Scholarly Publishers, and All We Have to Fear: How Psychiatry
Transforms Natural Fear into Mental Disorder (Oxford 2012), named best book of
the year by the American Sociological Association, Section on Evolution, Biology,
and Society. He is currently completing a book on Freud’s case history of Little
Hans and its significance in the history of psychoanalysis, to be published by
Routledge.
Introduction: Depression, One and Many
Jerome C. Wakefield and Steeves Demazeux
This collective volume takes a fresh look at the psychiatric diagnosis of “major
depressive disorder”, the disorder’s nature and its social meaning today. The hetero-
geneity of the conditions we call “depression” is so great that it raises difficult ques-
tions of individuation and identity. Major depression is one category of disorder in
the DSM-5 and ICD-10, yet it is virtually universally agreed that the conditions that
fall under that category constitute several different disorders caused by quite differ-
ent etiologies. Similarly, depression varies across cultures in the way it presents, the
way it is experienced, and the way it is valued or disvalued, so if it is so different,
what makes it the same condition of “depression” that is being studied across cul-
tures? Depression is the category of mental disorder most clearly recognized con-
tinuously since antiquity, yet it is also a category that has transformed and
dramatically expanded during the twentieth century, so what makes it the same
category over time? This is both a major intellectual challenge and a more immedi-
ate editorial challenge of explaining how the many diverse contributions to this
volume could possibly be talking about a common topic. In attempting to provide
an encompassing perspective, we acknowledge that some of the contributors to this
volume may well disagree (and that at times we two disagree), and put forward the
following thoughts in the spirit of offering one possible perspective among many.
J.C. Wakefield (*)

Silver School of Social Work and Department of Psychiatry,
New York University, New York, NY, USA
e-mail: [email protected]
S. Demazeux
Department of Philosophy, SPH Laboratory, Université Bordeaux Montaigne, Pessac, France
© Springer Science+Business Media Dordrecht 2016 1

J.C. Wakefield, S. Demazeux (eds.), Sadness or Depression?
History, Philosophy and Theory of the Life Sciences 15,
DOI 10.1007/978-94-017-7423-9_1
2 J.C. Wakefield and S. Demazeux
A Short or a Long History?
The historiography on depression indicates the profound difficulty of finding the

right balance for addressing in a unified way depression’s anthropological, social
and biological components. First of all, should depression be considered the result
of a short or a long history? If we rely merely on terminology, we should recall that
the medical use of the term “depression” as opposed to “melancholia” is rather
recent. Following scattered references to sadness as “depressed spirits” in the prior
centuries – including in Samuel Johnson’s Dictionary (Johnson 1755, 21) – Jean-
Etienne Esquirol characterized the condition of lypemania in 1838 as a “sad and
depressed passion” (our emphasis), becoming one of the first alienists to use this
metaphor inside a medical treatise. By the middle of the nineteenth century, the
substantive “depression” spread in the writings of many European psychiatrists,
such as French psychiatrist Jules Séglas who aimed at characterizing by this term a
new specific form of moral suffering with all the clinical features of melancholia but
without its component of delirium (see Lantéri-Laura 2003).
The history of melancholia seems easiest to trace back. It goes back to ancient
times (around fifth century BC) and to the theory of humors (“melancholia” means
“black bile disease”). In antiquity and until relatively recently, “melancholia” often
referred to conditions that involved delusions (“delirium”) and would likely be
labeled as schizophrenia today, such as a melancholic patient described by Pinel
who believed that he was actually dead and thus could not eat anymore (Starobinski
2012, 90). Today, melancholia is generally considered a severe form of depression,
but there is still controversy about whether the two clinical entities really overlap
with each other or should be distinguished. Despite a wave of studies some decades
ago that argued that no such distinction had been scientifically confirmed (Kendell
1976; Lewis 1934), many in psychiatry continue to argue that the distinction is real
and the histories divergent (Fink and Taylor 2007; Fink et al. 2007; Parker et al.
2010; Shorter 2007).
Some Arguments in Favor of the Long History View
Whereas some medical historians have documented the swarming multiplicity of

uses, theoretical assumptions, moral implications and treatment indications behind
the terms “depression” and “melancholia” (Starobinski 2012), other medical histo-
rians have insisted to the contrary on the “remarkable consistency” of the medical
condition that we now call depression (Jackson 1986, ix). The latter historians claim
that, notwithstanding the many changes in concepts, theories and treatments through
two and a half millennia, we can recognize in medical descriptions something like
a stable medical condition tantamount to our modern conception of major depres-
sive disorder, with a strikingly stable clinical picture. The individual is sad most of
the day, he cries a lot and has lost his appetite, his energy, his sleep and most of his
Introduction: Depression, One and Many 3
social interests, and often the individual cannot explain to himself and to others why
he is in such a state of low mood. An intense episode of sadness, combined with the
lack of a rational explanation for it in the circumstances of a person’s life, are the
two most traditionally mentioned characteristics from Aristotle (Jackson 1986, 32)
and Galen (1929) through Burton (2001) to Kraepelin (1915), and they remain
tempting reasons to speak of a common phenomenon of depressive episodes both
retrospectively and in our present time.
Some medical historians emphasize the dangers of retrospective diagnosis. As
Strarobinski observes, there is always something missing in the short clinical
accounts that we find in old books, most importantly the presence of the patient
(Starobinski 2012, 15). But is this a sufficient reason to condemn any retrospective
diagnosis? To take one historical example of many, when the philosopher David
Hume told the Comtesse de Boufflers about the “strange condition” of Lord
Chatham that rendered him incapable of making decisions, Hume surely was
describing something close to our modern concept of depression:
You ask the present state of our politics….[W]e are in greater confusion than usual; because
of the strange condition of Lord Chatham, who was regarded as our first minister. The pub-
lic here, as well as with you, believe him wholly mad; but I am assured it is not so. He is
only fallen into extreme low spirits and into nervous disorders, which render him totally
unfit for business, make him shun all company, and, as I am told, set him weeping like a
child, upon the least accident. Is not this a melancholy situation for so lofty and vehement
a spirit as his? And is it not even an addition to his unhappiness that he retains his senses?…
Meanwhile, the public suffers extremely by his present imbecility: no affairs advance: the
ministers fall in variance: and the King entertains thoughts of forming a new administration.
(Hume 1767)
The mysterious illness that gnawed at Lord Chatham intrigued many political
commentators of his time. How to explain that, as Lady Chatham reported to the
King, he suddenly became unable to make a decision about anything? Was he
affected by a real illness, as invoked in his Resignation Letter addressed to the
King in 1768? Or should we suspect political cowardice, as did some of his oppo-
nents? Resolving this question requires an investigation of the complex nexus of
causes and/or reasons that can explain his behavior at a particular time and in a
particular historical context, challenging us with endless ambiguities. The best
explanation could be moral or sociological rather than psychological or medical.
Yet even Hume identified “extreme low spirits” that are “nervous disorders” as a
possible explanation, distinguishing it from rank “madness” and thus from psy-
chotic conditions. Granting that basing our view of the history of depression on
patchy stories from the past has its methodological dangers, why should we deny
that many of our ancestors were affected by a condition that appears so common
nowadays? Should we refuse to allow individuals of the past the intuitive demarca-
tion that even they seem to have made between a normal episode of sadness and
pathological sorrow?
Those who consequently opt for a long history of depression would see the use
of the term ‘depression’ as simply a recent stylistic variant that refers to a condition
recognized since antiquity. It is true that in antiquity it was often what we would
now classify as “psychotic depression” – overlapping with what we now might

classify as schizophrenia – that fell under “melancholia.” And it is quite possible
that milder forms have gradually been coopted by this category with the advent of
“simple depression” and like states. Yet, many historical considerations support a
continuity within the changes.
While theories of depressive disorder have changed, the symptoms that indicate
the disorder have not. Writing in the fifth century B.C., Hippocrates provided the
first known definition of melancholia as a distinct disorder: “If fear or sadness last
for a long time it is melancholia” (Hippocrates 1931, 185). In addition to fear and
sadness, Hippocrates mentioned as symptoms “aversion to food, despondency,
sleeplessness, irritability, restlessness,” much like today’s criteria (Hippocrates
1923, 263). In another case, Hippocrates describes a woman who became morose
during grief as not taking to her bed but suffering from insomnia, anorexia, anxiety,
and somatic symptoms (Hippocrates 1923). Moreover, Hippocrates’s definition
indicated that it is not such symptoms alone but only symptoms of unexpected dura-
tion that indicate disorder. Hippocrates’s insistence that the sadness or fear must be
prolonged can be interpreted as a first attempt to capture the notion that dispropor-
tion to circumstances and thus lack of an explanation in terms of circumstances is
an essential aspect of depressive disorder.
A century after Hippocrates, Aristotle (or one of his students) in the Problemata
elaborated the distinction between a variety of normal mood states of sadness, on
the one hand, and pathological disease states, on the other. Aristotle clearly
expressed the idea that disordered sadness is disproportionate to events. He noted
that, if the black bile “be cold beyond due measure, it produces groundless despon-
dency” (Aristotle 1927, 165). Here “beyond due measure” refers to what is dispro-
portionate to the circumstances, making the resultant sadness “groundless.” Such
despondency, for example, “accounts for the prevalence of suicide by hanging
amongst the young and sometimes amongst older men too” (Aristotle 2000, 59).
Aristotle also inaugurated the tradition that has lasted to our own day of associating
depressive temperament or even depressive disorder with exceptional artistic and
intellectual ability, asking: “Why is it that all men who have become outstanding in
philosophy, statesmanship, poetry or the arts are melancholic, and some to such an
extent that they are infected by the diseases arising from black bile…They are all,
as has been said, naturally of this character” (Aristotle 2000, 57).
Further supporting a continuity of conception of depression, the ancients clearly
distinguished between melancholic disordered sadness and intense but normal sad-
ness with similar symptoms due to events in a person’s life. This distinction was
often illustrated with stories of a famous diagnostic triumph by Erasistratus (304–
250 B.C.), physician to King Seleucus of Syria, in which Erasistratus discovered
through shrewd observation that the King’s son, Antiochus, was not suffering from
melancholia as his symptoms suggested, but was instead suffering from unrequited
(and unexpressable) love – for his father’s young wife! As Aretaeus tells it:
A story is told, that a certain person, incurably affected, fell in love with a girl; and when
the physician could bring him no relief, love cured him. But I think that he was originally
in love, and that he was dejected and spiritless from being unsuccessful with the girl, and
appeared to the common people to be melancholic. He then did not know that it was love;
but when he imparted the love to the girl, he ceased from his dejection, and dispelled his
passion and sorrow; and with joy he awoke from his lowness of spirits, and he became
restored to understanding, love being his physician (Jackson 1986, 40).
Similarly, Galen (1929) describes a case in which he is unsure whether the prob-
lem lies in normal despair over some loss that is being hidden from the physician or
the development of a depressive medical disorder:
I was called in to see a woman who was stated to be sleepless at night and to lie tossing
about from one position into another. Finding she had no fever, I made a detailed inquiry
into everything that had happened to her, especially considering such factors as we know to
cause insomnia. But she either answered little or nothing at all, as if to show that it was
useless to question her. Finally, she turned away, hiding herself completely by throwing the
bedclothes over her whole body, and laying her head on another small pillow, as if desiring
sleep. After leaving I came to the conclusion that she was suffering from one of two things:
either from a melancholy dependent on black bile, or else trouble about something she was
unwilling to confess. I therefore deferred till the next day a closer investigation of this.
(Galen 1929, 213)
DSM-5 contains a note stating that the clinician must use judgment when diag-
nosing depression because intense normal responses of sadness to various losses
and stresses may resemble depressive disorder symptomatically. We may thus pre-
sume that many modern psychiatrists continue to be confronted by the same
dilemma facing Galen that challenges the symptom-based core of the modern defi-
nition of a depressive disorder.
What Is the Meaning of the Depression Epidemic

in the Twentieth Century?
Whatever the historical perspective we should embrace (the short or the long view),
one of the most intriguing and distinctive modern phenomena about depression is its
epidemic character. This supposedly devastating and recurrent psychiatric disorder
just a few decades ago was estimated to afflict perhaps 2–3 % of the population of
the United States over a lifetime (Klein and Thase 1997), whereas the latest and
most methodologically sophisticated studies indicate that the disorder occurs in
more than half of the U.S. population (Moffitt et al. 2010; Rohde et al. 2013). The
World health Organization (WHO) predicts that the situation will even get worse by
2020, with depression becoming the second major cause of worldwide disability.
How to explain such an epidemic expansion in prevalence and the corresponding
treatment and prevention efforts regarding the disorder that has come to be known
as “major depression”? In a huge literature devoted to this specific subject, one can
discern two basic hypotheses. The first hypothesis accepts the growth of depression
during the twentieth century as in some sense “real” and attempts to identify the
cause. Some researchers, for instance, have speculated that some novel toxic or
infectious agents or the influence of dietary changes may explain the epidemic of
depression. Others researchers have focused on changes in lifestyle, such as our

relationship with nature or lack of exposure to external light. Still others have con-
sidered such social changes as the rise of individualism, the development of neolib-
eralism, the culture of narcissism, social mobility, constant exposure to imagies of
those with greater beauty or wealth through the media, and the effects of these
phenomena on our psyches as possible causes of the epidemic of depressions. On
the other hand, it is pointed out that major traditional sources of dejection, such as
loss of children, poverty, and early death due to disease, have receded markedly in
the developed societies that nonetheless report high rates of depression.
The second hypothesis is that the overwhelming increase in the prevalence of
depression during the past century is mostly in some sense artificial. Epidemiological
data in psychiatry have never been very reliable, especially in community popula-
tions. Few studies exist before the 1970s, and they were rarely replicated and were
lacking a careful delineation between disorder and social distress (Horwitz and
Wakefield 2007, 205). The widely used diagnostic criteria for depression provided
in the American Psychiatric Association’s Diagnostic and Statistical Manual of
Mental Disorders (APA 2013) is clinically fuzzy, its boundaries have broadened
over time, and it is based on symptoms that can easily occur in normal sadness, so
that the mistaken “false positive” diagnoses of normal sadness as depressive disor-
der is possible. For example, recent changes in which a “bereavement exclusion”
from diagnosis with major depression was removed from the diagnostic criteria
implies that even intense sadness when mourning a relative can qualify as depres-
sive disorder. A positive aspect of this artificial expansion is that it makes depres-
sion more visible and thereby creates better support and social acceptance for a
disease that has long been considered shameful. A less optimistic perspective is that
the modern expansion of depression is a pathologization process that progressively
blurs the traditional and intuitive demarcation between normal sadness and patho-
logical sorrow and yields the medicalization of the normal emotions of ordinary life
(Horwitz and Wakefield 2007). This perspective raises concerns about the strategies
employed by the pharmaceutical industries over the past 40 years, resulting in very
high rates of consumption of antidepressants. The fact that in 1994, a selective sero-
tonine reuptake inhibitor called “Prozac” became the second top-selling drug in the
world is indicative of the scope of the social phenomena of depression using our
contemporary DSM-based definitions.
Depression is closely associated symptomatically not only with normal intense
sadness, but also with culpability and guilt, feeling stressed at work, excessive
fatigue, deep sorrow, general lassitude, and diffuse unhappiness. Because of its
medical nature, depression is the only one in this list that has a chance to get socially
accepted as an excuse for impaired role functioning. However, it will be accepted as
a social excuse only if, as the “sick role” demands, you show no complacency and
demonstrate a willingness to get better rather than accepting your condition
(Wakefield 2009, 2010). By contrast, lassitude (lassitude), tiredness (fatigatio) –
two terms that carry in old Latin, exactly like the word depressio, the same image of
exhaustion, of weariness, of a progressive slide down, of something being deflated –
have no positive place in society as justifiable, excusable phenomena that relieve

you from your social obligations. Indeed, the French philosopher Roland Barthes,
in one of his lectures at the College de France in 1978, wondered why tiredness is
so negatively connoted is our societies and undertook the philosophical rehabilita-
tion of tiredness as one of his figures of the “neutral” (Barthes 2005).
The same could largely be said of bereavement, except that for a long time in
human history there has been a strict social codification of the process of bereave-
ment. When an intimate dies, you are relieved of your social obligations for a cer-
tain time, after which society reasserts itself. Barthes noted in his diary a few days
after the death of his mother: “The measurement of mourning. (Dictionary,
Memorandum): eighteen months for mourning a father, a mother” (Barthes 2010,
28). According to the old dictionary that Barthes quotes, this measure was seen as
the normal expected duration of bereavement. Eighteen months is also approxi-
mately the duration of Barthes’ diary. The acceptable period of mourning today,
before it is reclassified as pathology, can be considerably shorter. The pathological
threshold was two months in DSM-IV, but even this threshold was removed in the
DSM-5, making it possible to diagnose the bereaved as disordered after just two
weeks of intense sadness. Barthes deplores the fact that our society today denies
mourning, leaving to the individual the moral duty to internalize his or her suffering
(Barthes 2010, 163). Whatever the intensity of his sorrow, Barthes categorically
refused the medical term of depression for describing his condition. He intention-
ally distorted the term’s meaning by inferring, for example, from the observation, “I
resist the world, I suffer from what it demands of me, from its demands,” to the
conclusion that “The world depresses me” (Barthes 2010, 135). Barthes refused to
consider himself to be suffering from a depression because admitting (in the passive
form) “I’m depressed” appeared to him as a kind of surrender that commands you
to clinically behave like a depressed person. That is, depression is a medical label
that carries contradictory meanings in the eyes of the patient. On the one hand, it
commonly functions as a welcome legitimate medical social excuse. On the other
hand, social or familial pressure that demands a medical definition of the sadness
may obscure its existential meaning to the individual.
“Diagnosis Creep” and the Philosophical Sociology of Concept

Deployment
The dramatic changes in estimated prevalence concerning depression raise another

question: Why is it so easy to expand diagnostic categories beyond the strict bounds
of mental disorder? There is of course the simple ambiguity that the term can be
used to refer to both pathological and normal emotions. Beyond that, there is a miss-
ing discipline of the “sociology of concept deployment” that would explore the
techniques, ambiguities, and fallacies by which concepts are expanded beyond their
previous bounds to encompass a larger domain with the acquiescence of those using
the concept. Perhaps part of this puzzle in the case of depression is not so much
conceptual but has to do with a sense of compassion, that people who are suffering
are in need and deserving of help and should be able to receive the help they need,
even if the source of their suffering is not a genuine medical disorder.
One important piece of the “concept deployment” puzzle has to do with psycho-
logical essentialism (Medin and Ortony 1989). Many concepts apply not only to
things that share apparent properties but to anything that shares some inferred
underlying essential nature with an initially identified class of prototypical cases.
Because we do not know the underlying essential processes that constitute the dys-
functions that occur in depressive disorder, it is possible to argue without fear of
being conclusively refuted that further processes that are considered normal sadness
might share that underlying essence and be disorders. Such essentialist extensions
of concepts can also be supported by a theory. For example, if one claims that mild
depression tends to lead to severe depression and thus tends to be prodromal for a
full-blown disorder, then one may tend to categorize milder states of sadness as
likely depressive disorders; and, if one theorizes about depression as lack of sero-
tonin, one may extend the concept to milder cases based on lowered serotonin.
Another reason it is easy to extend the concept of depression might be called the
“fallacy of prototype extension.” When trying to define the domain of application of
a concept, people commonly tend to focus on central, prototypical examples but not
to systematically address potential counterexamples, thus emphasizing necessary
conditions over sufficient conditions. If one tries to define the notion of a depressive
disorder, one will naturally be drawn to the idea that it is a matter of extraordinarily
high levels of sadness. The problem is that the definitional process includes no sys-
tematic counterexample formulation of cases of intense sadness that are not disor-
ders to ensure that the proposed definition is not only necessary but a sufficient
condition. The “dimensional” approach to diagnosis combined with such essential-
ist thinking leads to the classic “slippery slope fallacy” – the fallacy of thinking that
just because there is lack of any sharp dividing line between mild and severe depres-
sion, therefore there is no essential difference between the extremes. This leads to
the conclusion that sadness must be disorder “all the way down” to the mildest
cases. Thus, in some diagnostic formulations, even one or two depressive symptoms
can constitute “subthreshold” or “subsyndromal” depressive disorder.
Additionally, mental health professionals are heavily biased towards not missing
genuine cases and less concerned about false-positive diagnoses in which a normal
individual is mistakenly diagnosed as disordered. Professionals are apt to err on the
side of seeing pathology to avoid making a mistake that could lead to terrible con-
sequences for the misdiagnosed individual, whereas the impact of unneeded treat-
ment is not seen as so worrisome. The attempt to understand the concept of
depression and its extensive deployment within the mental health professions
requires cross-disciplinary perspectives from at least psychiatry, philosophy, and
sociology to understand our transformed application of this concept.
Integrating Biological and Social Views of Depressive Disorder
One opposition firmly embraced by most scholars is that between biological and
social-constructivist approaches to depression. Many of the authors in this volume,
while no doubt wanting to escape any such dichotomy, do tend to focus their atten-
tion on one or the other of these poles. Yet it is obvious both that there is a species-
typical biological substrate that forms the foundation for social constructions of
depression, and that human sociocultural malleability allows great scope to social
formulations. A “hybrid” conception attempts to encompass both truths by acknowl-
edging a biologically based etiology for mental disorder while affirming the role of
social construction in cultural manifestations of disorder (Wakefield 1992; Hacking
1999). Even if a mental disorder has a biological essence that is a real malfunction
of mental processes in the medical sense, its superficial features might vary with
social circumstances because underlying biological conditions may express them-
selves in a context-sensitive way.
If one assumes that sociocultural shaping involves alteration of brain tissue func-
tioning, then novel social constructions can yield genuinely novel dysfunctions (i.e.,
novel breakdowns in biologically designed capacities) as side effects. For example,
as technology advances, we are forced to make deliberative decisions about learn-
ing, eating, sex, reproduction, aggression, and play that were not needed in earlier
epochs in which natural motivational systems would have held sway. The tension
created by the provocation and exploitation of desire in market-driven economies
even while demanding extraordinary levels of control over these desires can yield
genuinely new pathologies.
When do the results of the interaction of biology and society become disorders?
The result of cultural sculpting of human beings in socially desired ways, from
stretching lips to developing autonomy to exploiting differences in mathematical
talent to create a technical elite, is not a disorder if there is no socially defined harm.
However, in the process of reshaping human beings as social artifacts, disorder
attributions do commonly arise in three ways.
First, the construction process can be pursued so relentlessly that damaging side
effects occur that constitute true disorders. For example, the chronic stress of con-
temporary competitive educational and occupational environments that wring as
much productivity as possible from the naturally talented can cause anxiety disor-
ders in the vulnerable.
Second, when novel social practices are embraced, dysfunctions that have existed
all along but been considered only minor anomalies because they have not caused
sufficient harm may be reevaluated, and their harm may now be deemed sufficient
to constitute a disorder. For example, minor dysfunctions in corpus collosum growth
caused no harm and thus were not disorders until cultures exploited human capaci-
ties to invent reading, which demands high brain-hemispheric information transfer
for which the corpus collosum is responsible. Consequently, those minor dysfunc-
tions have emerged as major obstacles to social participation and constitute the
genuine disorder of “dyslexia.”
Third, due to normal variations unfavorable to the social resculpting process,

some individuals may fail to adequately reach a constructed ideal. These individuals
are sometimes claimed to be defective and classified as disordered. However, such
judgments are conceptually questionable. When normal biological variation resists
conformity to social construction, that is best not considered a disorder no matter
how tempting it is for societies to use the “disorder” label as a cudgel to enforce
socially preferred change, because otherwise psychiatry becomes an oppressive
social control profession. The fallacy underlying such mislabeling is that cultural
ideology falsely declares the constructed ideal as “natural” so that when individuals
who are in fact quite normal do not match it, they are judged disordered.
Incorrectly labeling socially valued outcomes as natural and therefore classify-
ing normal variations that fail to manifest the socially desirable features as disorders
is not only incorrect but oppressive at its core. It encompasses such historical
episodes as classifying runaway slaves as suffering from “drapetomania,” and
classifying men who masturbated and women who experienced clitoral orgasms as
disordered during the Victorian era. In our own day, this fallacy encompasses label-
ing normal-range anxiety about public performances demanded by many of today’s
occupations as “social phobia,” labeling normal-range rambunctiousness in children
who have difficulty satisfying demands to sit quietly at their desks in school as
ADHD, and labeling those who are sad and therefore inefficient in their social role
performances as depressively disordered.
Overview of the Contributions
Always too close or too far: the phenomenon of depression is an object that seems
to accept no good focal length. This volume’s aim is to bring depression more
into focus by bringing together psychiatrists, philosophers, sociologists and
anthropologists to create a multidisciplinary composite of depression and shed light
on depression’s multifaceted nature. A second goal is to present a truly international
perspective on depression. It seemed important to encompass the experiences of
psychiatrists from different cultural contexts, but also to include scholars with
different theoretical backgrounds and who work within different methodologies.
The many areas that are covered include clinical research, epidemiology, neuro-
imagining, evolutionary psychology, psychoanalysis, sociology, medical anthropology,
philosophy, and translational research.
The volume contains 12 papers. The first five chapters (including this introduc-
tory the chapter, “Introduction: Depression, One and Many”) deal with overarch-
ing conceptualizations of depression.
In the chapter, “The Current Status of the Diagnosis of Depression”, British pro-
fessor of psychiatry Sir David Goldberg presents an overview of recent clinical,
epidemiological and genetic studies. He argues that depression is vaguely defined
and covers a heterogeneous mix of conditions, and overlaps with a wide range of
mental as well as somatic disorders that merge clinically with normality. Goldberg
concludes that recognizing this extreme heterogeneity – which contrasts with the
apparent homogeneity represented in classificatory systems and textbooks – is criti-
cal for working clinicians.
In the chapter, “The Continuum of Depressive States in the Population and the
Differential Diagnosis Between “Normal” Sadness and Clinical Depression”, Italian
professor of psychiatry Mario Maj addresses the problem of distinguishing normal
sadness from clinical depression. Observing that recent clinical and epidemiologi-
cal studies fail to establish clear diagnostic boundaries for depression, Maj contrasts
two rival approaches, the “pragmatic” versus the “contextual,” to establishing such
a boundary. The pragmatic approach, favored by both the DSM-5 and ICD-10
(World Health Organization 1992) diagnostic systems, claims that clinical utility
(e.g., usefulness in prognosis and treatment) is the major criterion for establishing
the boundary between normal sadness and depression. The contextual approach, by
contrast, aims at better taking into account all the contextual factors that indicate
whether sadness is a proportionate response to environmental circumstances, and
insists on the importance of the conceptual validity of the distinction. Maj examines
the strengths and weaknesses of both approaches, and concludes that neither
approach is completely satisfactory, thus that further qualitative research is needed
for resolving the issue.
In the chapter, “Beyond Depression: Personal Equation from the Guilty to the
Capable Individual”, French sociologist Alain Ehrenberg examines the “global
idiom” of depression that cuts across contemporary societies. He argues that the
replacement of psychoanalytic theories by the cognitive neurosciences has led to a
reconceptualization of depression, with a new emphasis on individual autonomy
and the capacity for emotional self-control. Whereas at the end of the nineteenth
century the depressed individual was conceived of as a guilty individual, he or she
is now seen as an individual whose emotional and action capacities are dysfunc-
tional and need to be restored. This transformation has influenced our view of peo-
ple’s responsibility for their physical and psychological health. Ehrenberg concludes
that depression should be seen not only as an individual disorder but as one pro-
foundly connected with our ways of being affected by others and our ways of acting
as autonomous individuals in our contemporary societies.
In the chapter, “Depression as a Problem of Labor: Japanese Debates About
Work, Stress, and a New Therapeutic Ethos”, Japanese professor of anthropology
Junko Kitanaka traces the evolution of the Japanese national debate about depres-
sion during the 1990s, which she argues was connected to feelings of increasing
stress in the workplace. She describes and evaluates the recent transformation in
Japanese culture in which depression became the target of public surveillance. This
shift in the conceptualization of depression, from a “private matter” to a “public ill-
ness” sheds light on the social nature of depression, and especially its relationship
with recent development of the neoliberal economy.
The chapters “Darwinian Blues: Evolutionary Psychiatry and Depression”, “Is
an Anatomy of Melancholia Possible? Brain Processes, Depression, and Mood
Regulation” and “Loss, Bereavement, Mourning, and Melancholia: A Conceptual
Sketch, in Defence of Some Psychoanalytic Views” examine depression from

three very different theoretical perspectives: evolutionary, neurophysiological, and
psychoanalytic.
In the chapter, “Darwinian Blues: Evolutionary Psychiatry and Depression”,
Canadian philosopher Luc Faucher critically examines two recent evolutionary
models of depression: Nesse’s low mood model, and Andrews and Thomson’s
“analytical rumination” model. The author describes the strength and weaknesses of
these two models, and their links with previous models (like the “social competi-
tion” model developed by Price or the “bargaining model” proposed by Hagen). He
concludes that, despite the fact that the speculative nature of these models prevents
us from applying them as established doctrine in the clinic, evolutionary scenarios
still can play a “heuristic function” in psychiatry. Faucher argues, however, that it is
doubtful that evolutionary psychology can one day constitute the “basic science”
that some psychiatrists, such as Nesse, envision.
Could future neuroscience shed more light than evolutionary psychology on the
understanding of depressive mechanisms? In the chapter, “Is an Anatomy of
Melancholia Possible? Brain Processes, Depression, and Mood Regulation”,
French philosopher Denis Forest identifies many weaknesses in the current neuro-
biological approach to depression, but argues that these problems can be addressed.
The author calls for further conceptual analysis of mood and affective states, and
advocates for a more elaborate epistemological reflection on the interdependence
between physiological and emotion regulation mechanisms. Finally, he argues for
a multidisciplinary approach including neuroscience, moral philosophy and social
science that would encompass the several kinds of explanations provided in differ-
ent disciplines.
In the chapter, “Loss, Bereavement, Mourning, and Melancholia: A Conceptual
Sketch, in Defence of Some Psychoanalytic Views”, French philosopher and psy-
choanalyst Pierre-Henri Castel, through an examination of Henry James’ story,
“Altar of the Dead”, appraises the psychoanalytic conceptions of melancholia and
mourning put forward by Karl Abraham, Sigmund Freud, Melanie Klein and
Jacques Lacan. Castel insists that the central dimension of any depressive state –
commonly neglected in behavioral approaches – is the intentionality of the patient’s
loss. What is lost to whom? What determines the choice to mourn and live with the
loss versus in effect to die with the lost person? These simple questions are crucial
for clinical practice and offer a complex view that illuminates the parallel that often
exists between mourning and melancholia concerning the lost object. This chapter
also offers an implicit argument that clinicians can benefit greatly from studying not
only science articles and medical textbooks, but also literature and humanities.
The chapters “Suffering, Meaning and Hope: Shifting the Focus from Depression
in Primary Care”, “An Insider View on the Making of the First French National
Information Campaign About Depression” and “Extrapolation from Animal Model
of Depressive Disorders: What’s Lost in Translation?” examine depression in specific
contexts: primary care, public health, and animal research.
In the chapter, “Suffering, Meaning and Hope: Shifting the Focus from
Depression in Primary Care”, British physician and medical philosopher Christopher
Dowrick argues that, despite its being one of the most frequently diagnosed mental
disorders in primary care settings, “the diagnosis of depression is not fit for the
purposes of primary care.” The author lists and analyses the defects of the “depres-
sion” label: it lacks validity, it lacks utility, it has iatrogenic effects, and it lends
itself to a reductionist perspective. Dowrick encourages the development of a new
conceptual framework, nourished with medical knowledge as well as philosophical
and political insights. Dowrick concludes by highlighting the centrality of two con-
cepts for clinical settings: coherence (as opposed to the fragmented individual that
medical textbooks deal with) and engagement (as a remedy for the neglect of the
intersubjective structure of our emotional states in medical literature). This new
perspective, the author claims, would help develop “a theory of the person based not
on passivity but on agency and creative capacity”.
In the chapter, “An Insider View on the Making of the First French National
Information Campaign About Depression”, French sociologist Xavier Briffault
investigates the implications of depression diagnosis for public health strategies.
Briffault draws on his personal experiences working on the implementation of the
first French national information campaign on depression in 2007, to identify meth-
odological difficulties related to such national campaigns. To positively impact the
population, a national information campaign must rely on a broad consensus
amongst experts as well as rigorous scientific evaluation. Unfortunately, neither of
these goals were attained at the end of the French national campaign process. Given
the harsh ideological controversies that exist concerning depression (especially in
France, where psychoanalytic theories are still influential), the national campaign
turned into a battle ground amongst professionals. Briffault provides many illustra-
tions of the negotiations between the different parties that occur in such a campaign,
and describes the largely hidden yet important role played by DSM in the French
debate.
In the chapter, “Extrapolation from Animal Model of Depressive Disorders:
What’s Lost in Translation?”, French philosopher Maël Lemoine explores the theo-
retical underpinnings of animal models of depression, identifying the main episte-
mological and methodological difficulties confronting such models. Lemoine asks
when, and on what grounds, we can say that an animal model is successful, arguing
that the main difficulties lie not in the mental nature of depression but in its fuzzy
clinical characterization (its exophenotype). He takes the example of the mono-
amine hypothesis of depression, which is supported by a variety of animal models
related to each other in complex ways. Lemoine distinguishes between mosaicism
of animal models (the modelling of a disease by the way different animal models
operate at different levels of explanation) versus chimerism of animal models (dif-
ferent animal models are used in order to instantiate one specific aspect or part of a
disease explanation). His analysis illuminates the complex ways animal models and
translational psychiatry may help to lead to a progressive reconceptualization of our
prescientific notion of depression.
Finally, the volume ends with the chapter, “Psychiatry’s Continuing Expansion
of Depressive Disorder”, an epilogue in which American philosopher of psychiatry
and clinician Jerome C. Wakefield and sociologist Allan Horwitz review recent
developments and provide a retrospective account of the controversial influence of

their book, The Loss of Sadness, initially published in 2007, on the North-American
debate concerning depression. Although their critical analysis of the decontextual-
ized symptom-based definition of major depression in DSM-IV was widely praised,
the revision of the DSM-5 moved in the opposite direction to the one they sug-
gested: DSM-5 removed the one contextual criterion in the definition of major
depression, i.e. the bereavement exclusion criteria. Wakefield and Horwitz, in this
final chapter, give a comprehensive overview of the recent scientific debate concern-
ing depression, and document the ever-increasing tendency of modern societies to
pathologize normal sadness.
Acknowledgment This volume grew out of a conference held in Paris in June 2010 on the occa-
sion of the publication of the French translation of Horwitz and Wakefield’s book, Loss of Sadness,
titled “Tristesse ou depression?” [Sadness or Depression?]. This international conference, orga-
nized by Françoise Parot and Steeves Demazeux, was financed by the project PHS2M (‘Philosophie,
Histoire et Sociologie de la Médecine mentale’) and supported by the Agence Nationale pour la
Recherche (ANR-08-BLAN-0055-01). We want to express our deep gratitude to the director of the
PHS2M, Pierre-Henri Castel, to Françoise Parot – who translated the Loss of Sadness into French,
and who led this collective project – and to all the participants in this initial event: Derek Bolton,
Xavier Briffault, Pierre-Henri Castel, Françoise Champion, Christopher Dowrick, Alain Ehrenberg,
Luc Faucher, Denis Forest, Bernard Granger, David Healy and Fernando Vidal. We are grateful to
David Goldberg, Allan Horwitz, Junko Kitanaka, Maël Lemoine and Mario Maj who later accepted
invitations to join the project. Finally, we would like to thank co-editor Philippe Huneman and
Springer’s Ties Nijssen for their complete support and confidence in this project throughout this
long publication process.
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The Current Status of the Diagnosis
of Depression
David Goldberg
Abstract The term “depression” is an umbrella that covers a large number of het-
erogeneous depressive disorders, with symptoms overlapping with other common
mental disorders on the one hand, and chronic systemic disease on the other. It cov-
ers both disorders that definitely benefit from recognition and treatment by the clini-
cian, and those that can be thought of as homeostatic reactions to adverse life events,
which will remit spontaneously whether or not they are detected. The former group
includes depressions following severe loss events in vulnerable individuals.
Typical bereavement reactions can readily be distinguished from depressive dis-
orders, and requires only supportive care from clinicians. However, bereavement
can also precipitate a depressive disorder in vulnerable people which most definitely
benefits from treatment, and has additional features not usually seen in the more
usual bereavement reactions. Vulnerability factors include genes, early maternal
attachment, adverse childhood experiences and personality factors.
In their relationships with other physicians, what has come to be known as “major”
depression is the flagship of psychiatry – the condition that general physicians com-
monly neglect to detect, but which co-occurs with many chronic physical disorders
that produce disability. It is often referred to as though it is a homogenous concept,
and many countries have mounted national campaigns aimed at improving detection
rates (Regier et al. 1988a; Paykel et al. 1997; Jorm et al. 2006).
In several other areas of the classification of mental disorders, we have come to
acknowledge that there are spectrums of disorder, for example, schizophrenias,
autistic disorders and eating disorders. It will be argued in this chapter that there are
a wide range of depressive disorders, and that the manifestations of depressive dis-
orders are influenced by genetic factors, early childhood adversity and pre-morbid
personality. These factors help to determine which of the overlapping syndromes of
depression a particular individual is likely to develop. Depression also merges into
normality and frequently occurs as a transient reaction to a wide range of adverse
D. Goldberg (*)
Psychiatry Research Trust, Institute of Psychiatry, London, UK

J.C. Wakefield, S. Demazeux (eds.), Sadness or Depression?
DOI 10.1007/978-94-017-7423-9_2
18 D. Goldberg
circumstances. The current concept is a blunderbuss approach which gathers

together a heterogeneous collection of common disorders under a single umbrella.
The Case for Heterogeneity
When once recalls that the DSM diagnosis should be made when a patient – in addi-
tion to one of the required symptoms – has any four out of eight other symptoms, and
then recalls that several of these are opposites of one another, it is easy to see how this
heterogeneity might arise. For example, a patient who has psychomotor retardation,
hypersomnia and gaining weight is scored as having identical symptoms as another
who is agitated, sleeping badly and has weight loss. Lux and Kendler (2010) studied
depression in a sample of twins and distinguished between “cognitive” and “neuro-
vegetative” symptoms, and show that these had different relationships to a larger set
of potential validators. They conclude that their results “challenge our understanding
of major depression as a homogeneous categorical entity”. Others have been able to
separate the various depressive symptoms, and to compare the relative efficiency of
each symptom to making the diagnosis (McGlinchey et al. 2006). Jang et al. (2004)
factor analysed a larger set of depressive symptom scales, and found that they could
identify 14 different subscales, which had rather low inter-correlations, and very dif-
ferent heritabilities. Given these findings, to declare that all those satisfying the
DSM-5 criteria for the diagnosis of “Major Depressive Disorder” are suffering from
the same disorder seems like magical thinking.
Can Homeostatic Responses to Adverse Circumstances

Be Included as Cases of Depression?
Epidemiological studies (Regier et al. 1988b; Melzer et al. 1995; Andrews et al. 2001)
reveal such high prevalence of depression in the developed world that some have sup-
posed that such syndromes in the community often represent transient homeostatic
responses to internal or external stimuli that do not represent true psychopathologic
disorders (Regier et al. 1998). It is certainly true that many people develop an episode
of depression after a loss event, or in response to some other transient, adverse circum-
stance. In a paper prepared in the preparations for DSM-5, it is clearly stated that a
mental disorder must not merely be an expectable response to common stressors and
losses (Stein et al. 2010). It has also been shown that the public does perceive depres-
sive symptoms as an indication of mental disorder when occurring in the context of
adverse life events (Holzinger et al. 2011). Maj (2011) has considered the differentia-
tion between a depressive illness and normal sadness, and argues that the latter is
always triggered by a life event and appears to be proportionate to that event. By
contrast if depression is triggered by a life event it is disproportionate to that event in
its intensity and duration, and in the degree of the functional impairment it produces.
The Current Status of the Diagnosis of Depression 19
We know, from the large placebo response to antidepressants that many milder cases
remit without specific treatment, suggesting that they are indeed homeostatic responses
to life stress, as others have suggested (Wakefield 1997). Even cases of moderate
severity may respond to non-specific psychological interventions like problem solv-
ing (Gath and Catalan 1986). All these arguments appear to support the idea that what
passes for depression in community surveys are often merely gloomy people with
transient disorders, whose distress should not be medicalised.
The concept of “disproportionate” depression is a slippery concept, as the clini-
cian may suppose that if he or she had experienced that particular event they would
not have developed the particular set of symptoms of the patient before them: but the
clinician may well be much less vulnerable to developing symptoms, and may not
justifiably know how stressful the situation was to that individual. The link between
severe loss events and depression was first conclusively demonstrated by Brown and
Harris (1967), who showed that severe loss events occurred in 68 % of community
onset cases of depression among a population of working class women, in contrast to
23 % of normal controls. While this undoubtedly establishes severe loss events as
precipitants of depressive episodes, we may make two further observations: 32 % of
onsets of depression do not follow severe loss events, and the fairly high rate of loss
events in the control population is not followed by an onset of depression for a sub-
stantial proportion of those so exposed. In other words, many people are relatively
resilient in the face of loss, or at any rate to not develop depression.
It is also important that while sadness is a single, very common experience, that
the diagnosis of depression refers to the development of a set of at least five symp-
toms, present for most of the time in the previous two weeks, and is associated with
disability and distress. This goes well beyond the simple experience of sadness, and
frequently persists for much longer than two weeks. Furthermore, a range of psy-
chological and pharmacological interventions produce much better results than a
simple placebo (NICE 2004).
Only a small minority of depressed people are seen by psychiatrists, the great
majority are seen in primary care and general hospital settings, usually presenting
to doctors with somatic symptoms. Having excluded a physical cause for these
symptoms, the doctor needs to recognise the depressed state, and offer an interven-
tion for depression. The presenting somatic symptoms often remit provided the
depression responds to the intervention offered.
How Can Bereavement Be Distinguished from Depression?
The psychological sequelae of the death of a loved one are themselves quite hetero-
geneous. In most cases, there is very little difficulty, since a normal bereavement
consists of quite distinctive phenomena which are quite unlike depression. Sigmund
Freud (1917) pointed this out in a famous paper called “Mourning and Melancholia”
(see Castel, this volume), and made the point that whereas in mourning, time is
needed for reality-testing to “free the ego of its libido of the lost object, the complex
20 D. Goldberg
of melancholia behaves like an open wound, drawing to itself energies…from all

directions, and emptying the ego until it is totally impoverished”. In more prosaic
language, during bereavement the person grieves for the lost person, and the grief
comes in waves, rather than being a constant phenomenon. Nor does the survivor
usually experience self hatred and wish to die. The following excerpt is from an
authoress (Jamison 2009) who has experienced both depression and bereavement:
Time alone in grief proved restorative. Time alone when depressed was dangerous. The
thoughts I had of death after (my husband’s) death were necessary and proportionate. They
were of his death, not my own. With depression, however, it was my own death I sought out.
In grief, death occasions the pain. In depression, death is the solution to the pain….My
mood, fixedly bleak during depression, was not so during grief. It was mutable and com-
monly rose in response to the presence of my family and friends. I was generally able to
meet the demands of the world. ….Even during the worst of my grief I had some sense that
this would happen, that the weather would clear. I did not have this faith during the merci-
less months of depression.
However, medical classifiers love these polarities, and like to describe these
two phenomena as though they are quite different. Unfortunately real life is more
complex, since a bereavement can also precipitate a depressive illness, so the
clinician must listen carefully to the patient’s experience before deciding that
this is a typical case of bereavement, deserving of sympathy and perhaps symp-
tomatic and supportive help, rather than treating a depressive episode. The peo-
ple with typical bereavement are much less vulnerable to loss events than those
who become depressed when bereaved, and it is important to understand what is
known about the determinants of vulnerability. Some people develop depression
after adverse events that cause only transient reactions in more resilient people,
while others do not become depressed until they have experienced prolonged and
severe adverse experiences.
Some Determinants of Vulnerability to Depression
Caspi et al. (2002) used the Dunedin birth cohort to show that the extent to which
stressful life events were followed by depression is partly determined by the 5HT
transporter gene on chromosome 17. With two long version of the gene, there was
only a slight relationship, so that the probability of later depression rose from about
9 % with no stressful events, to about 12 % with four or more events. With the gene
heterozygous (one long, and one short version) the probability rose to about 24 %,
and with a double short version of the gene the probability rose to nearly 39 %.
There have been several replications of this finding since the original paper (Eley
et al. 2004; Kendler et al. 2005; Wilhelm et al. 2006). It would therefore appear that
part of the explanation for the greater vulnerability of some individuals to life stress
is the presence of a particular version of a gene – about a third of the Dunedin popu-
lation have the double short version of the gene, with a further 51 % being hetero-
zygous, and therefore less highly susceptible to stressful events.
This genetic variant – having either a double short (ss), or one long and one short
gene (ls) – has also been shown to interact with the quality of maternal responsiveness
to the child. Barry, Kochanska, and Philibert (2008) also showed by prolonged natu-
ralistic observation of 88 mother infant pairs, that there was no such relationship for
those homozygous for the long gene (ll). However, with ss and ls infants, low mater-
nal responsiveness was associated with very poor attachment, while high respon-
siveness was associated with high infant attachment (similar to those with the ll
gene); medium maternal responsiveness was intermediate between the two. Negative
early experience amplified the risk conferred by the short 5-HTT allele, whereas
positive early experience, while it served to buffer that risk, did not appear to lead
to better outcomes than outcomes for children without the genetic risk.
If the mother is responsive to her infant, normal attachment occurs whatever the
maternal genes, but the combination of an unresponsive mother and either ss or ls in
the 5HT transporter genes produces insecure attachment. Disorders of maternal
attachment may occur as a result of maternal depression, or a failure of the mother
to bond with the infant for other reasons.
There is also evidence that adversity in the form of either neglect and physical
abuse in early and middle childhood may further increase vulnerability to stressful
events. As genetic contributions have been introduced into research designs it has
become increasingly clear that some individuals contribute to the onset of their own
adverse environments and that genetic effects may contribute to psychopathology
indirectly through their influence on the child’s behaviour (Rudolph et al. 2000).
The Importance of Anxiety in Depressive States
Epidemiological studies of mental disorders in the community all show substantial

co-morbidity between depression and generalized anxiety disorder (GAD). This
occurs despite the fact that GAD has to last 6 months before it is counted, whereas
depression only needs to have lasted 2 weeks. In a large study of patients attending
primary care in 11 countries, if the duration of symptoms required for GAD is short-
ened from 6 months to 1 month, the prevalence of “co-morbid” depression and GAD
goes up from 3.4 to 5.7 %, while the prevalence of depression without anxiety drops
from 4.7 to 2.3 % (Goldberg et al. 2011). Provided that anxious depression refers to
the simultaneous experience of symptoms of both anxiety and depression, it is there-
fore more than twice as common as depression without anxiety. Anxious forms of
depression are indeed the commonest forms of depression in general medical settings,
although the anxious symptoms are frequently missed. Longitudinal studies have
shown that co-morbid cases of depression and anxiety have experienced more severe
adversity in early childhood (Moffitt et al. 2007; Richards and Goldberg 2008).
These co-morbid cases (major depression plus generalized anxiety disorder)
have a worse outlook and a longer course than depression occurring on its own, and
the suicide rate is also higher in these cases. These differences are consistent for
both major depression and bipolar disorder when anxious symptoms are present
22 D. Goldberg
(Goldberg and Fawcett 2012). There is consistent evidence that there are personality
differences when anxious symptoms are also present, with higher score on negative
affect (neuroticism) (Goldberg et al. 2009). When anxious symptoms are absent, the
depressive disorders is likely to have less severe depressive symptoms, and to have
parents with an excess only of depressive symptoms on their own; in contrast, anx-
ious depressives have parents with a wide range of common mental disorders, also
including mania (Goldberg et al. 2014). Using Cloninger’s personality constructs,
this study also showed that while non-anxious depressives were no more likely to be
harm avoidant than controls, the anxious depressives were likely to be high on harm
avoidance and reward dependence.
There is some suggestive evidence that there are also biological differences
between anxious and non-anxious depression. In an early study (Meller et al. 1995).
adrenocorticotrophic hormone (ACTH) and cortisol levels were measured in 14
patients with anxious depression following exogenous cortisol releasing hormone
(CRH) challenge. Compared to 11 patients with non-anxious depression and 27
healthy controls, subjects with anxious depression exhibited a significantly attenu-
ated response. However, patients were not required to be medication free at the time
of testing, and depressed patients could meet criteria for either major depression or
bipolar disorder. In a structural neuro-imaging study, 49 patients with anxious
depression were compared with 96 patients with depression without anxiety and
183 healthy controls. Those with anxious depression had increased grey matter vol-
ume in the superior temporal gyrus, extending into the posterior middle temporal
gyrus and inferior temporal gyrus in the right hemisphere when compared to the
depressed group without anxiety (Inkster et al. 2011).
Cases of depression with apathy, psychomotor slowness low energy therefore
appear to have quite different characteristics than the more common anxious depres-
sives, yet both are given the same name: major depressive disorder. This is perhaps
the most important sub-form of depression, with fundamental differences from the
anxious forms of depression. This important group of depressions has been much
less well studied than the anxious depressions, partly because they have been
defined by exclusion, and partly because they are buried in the overall concept of
“major depression”.
Multiple Co-morbidity, or Depressive Syndromes Influenced

by Personality?
The term “co-morbidity” was applied by Alvan Feinstein (1970) to refer to those
cases in which a ‘distinct additional clinical entity’ occurred during the clinical
course of a patient having a particular illness (italics added). In its original meaning,
it referred to “a medical condition existing simultaneously but independently of
another condition”. If the two disorders are completely unrelated, for example isch-
aemic heat disease and carcinoma of the prostate, this makes good sense, but it is
also used to refer to conditions which are highly related to each other, such as
anxiety and depression. It is also extended to the overlapping syndromes of com-

mon mental disorders, so that a person who develops a depressive illness with
obsessional symptoms and panic attacks will be said to suffer from ‘co-morbid’
major depression, obsessional compulsive disorder and panic disorder.
There is nothing wrong with this, provided it is used merely to catalogue the
symptoms that are present in a particular patient, and to direct the clinician to par-
ticular interventions. Unfortunately it tends to create the idea in the clinician’s mind
that the patient is suffering from three independent disorders, which happen to be
present at the same time.
Karl Jaspers (1923) argued that below the severe group of disorders (psychoses
and organic disorders of the brain) were the ‘psychopathien’, which comprise
abnormal personalities and the neuroses. These are “phenomena which continually
keep merging into one another…there is no sharp dividing line between types (of
neuroses and personality disorders) nor is there a decisive borderline between what
is healthy and what is not. A diagnosis remains typological and multi-dimensional,
including a delineation of the type of personality”.
There are two different ideas here: rather than different diseases, we should think
of overlapping syndromes; and in making sense of these we should consider the
pre-morbid personality of the patient. These provide a key to some of the various
depressive syndromes.
People who are normally punctual, orderly and conscientious and who are vul-
nerable to affective disorders will, when faced with a severe life event, develop
severe and distressing obsessional and compulsive symptoms. When the accompa-
nying depressive symptoms have been treated, these will disappear. The person has
been suffering from one disorder, not two.
In similar manner, a habitually anxious person may develop panic attacks when
depressed, and an introspective person with mild health concerns may develop quite
severe hypochondriacal symptoms when depressed. The combinations of symptoms
experienced by depressed individuals are by no means as neat as medical textbooks
suggest – these are overlapping syndromes, rather than independent disorders
(Goldberg 2011).
However, there are four other, important forms of depressive illnesses.
Depression Presenting with Somatic Symptoms
In general medical settings, this is by far the most common presentation of depres-
sive illness. These patients are experiencing the symptoms that occur in depression,
but their main reason for consulting is to find the cause, and obtain alleviation for,
distressing somatic symptoms. When no cause can be found for these symptoms,
the clinician may consider the depressive symptoms as a cause for these pains and
discomforts. There is now impressive evidence for inflammatory changes in depres-
sion, and one possible explanation for these pains are pro-inflammatory cytokines
(Capuron and Miller 2004; Zunszain et al. 2011).
24 D. Goldberg
Whatever the cause, the most rational management of these patients is to help
them with their depressive symptoms, and to explain that their pains are real, and
not imaginary. The best management strategies for these forms of depression are
described elsewhere (Rosendal et al. 2009; Olde Hartman et al. 2013).
Depression Accompanying Chronic Physical Illnesses
These depressions are often poorly recognised by generalists, whose attention is

largely for the real physical disorder, and typically confine themselves to the treat-
ments for it. Rates of depression are at least double that among the healthy in a wide
range of chronic physical disorders, and in some may be five times the usual rate
(Goldberg 2010).
Diagnosis of these depressions is complicated by the fact that four of the “diag-
nostic features” of depression may well be caused by the physical illness, including
fatigue, poor sleep, poor appetite and weight loss. This may cause confusion since
no clear threshold for the numbers of symptoms needed for a diagnosis seems to
exist if such symptoms are to be discounted. However, if there is a positive reply to
either of the usual two screening questions, it is only necessary to ask three addi-
tional questions dealing with poor concentration, ideas of worthless and thoughts of
death. A total of three symptoms or more from this list of five symptoms allows
depression to be diagnosed with high sensitivity and specificity, when assessed
against the full list of criteria (Zimmerman et al. 2006; Andrews et al. 2008).
Successful treatment of the depression is associated with a lower mortality and bet-
ter collaboration with the necessary physical treatments.
Such patients report a poor quality of life, and experience more pain from their
physical illness than they would if there depression was treated. The special task of
the physician is to reach agreement with the patient that he or she is indeed depressed,
and to explain the effects that this is having on the quality of the patient’s life, the
severity of any pains that are experienced, and the disability associated with the
physical illness. The range of treatments that are effective in depression among the
healthy are all effective in these patients, and the only special measure required of
the clinician should an antidepressant drug be used is to guard against harmful inter-
actions between the antidepressant and drugs used for the physical illness.
Pseudo-demented Depression
In older people, depression may present as an apparent dementia, but the presenting
symptoms turn out to be due to inattention and impaired concentration, while symp-
toms of depression are undoubtedly present and may be elicited by direct enquiry. It
is important to grasp that there is no clear dividing line between early dementia and
the apparent dementias referred to here: there may well be mild, early signs of
organic damage, but when a depressive process is added the clinical picture may
resemble a definite dementing illness.
The special task here is to reassure both patient and carer that the memory prob-
lems are not due to advanced cerebral disease, and are likely to improve a great deal
with treatment of the depression.
Depression Due to Drugs, Both Licit and Illicit
The list of drugs that can themselves cause depression is a long one, and includes
drugs prescribed by doctors, excessive use of alcohol, as well as a wide variety of
‘recreational’ drugs and other toxic agents. Many drugs have been said to cause
depression on slender evidence, but among those for which the evidence is good are
included β-blockers, steroids, some anti-viral agents and digoxin (Patten and Love
1993; Zdilar et al. 2000). Among legal drugs, alcohol is easily to most important
agent producing depression.
Conclusion
While these various forms of depressive illness need to be known and recognised by
all working clinicians who are not trained psychiatrists, there are in fact strong argu-
ments for continuing to see them all as different varieties of depressive illnesses,
despite their aetiological and clinical heterogeneity. While many cases of depres-
sion can be regarded as homeostatic reactions to adverse circumstances, it is impor-
tant to recognise that such reactions can be prolonged, and are accompanied by both
distress and disability.
It must also be recognised that an individual’s vulnerability to adverse circum-
stances is determined by factors both inherited and acquired by interactions between
genes and environment, and by various forms of child abuse. This helps to explain
the wide variety of reactions to a bereavement, ranging from any culturally sanc-
tioned bereavement reaction to typical depressive illnesses.
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The Continuum of Depressive States
in the Population and the Differential
Diagnosis Between “Normal” Sadness
and Clinical Depression
Mario Maj
Abstract One of the principles of the “neo-kraepelinian credo”, articulated in the

1970s, was that “there is a boundary between the normal and the sick”. In other
terms, it was maintained that there is a clear, qualitative distinction between persons
who have a mental disorder and persons who do not. A corollary to this principle
was the statement that “depression, when carefully defined as a clinical entity, is
qualitatively different from the mild episodes of sadness that everyone experiences
at some point in his or her life”. Apparently in line with this statement was the
observation that tricyclic antidepressants were active only in people who were clini-
cally depressed; when administered to other people, they did not act as stimulants
nor did they alter the subjects’ mood. Today the picture has changed dramatically.
Taxonomic studies have failed to support the idea that a latent qualitative difference
exists between major depression and ordinary sadness, arguing instead in favor of a
continuum of depressive states in the general population. We are left, therefore, with
two competing approaches: a “contextual” approach, which assumes that the dif-
ferential diagnosis between “true” depression and “normal” sadness should be
based on the presence or not of a triggering life event and on whether the response
is proportionate to that event in its intensity and duration; and a “pragmatic”
approach, positing that the boundary between depression and “normal” sadness
should be based on issues of clinical utility (i.e., thresholds should be fixed – in
terms of number, intensity and duration of symptoms, and degree of functional
impairment – which are predictive of clinical outcomes and treatment response).
This chapter summarizes the strengths and weaknesses of these two approaches.
M. Maj (*)
Department of Psychiatry, University of Naples SUN, Naples, Italy

DOI 10.1007/978-94-017-7423-9_3
30 M. Maj
The Evolving Target of Psychiatry
There was a time when the target of the psychiatric profession was very clear and
widely accepted. It was “madness”, that is, a few patterns of behaviour and experi-
ence which were clearly beyond the range of normality (Maj 2012a). The crucial
characteristic of those patterns, easily recognizable also by non-professionals, was
the apparent lack of meaning: ideas or perceptions without any foundation in real-
ity; emotions or behaviours that were clearly irrational. This “breakdown of ratio-
nality” (Bolton 2008) was more or less explicitly ascribed to some alteration in the
functioning of the brain (“mental illnesses are diseases of the brain”).
In the perception of part of the general public, of some colleagues of other medi-
cal disciplines, and, paradoxically, of some fervent critics of old asylums, this tradi-
tional target of psychiatry has remained unchanged: psychiatry only deals with
people who are “mad”.
However, the actual target of the psychiatric profession has changed dramatically
in the past decades. It has become a wide range of mental disorders, several of
which do have a “meaning” that can be reconstructed. The presence of a “dysfunc-
tion” in these conditions is still hypothesized but, according to the DSM-5, it is “a
dysfunction in the psychological, biological, or developmental processes underly-
ing mental functioning” (American Psychiatric Association 2013). So, the presence
of an alteration in the functioning of the brain is no longer a prerequisite.
Since several of these disorders are obviously on a continuum with normality,
fixing a boundary between what is normal and what is pathological has become
problematic. This boundary is often determined on pragmatic grounds, or on the
basis of “clinical utility” (i.e., prediction of clinical outcomes and response to treat-
ment), although this pragmatism may involve some tautology (in fact, requiring that
a diagnostic threshold be predictive of response to treatment seems to imply that a
condition becomes a mental disorder when there is an effective treatment available
for it) (Maj 2012b). Furthermore, there are mental disorders (depression is a good
example) for which several different treatments are available, the response to which
may be predicted by different diagnostic thresholds (e.g., the threshold predicting
response to interpersonal psychotherapy is likely to be different from that predicting
response to selective serotonin reuptake inhibitors (SSRIs), which in its turn is dif-
ferent from those predicting response to tricyclic antidepressants and to electrocon-
vulsive therapy).
In this new scenario, psychiatry has become the focus of opposite pressures.
On the one hand, the profession is being accused of unduly pathologizing ordi-
nary life difficulties in order to expand its influence (e.g., Horwitz and Wakefield
2007; Stein 2010). This criticism becomes harsher when the above-mentioned evo-
lution of the target of psychiatry from “madness” to a range of mental disorders is,
in good or bad faith, ignored: pathologizing ordinary life difficulties becomes “mak-
ing us crazy” (Kutchins and Kirk 1997). Of course, the argument is presented with
greater fervor when the perceived undue “pathologization” occurs in children or
The Continuum of Depressive States in the Population and the Differential… 31
adolescents, or when it is considered to be a consequence of an alliance between

psychiatry and the pharmaceutical industry.
On the other hand, the psychiatric profession is being pressured to go beyond the
diagnosis and management of mental disorders, acting towards the promotion of
mental health in the general population (e.g., World Health Organization 2001;
World Health Organization Regional Office for Europe 2005). Within this frame-
work, especially in those countries in which community mental health services are
most developed and psychiatrists are leading such services, there is a call for deal-
ing with “mental health problems” that are not proper mental disorders, such as the
serious psychological distress occurring as a consequence of a natural disaster or
the ongoing economic crisis. Furthermore, psychiatrists are being pressured to diag-
nose and manage proper mental disorders as early as possible, which means dealing
with a variety of conditions that may be “precursors” or “prodromes” of those dis-
orders, but more frequently are not, with the unavoidable risk of, again, pathologiz-
ing situations that are within the range of normality.
Indeed, the ongoing economic crisis is having a significant impact on the mental
health of the population in many countries, especially where scarce social resources
are available to protect people who become unemployed, indebted or poor due to
the crisis (Wahlbeck and McDaid 2012). Mental health services are often called to
intervene, in a situation of uncertainty and confusion about roles and competences.
A couple of recent episodes from my own country, Italy, are emblematic in this
respect. In 2012, a group of widows of entrepreneurs who had committed suicide,
allegedly as a consequence of economic ruin, marched in an Italian town under the
slogan “Our husbands were not crazy”. “It was despair, not mental illness, which
brought my husband to do that”, one of them said (Alberti 2012). In the same period,
in another Italian town, the widow of an entrepreneur who had committed suicide
blamed the professionals of a mental health service because they had not hospital-
ized him compulsorily. They had found him worried about his economic problems,
but they had thought he did not have a mental pathology. “He was depressed. They
should have hospitalized him”, the widow said (Di Costanzo 2012). So, psychiatry
is being blamed on the one hand for unduly pathologizing and stigmatizing under-
standable psychological distress, and on the other for not pathologizing that same
distress and not managing it as if it were a proper mental disorder.
Equally emblematic is the recent discussion on “attenuated psychosis syndrome”
and “juvenile bipolar disorder” (the former proposed for inclusion in the DSM-5
and finally included only in the Section III for conditions requiring further study;
the latter never included in the DSM, despite considerable lobbying). On the one
hand, the need is emphasized to diagnose and manage schizophrenia and bipolar
disorder as early as possible, even before the typical clinical picture becomes mani-
fest, in order to improve the outcome of those disorders; on the other, concern is
expressed about the risks involved in false-positive diagnoses, especially in terms of
social stigma and self-stigmatization, and of misuse of medications (e.g., Corcoran
et al. 2010; Parens et al. 2010).
32 M. Maj
The Differentiation between “Normal” Sadness and Clinical

Depression
The issue of the boundary between “normal” sadness and “true” depression should
be considered in the light of the above scenario.
One of the principles of the “neo-kraepelinian credo”, articulated by Gerard
Klerman in the 1970s (Klerman 1978), was that “there is a boundary between the
normal and the sick” (i.e., there is a clear, qualitative distinction between persons
who have a mental disorder and persons who do not). A corollary to this assumption
was the statement that “depression, when carefully defined as a clinical entity, is
qualitatively different from the mild episodes of sadness that everyone experiences
at some point in his or her life” (Blashfield 1984). Apparently in line with this state-
ment was the observation that tricyclic antidepressants were active only in people
who were clinically depressed; when administered to other people, they did not act
as stimulants nor did they alter the subjects’ mood.
Today the picture has changed dramatically. Taxonomic studies, carried out in
clinical and non-clinical samples, have failed to support the idea that a latent quali-
tative difference exists between major depression and ordinary sadness, arguing
instead in favor of a continuum of depressive states in the general population (e.g.,
Ruscio and Ruscio 2000). The only possible exception is a nuclear depressive syn-
drome, roughly corresponding to what is currently called melancholia, which does
seem to differ qualitatively from normal sadness in some respects (Grove et al.
1987). Whether this condition represents a distinct disease entity, as advocated by
some experts, or corresponds to the most profound states of depression, in which
there is probably the recruitment of further neuronal circuits, so that the clinical
picture is more complex and with a more prominent biological component, remains
open to research. The fact that in many people with recurrent depression some epi-
sodes are melancholic and some are not (Melartin et al. 2004) seems to support the
latter notion, i.e., that melancholia is a marker of the severity of depression. Anyway,
the notion that there is always a qualitative difference between “true” depression
and “normal” sadness appears today very hard to maintain.
So, given the current state of knowledge, we are left with two competing
approaches, which I have called, respectively, “contextual” and “pragmatic” (Maj
2011). The “contextual” approach assumes that there is a basic difference between
depression and “normal” sadness: the latter is always triggered by a life event and
appears to be proportionate to that event; the former is either not triggered by a life
event or, if triggered by an event, is disproportionate to that event in its intensity and
duration. The “pragmatic” approach posits that the boundary between depression and
“normal” sadness should be based on pragmatic grounds (i.e., thresholds should be
fixed – in terms of number, intensity and duration of symptoms, and degree of func-
tional impairment – which are predictive of clinical outcomes and treatment response).
The “contextual” approach is certainly more appealing to the general public. In
fact, a recent population study carried out in Germany (Holzinger et al. 2011)
concluded that ordinary people do not tend to perceive depressive symptoms as an
indication of the presence of a mental disorder when they occur in the context of
adverse life events. In contrast, nearly two-thirds of the almost 5,000 psychiatrists
participating in a recent survey of the World Psychiatric Association and the World
Health Organization (Reed et al. 2011) stated that the diagnosis of depression should
be made if the syndrome is present, even if it appears to be a proportionate response
to an adverse life event.
Indeed, the “contextual” approach has several weaknesses.
First, the presence itself of a depressive state can lead to a significant increase in
reports of recent stressful events (Cohen and Winokur 1988), since many depressed
people tend to attribute a meaning to events that are likely to be neutral. Second, the
presence of a depressive state may expose a person to adverse life events: in fact, the
relationship between depression and so-called “dependent” events (i.e., events
which can be interpreted as a consequence of the depressive state, such as being
fired from a job or being left by a fiancé) is much stronger than the relationship
between depression and other events (Williamson et al. 1995).
Third, whether an adverse life event has been really decisive in triggering a
depressive state may be difficult to establish in many cases, and in any case requires
a subjective judgment by the clinician, likely resulting in poor reliability. This has
been well known since the 1930s, when Sir Aubrey Lewis, testing a set of criteria
aimed to distinguish between “contextual” and “endogenous” depression, con-
cluded that most depressive cases were “examples of the interaction of organism
and environment”, so that “it was impossible to say which of the factors was decid-
edly preponderant” (Lewis 1934).
Fourth, the few studies comparing definitely situational with definitely non-
situational major depressive disorder, defined according to Research Diagnostic
Criteria (RDC, Spitzer et al. 1975), reported that the two conditions were not differ-
ent with respect to demographic, clinical, and psychosocial variables (e.g.,
Hirschfeld et al. 1985). Similarly, in a study comparing five groups of depressed
patients differing by the level of psychosocial adversity experienced prior to the
depressive episode, Kendler et al. (2010) found that the groups did not differ signifi-
cantly on several clinical, historical, and demographic variables.
Finally, the clinical utility of the proposed contextual exclusion criterion in terms
of prediction of treatment response appears very uncertain. Currently available
research evidence suggests that the response to antidepressant medication in major
depressive disorder is not related to whether or not the depressive state was pre-
ceded by a major life event (Anderson et al. 2000). Furthermore, interpersonal psy-
chotherapy is based on the assumption that depression is often understandably
related to a disturbing life event, and that “if the patient can solve the life problem,
depressive symptoms should resolve as well” (Markowitz and Weissman 2004).
This begs the question of whether we should conclude that all cases in which inter-
personal psychotherapy is effective are not “true” cases of depression (Maj 2012b).
The “pragmatic” approach, however, is not free from problems. The duration
criterion fixed by the DSM-5 (at least two weeks of depressive symptoms) has not
been supported by research (e.g., Kendler and Gardner 1998), while the functional
criterion (a clinically significant degree of distress or psychosocial impairment) has
34 M. Maj
been found to be redundant by most clinical and epidemiological studies (e.g.,

Mojtabai 2001; Zimmerman et al. 2004; Wakefield et al. 2010).
The symptomatological threshold (presence of at least five depressive symp-
toms) has been extensively tested by empirical research, but has not received a con-
vincing validation. Actually, an increasing number of depressive symptoms has
been found to correlate in a monotonic fashion with a greater risk for future depres-
sive episodes, a greater functional impairment, a higher physical comorbidity, and a
more frequent family history of mental disorders (Kessler et al. 1997). When a point
of rarity has been reported, it usually corresponded to a threshold higher than that
fixed by the DSM-5. For instance, Kendler and Gardner (1998) found that the risk
for future depressive episodes was substantially greater in subjects with seven or
more symptoms than in those with six symptoms, while Klein (1990) reported that
the risk for mood disorder was significantly higher in relatives of patients with six
or more depressive symptoms than in both those with four or five symptoms and
those with non-affective disorder.
The notion that the threshold fixed by the DSM-5 may be too low is also sup-
ported by some research concerning the prediction of response to pharmacological
treatment. Paykel et al. (1988) found that the superiority of amitriptyline over pla-
cebo was more substantial when the initial score on the 17-item Hamilton Rating
Scale for Depression (HRSD-17) was between 16 and 24, less substantial when it
was between 13 and 15, and non-significant when it was between 6 and 12. The
authors reported that 13 % of patients with RDC major depression were among
those with HRSD-17 scores between 6 and 12, while 34 % had a score between 13
and 15. So, almost one half of the patients with a diagnosis of major depression
according to RDC (which are almost identical to DSM-5 criteria) were in the groups
showing a non-significant or “less substantial” response to pharmacotherapy.
Similarly, Elkin et al. (1989) found that, among patients with an RDC diagnosis of
major depressive disorder, those with an initial score of less than 20 on the HRSD-
17 (more than 60 % of the sample) did not recover more frequently with imipramine
than with placebo plus clinical management, whereas patients with an initial score
of 20 or more did significantly better.
However, other studies, using psychosocial impairment as a validator, reported
that this impairment was not different in people with two to four depressive symp-
toms compared to those with five or more symptoms (e.g., Broadhead et al. 1990),
which seems to suggest that the threshold proposed by the DSM-5 may be too high.
Notably, the RDC and the DSM-III and its successors assume that all depressive
symptoms (with the only exception of depressed mood and loss of interest or plea-
sure) have the same “weight” for diagnostic purposes, which may not actually be
the case (e.g., Wakefield and Schmitz 2013).
It is worthwhile to observe that the ICD-10 definition of a depressive episode
(World Health Organization 1999) is not consistent with the DSM-5 criteria. In fact,
the ICD-10 fixes a threshold for mild depressive episode requiring the presence of
at least four depressive symptoms (including at least two of the core symptoms of
depressed mood, loss of interest and enjoyment, and increased fatiguability), none
of which should be present to an intense degree, and a threshold for severe depres-
sive episode requiring the presence of at least seven depressive symptoms, including
all the above mentioned core symptoms, some of which should be of severe inten-
sity. It is further specified that “an individual with a mild depressive episode is usu-
ally distressed by the symptoms and has some difficulty in continuing with ordinary
work and social activities, but will probably not cease to function completely”,
whereas “during a severe depressive episode it is very unlikely that the sufferer will
be able to continue with social, work, or domestic activities, except to a very limited
extent”. So, although the “pragmatic” approach is adopted by both our main diag-
nostic systems, the thresholds they provide are not consistent, and a person may
have a depressive episode according to the ICD-10 but not to the DSM-5.
It is clear that neither the “contextual” nor the “pragmatic” approach, in their
current formulations, are really able to guide the clinician in the differential diagno-
sis between “true” depression and “normal” sadness.
Excluding the diagnosis of depression simply because the depressive state looks
understandable and proportionate to a recent life event involves the risk of automati-
cally depriving people with a severe and disabling condition of a treatment they may
require. Every experienced clinician is able to recall several cases in which he him-
self or a colleague made that mistake, with serious, sometimes tragic, consequences.
On the contrary, making the diagnosis of depression if clinical criteria are fulfilled
does not necessarily imply that the person will receive a treatment, and certainly not
that he will receive a pharmacological treatment. It will be in the phase of the clini-
cal characterization of the individual case, which follows the phase of the diagnosis,
that the circumstances in which the depressive state emerged will be considered,
along with many other variables, and this may lead to the decision not to treat
(watchful waiting), or to prescribe a psychotherapy which may be just supportive,
or to prescribe a pharmacological treatment chosen among the many available, or to
prescribe a combination of a psychotherapy and a pharmacotherapy.
On the other hand, the thresholds currently fixed for the diagnosis of major
depression following the “pragmatic” approach are not consistent and not convinc-
ingly validated, and the notion itself of a single symptomatological threshold being
predictive of response to whatever treatment seems now unreasonable. It is clear that
the introduction of several evidence-based psychotherapies and of SSRIs has con-
tributed to lower the threshold for the diagnosis of depression in ordinary clinical
practice, because those interventions seem to work in milder depressive states which
did not respond to tricyclic antidepressants (or in which the risk-benefit ratio of
those medications was clearly unfavorable). So, response to different interventions
may be predicted by different diagnostic thresholds. That the availability of new
effective treatments may influence the perceived boundary between what is normal
and what is pathological is certainly not unique to psychiatry. For instance, infertil-
ity has been regarded as a fact of life for many centuries, being acknowledged as a
disease only when effective reproductive techniques became available (Elliott 1999).
Overall, an analogy seems to emerge between depression and some common phys-
ical diseases such as hypertension and diabetes, which also are on a continuum with
normality in the general population, with at least two thresholds identifiable along that
continuum: one for a condition deserving any kind of clinical attention (which may
36 M. Maj
just be watchful waiting) and another for a state requiring pharmacological interven-
tion. In the case of depression, the former threshold is likely to be lower than that fixed
by the DSM-5, while the latter is certainly higher. Both thresholds may need to be
based on the overall severity of depressive symptoms in addition to their number.
Contrary to our colleagues diagnosing and treating hypertension and diabetes,
we do not have laboratory tests on which to base the above thresholds. This makes
the role of the experience and wisdom of the clinician, and the need for diagnostic
manuals to guide clinical practice, much more significant in psychiatry than in other
medical disciplines.
The detailed description of proper mental disorders provided by current diagnos-
tic systems, however, may not be sufficient, especially for psychiatrists working in
a community setting. We may also need a description of ordinary responses to major
stressors (such as bereavement, economic ruin, exposure to disaster or war, disrup-
tion of family by divorce or separation) as well as to life-cycle transitions (e.g.,
adolescent emotional turmoil). The DSM-5 attempt to describe “normal” grief as
opposed to bereavement-associated depression, in order to guide differential diag-
nosis, is a first step in this direction.
Furthermore, we may need a characterization of the more serious responses to the
above stressors that can be brought to the attention of mental health services although
not fulfilling the criteria for any mental disorder. The serious and potentially life-
threatening psychological distress related to economic ruin, in which shame and
despair are the most prominent features and the diagnostic criteria for depression are
often not fulfilled, is a good example. The current delineation of “adjustment disor-
ders” in both the DSM-5 and ICD-10 is too generic and ambiguous to be useful for
differential diagnostic purposes and as a guide for management.
Of course, other mental health professionals (and perhaps other professionals
outside the health field) will have to collaborate with psychiatrists or even take the
lead in those characterizations. This may hopefully contribute to the construction of
a transdisciplinary, clinically relevant, body of knowledge in the mental health field,
whose existence is at present arguable (Maj 2012a).
Further research is clearly needed to refine the thresholds for the diagnosis of
depression and for the assessment of the severity of a depressive episode. Further
qualitative studies are also needed to explore the subjective experience of depressed
persons, and the possible differences between this experience and that of ordinary
sadness. A more precise characterization of individual depressive symptoms is
required, as well as an exploration of the predictive value of individual symptoms
and specific symptom clusters, with respect to different outcome measures and
response to different treatments. Further research on the validity and clinical utility
of the construct of melancholia is also warranted.
Meanwhile, however, it should be clarified that the fact that a diagnosis of depres-
sion is made does not imply that the person is “mad”, nor that his brain is not
functioning well, nor that he necessarily needs an intervention, and certainly not
that he must be treated with a psychotropic drug. This clarification is likely to reduce
significantly the philosophical, social, and ethical implications that the debate on
this issue obviously has at the moment.
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Beyond Depression: Personal Equation
from the Guilty to the Capable Individual
Alain Ehrenberg
Abstract The aim of this chapter is to propose a sociological definition of mental

health problems and practices. Due to the wide range of practices (from psychosis to
self-help), this task is approached as a global idiom, enabling the formulation of mul-
tiple tensions and conflicts of contemporary modern life, and providing answers for
acting on them—in the family, work and workplace, between couples, in education,
etc. The centrality of emotional issues in our society can be described as a form of
“mandatory expression” (Marcel Mauss), which characterizes an attitude toward con-
tingency or adversity in a global context where autonomy is the supreme value. From
this perspective, mental health can be seen as an individualistic way of dealing with
what the ancients called the ‘passions’; it is the name individualistic society has given
to what was referred to as the ‘passions’. Mental health is concerned with our ways of
being affected by our ways of acting, and our ways of acting on these afflictions. A
transversal viewpoint is presented, of which depression is only one aspect, at three
intertwined levels of changes regarding: (1) the configuration of values and norms; (2)
the concept of mental health; (3) the type of knowledge that dominates psychiatry and
mental health fields, that is, the progressive replacement of psychoanalysis by cogni-
tive neuroscience as the main type of knowledge of the human mind since the 1980s.
Reports on mental health published by health and political organizations, generally

indicate that between 20 and 25 % of the population of any developed society is
affected by a “mental illness”, but primarily by anxiety and mood disorders, and
most notably, depression. The area of mental health refers to a large spectrum of
problems, ranging from psychosis to personal development, self-help, and enhance-
ment, or what psychiatrists have called “positive mental health” (Vaillant 2008). So,
it comes as no surprise that the number of persons affected and, consequently, the
cost to society are huge – from 3 to 4 % of the GDP of EU countries (European
Commission 2005). Today, mental health certainly is a central public health issue,
but contrary to cancer for instance, it is not only such an issue.
A. Ehrenberg (*)
CNRS (Centre National de la Recherche Scientifique), Université Paris-Descartes, Cermes3
(Centre de recherche, médecine, sciences, santé, santé mentale, société), France

DOI 10.1007/978-94-017-7423-9_4
40 A. Ehrenberg
The main difference between traditional psychiatry and modern mental health
can be expressed very simply: psychiatry is a local idiom, specialized in the
identification of particular problems. Mental health, because of large domain it
encompasses, is a global idiom, enabling the identification of multiple tensions
and conflicts of contemporary modern life, and, moreover, providing solutions.
That is, the practice of mental health is concerned with identifying problems
generally linked to social relationships, seeking reasons to explain them, and
finding solutions. Today, mental health is not only about the struggle against
mental illness, it is also a way of addressing multiple problems in ordinary soci-
ety—in the family, work and workplace, between couples, in education, etc.
Mental health concerns not only health, but also the socialization of the modern
individual. It addresses the essential elements of individualistic society, such as
self-value, the opposition between responsibility and illness, and the ability to
succeed in life. It raises moral questions concerning good and evil, justice and
injustice, dignity and shame.
One has to elaborate further about the central place mental health has come to
occupy in our way of life.
In “Understanding a Primitive Society”, a discussion on the concept of objective
reality with anthropologist Edward Evans-Pritchard and philosopher Alasdair
McIntyre, published in 1964, Peter Winch explains that the magical rites of the
Azandes observed by Evans-Pritchard “express an attitude to contingencies; one,
that is, which involves recognition that one’s life is subject to contingencies, rather
than an attempt to control these”. These rites:
emphasize the importance of certain fundamental features of their life […] We have a
drama of resentment, evil-doing, revenge, and expiation, in which there are ways of
dealing (symbolically) with misfortunes and their disruptive effects on man’s relations
with his fellows, with ways in which life can go on despite such disruption (Winch
1964, 321).
The idea I’ll develop here is that the centrality of emotional issues in our soci-
ety can be described as a form of “mandatory expression” (Mauss 1921/1969),
which characterizes an attitude toward contingency or adversity in a global con-
text where autonomy is our supreme value. From this perspective, mental health
can be seen as an individualistic way of dealing with what the ancients called the
‘passions’; it is the name individualistic society has given to what was referred to
as the ‘passions’. Mental health, as we shall see, is about our ways of being
affected by our ways of acting, and about our ways of acting on these
afflictions.
Here I present a transversal viewpoint, of which depression is only one aspect, at
three intertwined levels of changes regarding: (1) the configuration of values and
norms; (2) the concept of mental health; and (3) the type of knowledge that domi-
nates psychiatry and mental health fields, that is, the progressive replacement of
psychoanalysis by cognitive neuroscience as the main type of knowledge of the
human mind since the 1980s.
Beyond Depression: Personal Equation from the Guilty to the Capable Individual 41
The Configuration of Values and Norms: Guilt and Discipline,

Capability and Autonomy
In attempting to understand the anthropological place of mental health issues today,

one should primarily consider the encompassing values and norms of society.
Following a Durkheimian perspective, human and social affairs have to be
approached in terms of collective representations. Collective representations are not
constraints that come from outside; they are expectations that determine, or rather
constitute, us by affecting us in a total manner. For instance, and to put it briefly, in
traditional African lineage society, it is of crucial importance to respect one’s ances-
tors (and the social ideal is to become an ancestor); in traditional Indian caste soci-
ety, it is to abide by one’s degree of purity; in modern individualistic society, it is to
become someone by oneself. Recently, this question of becoming oneself has
changed. I would summarize the change as follows: we have witnessed a shift from
the guilty and disciplined individual to the capable and autonomous individual. This
shift occurred during the second part of the twentieth century.
The concept of autonomy today designates many aspects of social life and has to
be historically described in two steps. Autonomy first emerged as a collective aspi-
ration in developed societies between the end of Second World War and the 1970s,
an aspiration towards greater choice or independence and more equality—in which
equality between men and women, and therefore the rise of woman as individual, is
the epicenter. Between the 1970s and the 1980s it has become the common condi-
tion and has pervaded social relationships beyond the dynamic of emancipation: it
has widened to action itself where individual initiative is highly valued, notably
through the transformations of the workplace and capitalism where flexible work
implies the autonomy of workers. Values and norms of choice, self-ownership, and
individual initiative value the three dimensions of independence, cooperation, and
competition. This change modifies the relationships between the agent and his or
her action; it increases the responsibility of the agent regarding his or her own
action. The consequence is that everything that concerns individual behavior, the
mobilization of personal dispositions, and notably the ability of the individual to
change by himself, to be the agent of his own change (in short, “personality”) is a
major social and political preoccupation.
I summarize this change as a shift from autonomy-aspiration to autonomy-
condition. It must be added that these aspects can be understood and valued differ-
ently according to a given society: for instance, autonomy unifies the US, where the
self-motivated individual is a major collective representation, but divides France,
where it tends to represent an abandonment of the individual and society to market
forces (Ehrenberg 2010, Italian version 2010, German 2011).
Today autonomy has become our common condition; it is a normative expecta-
tion for everyone, and not a choice you have the liberty to make.
The history of depression incarnates this change. It accompanied the shift from
guilt and discipline to capability and autonomy during the second half of the twen-
tieth century. It has progressively occupied the place of Freudian neurosis, that is,
42 A. Ehrenberg
the pathology of guilt, and has become the shadow of the individual normed by
autonomy. I will summarize the shift as follows. In a form of life organized by tra-
ditional discipline, the question was: am I allowed to do it? When reference to
autonomy dominates the concept of society, when the idea that everyone can become
someone by oneself becomes an ideal embedded in our mores, the question is: am I
able to do it? Neurotic guilt has not disappeared; it has taken the form of depressive
insufficiency. My hypothesis is that, if melancholy was the illness of the exceptional
man during the sixteenth century Renaissance, and if during the Romantic Era, it
was at the crossroads of creation or genius and unreason (Klibanski et al. 1964), it
is now the situation of everyone, because contemporary individualism consists in
having democratized the idea that any one could be exceptional. In fact, the history
of contemporary depression must be approached in two steps: from the 1940s to the
beginning of the 1970s, depression was considered to be a subfield of neurosis, and
hence remained attached to the categories of conflict, guilt, and desire; since then, it
has been reconceptualized by psychoanalysts as a narcissistic pathology where top-
ics centered on desire lost ground in favor of a problematic centered on object loss,
subjective identity, and shame, which subordinated feelings of guilt. It seems it is
less desire that was at stake than a feeling of permanent insecurity. Depression has
become a pathology of greatness, developing feelings of insufficiency regarding
social ideals. It has been a major expression of the democratization of the excep-
tional. This shift of our configuration of norms and values has set the individual on
an axis that goes from capability to incapability (Ehrenberg 1998 English transla-
tion 2010). In this shift, personal assertion, or the capability to assert oneself, appro-
priately becomes a core element of socialization at every level of the social
hierarchy.
We have been faced with new life trajectories and new ways of living affecting
the family, employment, education, relationships between generations, and so on.
Along with this we have witnessed the end of the welfare state of the twentieth
century. This change indicates that we are living in a type of society where we all
have to invest ourselves personally in numerous and heterogeneous social situa-
tions. Individual capability to act as an autonomous self has become a major point
of reference. It embodies our ideals of personal accomplishment.
This is a change in what can be called “personal equation”. In the previous
discipline-based system, the aim of behavior regulation was the docile individual,
and values of autonomy, like choice or individual initiative, were subordinated: in
this light, personal equation was weak. In the new autonomy-based system, the aim
of regulation is one’s personal initiative, and each person has to adopt a line of con-
duct: personal equation is strong. For instance, think of the shift from qualifications
in the Taylorian/Fordian workplace to skills in the flexible workplace, and notably
social skills with which an emotional dimension has emerged related to increased
self-control. These skills condition the possibility to adopt a line of conduct in a
type of management of the workforce where the problem is no longer how to coor-
dinate the action from a centralized direction, but how to make people cooperate
with each other. In the discipline-based system, the regulation of action consisted of
a discipline of the body; in the flexible organization it consists of a mobilization of
their personal commitment. In both cases, the individual has to “self control”, to
“self regulate”, but the style of social constraint is different. Today, work is consti-
tuted by interdependent relationships between human beings. The source of effi-
ciency in the workplace is both the relationship and the individual. These capacities
are required at every hierarchical level of companies because we are faced with a
type of temporality characterized by uncertainty. In this context, emotional control
is a major skill.
The meaning of discipline itself has changed: it is subordinated to the design of
getting individual initiative, therefore abilities to self-motivate and self-activate. It
tends to self-discipline. Where the problem previously was to render the individual
docile and useful, as philosopher Michel Foucault put it (Foucault 1975), now it is
to develop abilities to self-activate and to self-control. The aim of discipline is not
obedience mainly; it is a means to develop abilities of empathy and self-reliance
(Ehrenberg 2010).
Capacities for good socialization have a triple aspect: cognitive, social, and emo-
tional. There is a new dimension of personal responsibility in social life.
Consequently, relations between responsibility, capability, and emotional self-
control are crucial for public policies.
The point I want to make here is that the contemporary concern about the
treatment of personality is not primarily about an upsurge in psychological dis-
orders. It is about the normative changes of our ways of acting in society, there-
fore about our new forms of socialization and its consequences for inequalities
and poverty. In this society, individual subjectivity has become a major issue
because it emphasizes problems of self-structuring. Without this self-structuring,
it is difficult to act by oneself in an appropriate manner. It was never a central
concern in a society of mechanical discipline. The consequence of the shift from
discipline to autonomy is a demand for an increased capacity of emotional self-
control. At the same time, our social relationships are more frequently formu-
lated in a language of affect and emotions, distributed between the good of
mental health and the bad of psychic suffering. This leads me to the second level
of change.
From Psychiatry to Mental Health: The New Morbidity
Self-motivation, self-activation, self-control, self-discipline, self-regulation: there

is, of course, a strong relationship between these notions and the predominant place
occupied nowadays by mental health issues in social life. Generalized attention to
mental health and psychic suffering is a major reference point for
individualization.
Depression certainly is the clinical entity through which changes appear in guilt
and in reasons to feel guilty in society. But since its reconceptualization 40 years
ago, numerous entities have appeared that have made up the field of mental health.
Changes in personal equation have been accompanied by a new morbidity of a
44 A. Ehrenberg
behavioral nature, which is the pathology of the capable individual, of which the
depression reconceptualized, either by psychoanalysis or biological psychiatry.
Capable individual is an expression of a system of social relationships where choice,
individual initiative, self-ownership, and ability to act as an agent of one’s own
change are supreme values.
This new morbidity, which is not only a matter for the particular area of mental
illness, but above all for the general field of social life, has been instituted as a major
issue in the workplace, education, and family—stress and burnout, ADHD, school
phobia, and intra family violence. It highlights two major changes. The first change
is the status of symptom: the mental disorder is an expression of difficulties related
to socialization in one way or another, and criteria related to social functioning have
become essential—this is the rise of axis five in the DSM-III, dedicated to the
assessment of adaptive functioning in the past year (Millon 1983). Though axis 5
was removed from the fifth version, functioning remains at the center of profession-
als’ concern. The second change is related to the style of unhappiness: the feeling of
not being able to be good enough or not being able to mobilize oneself into action
is at the core of the evil; the inability to act and to project oneself in the future is at
the core of the difficulties of the subject.
The evolution of American pediatrics is typical of the change regarding func-
tioning. In 1975, the American Academy of Pediatrics introduced the concept of
« new morbidity » to designate non-infectious problems affecting children and
families whose prevalence were on the rise. In 1991, it released a report on the
role of the pediatrics in the future. Its first sentence asserts that “societal changes
have engendered significant changes in the delivery of health care” (American
Academy of Pediatrics Task Force 1991, 401) in which social dimensions have
a central place. The new morbidity is behaviorial, and the concept of behavioral
health earns a new value, from toddlers to young adults. Now, social, develop-
mental, and behavioral problems are the core of the profession of pediatrics.
Two other reports followed, in 2001 and 2012, which went in the same direc-
tion. This morbidity represents a “shift in the understanding of what has an
impact on children and families health” (American Academy of Pediatrics,
Committee on Psychosocial Aspects of Child and Family Health 2001, 1228).
Disparities, claims the 2012 report, “threaten the democratic ideals of our coun-
try in weakening the national creed of equality of opportunity”. This is a “sig-
nificant change of paradigm” (Shonkoff et al. 2012): through developmental
approaches, which aim to reducing pathologies of adulthood with early inter-
vention in childhood, a shift occurred from a sick-care model to a health-care
one.
In a nutshell, the new morbidity and the new health is behavior, and behavior is
individual autonomy. It is less disobedience that counts than lack of empathy for
others and lack of self-reliance, which are disclosed by the behavior, and have long-
term disadvantageous consequences for socialization.
The accent put on early intervention and the developmental approach high-
lights a fundamental element of autonomy: the relationship with time. Because
mental health deals with pathologies of relational life that disable individual
freedom, it appears to be an ensemble of practices where personal transformation

is a key value, which amounts to practices conceived in terms of a relation to
time centered on uncertain and unstable futures. Changes in our relationship to
time and the rise of our worry for emotional and drive control are closely
connected.
Regarding the most common disorders (mainly depression and anxiety disor-
ders), let’s take some examples in the UK to illustrate the idea of a global idiom
in which emotional self-control and autonomy are intertwined. For instance, the
famous report on depression published by economist Richard Layard (professor
at the LSE&PS) in 2006, in the context of “Initiative for Improving Access to
Psychological Therapy” (IAPT) prepared by National Health Service and
launched in 2008, claims that anxiety and depression disorders are the main
social issue today and that the primary cause of misery is not poverty, but “men-
tal illness”. Why? Because “mental illness” is related to behavior, and behavioral
problems are considered to be the most challenging aspects of our society by
Layard and other “happiness economists”. The report proposed recruiting 10,000
therapists specialized in CBT to alleviate this new social scourge (Center for
Economic Performance’s Mental Health Policy Group 2006). The same year, the
Institute for Public Policy Research (IPPR), a progressive British think tank,
published Freedom’s Orphans. In this report, the authors “used two large surveys
that followed young people born in 1958 and 1970, and shows that in just over a
decade, personal and social skills became 33 times more important in determin-
ing relative life chances” (Margo et al. 2006, viii). Several reports were pub-
lished in the UK on the topic of “character capabilities” as targets for early
intervention public policy against child poverty. For instance, Demos, and its
“Character Inquiry” of 2011:
The aim of The Character Inquiry is to investigate the potential of focusing on character,
and character development, to help achieve greater levels of wellbeing in society and among
individuals […] The capabilities that enable individuals to live ethically responsible and
personally fulfilling lives […] consist of the ability to apply oneself to tasks, to empathize
with others and to regulate one’s emotions (Lexmond and Grist 2011, 10).
Focus, empathy, and self-control are three key words of autonomy. Another
report published by IPPR in 2009 about personal advisers, who have a pivotal role
in welfare-to-work, is entitled Now it’s Personal. Personal Adviser and the New
Work Public Service. It notably underlines:
[…] evidence that new training techniques such as the Cognitive Behavioral Interviewing
technique can encourage a more open and productive dialogue between adviser and client,
enabling discussions to move onto employment related goals more quickly (McNeil 2009,
6).
The same year a report was published by Carol Black, director of NHS (National
Health Service), which proposed changing the conception of fitness and disability
at work from a “sick” to “fit for work” model. Following these various reports and
recommendations, a plan for developing psychotherapy training and access has
been launched in 2010. As the Minister for care service put it in his foreword,
46 A. Ehrenberg
“talking therapies are a major element of our cross-government mental health strat-
egy” (Department of Health 2011, 2).
This example highlights an extension of psychotherapy to problem-solving, that
is, a form of coaching: social functioning is added to and intertwined with
psychopathology. Such interventions are conceived as forms of empowerment to
develop individual’s capacities to rely on themselves by helping them to support
themselves through accompaniments whose purpose is to make them the agents of
their own change. It is crucial to understand that mental health issues are at the core
of today’s public policy, which have larger targets than strictly psychiatric prob-
lems. The shift from a sick-model to a health model means mental health is about
how to achieve good socialization in a world where ability to decide and act by
oneself pervades social relationships, and is the common condition. Mental health
acts on our mores and habits. Similarly to civil religion for Rousseau, it fosters a
“feeling of sociability” (Rousseau 1762/2001).
Regarding psychiatric patients affected by severe and enduring mental illnesses,
like schizophrenia, new approaches have also emerged since the 1970s that are cen-
tered on the idea of autonomy. They result from a major change in psychiatric insti-
tutions, one that makes the autonomy of the patient the goal and the means of the
treatment. This change is the end of the “total institution” described by sociologist
Erving Goffman half a century ago (Goffman 1961). The paradox is that Goffman
published his book at a point when the dynamic of deinstitutionalization was just
beginning. Today, the psychiatric patient has to live in a community and not in a
hospital. The issue of being able to live an autonomous life is at the heart of treat-
ments; that is, social relationships have become a major aim. Psychosocial inter-
ventions (self-management, psychoeducation, cognitive remediation, etc.) aim to
improve a patient’s skills to live in ordinary social life. The emergence of his or her
voice has accompanied a double change in the style of action: from “acting on” the
patient to “acting with” him or her, on one hand; and from the emphasis put on the
pathology (on the deficit, on the handicap) to the potential to enhance his or her
strengths, on the other. To enhance the patient’s potential is a means to better fight
against the pathology, the handicap or the deficit. Beyond the clinical stability of the
patient, a new goal appeared about 30 years ago, supported by the so-called
Recovery movement: the possibility to have a more accomplished and rewarding
life as a person, despite the illness (see notably Hopper 2007). Here, also, social
functioning is a major concern.
This new understanding of mental illness—as involving the general domain of
social life—has been instituted as an organizing vision in workplaces, education,
and family life. This vision obviously implies that mental health practices deal with
the relations between individual afflictions and social relationships. A mental disor-
der is typically seen as the expression of difficulties linked to socialization, that is,
with social functioning viewed as essential for individual well-being. This is not so
much a “medicalization” of behaviors (as sociologists have too often implied [see
Conrad 2007, for instance]). What it represents, rather, is a complementary change
both in medical practices and in social relationships, an understanding of which
requires a descriptive approach.
From Psychoanalysis to Cognitive Neuroscience
During the last three or four decades, psychoanalysis has declined in favor of the
rise of cognitive neuroscience. The word “cognitive” means that neuroscience aims
to combine two areas: neurophysiology and psychology. The concept of emotion is
conceived of as information processing, hence its cognitive dimension.
The general issue I explore is the following: through neuroscience there is a
change of the relationships between neuropathology and psychopathology, patholo-
gies of lesion and pathologies of function. Notably, there is a strong trend today to
merge these two kinds of pathology into a single neuropsychiatric kind, one in
which reference to the brain as the biological system on which one can explain as
much psychopathology as neuropathology, is the supreme value (See Ehrenberg
2004, 2008/2010). In this context, my aim is to understand how references to the
brain and cognition have entered into social life and the collective imagination, how
people use them and if it makes a difference in their life.
Following the model of total knowledge that psychoanalysis has pretended to be,
cognitive neuroscience has become a psychology, sociology, and a philosophy.
Total knowledge has an anthropological nature, in the sense that it addresses the
question: what is man made up of? Today, it seems that a genuine science of human
behavior tends to replace a psychoanalytic science, regarding which the status of
science has remained doubtful. A genuine science is a science able to prove its
propositions in the laboratory with the use of standardized methods without which
there is no such thing as science. The therapeutic hopes invested in cognitive neuro-
science seem analogous to those of psychoanalysis a few decades ago.
This transformation occurred for many reasons, but I want to underscore the
anthropological one, from the guilty to the capable individual.
For Freud, civilization is based on the repression of drives, and, as he wrote in
“the Id and the Ego” (Freud 1981), the superego is like a garrison in a town. I would
qualify his claim: it is the form of life on which psychoanalysis was born which was
based on this repression, and not civilization in general. The core moral feeling of
Freud’s thought is guilt; as he wrote in the same article, the patient doesn’t feel
guilty, he feels sick. Freud’s thought was about guilt and desire. Guilt feelings are
disguised in symptoms, which are the expression of forbidden desires. Desire is a
conflicting entity for Freud. Psychoanalysis was founded on an anthropology of the
guilty individual at a time when the social normative and value systems were based
on mechanical discipline. What is at stake in psychoanalysis and in the practice of
the talking cure is a set up for “passionate utterance”, to use an expression by
Stanley Cavell, “an invitation to improvisation in the disorders of desire” (Cavell
2005). Where one’s own conflicting desire can appear, desire and conflict being
necessarily intertwined—desire being something closer to passion and passivity
than to action and activity. When this form of life began to be shaken, psychoana-
lysts started to think that Narcissus had replaced Oedipus, the ideal ego, and the
surperego. They deemed that their patients were subjected more to anxieties of loss
rather than of conflict. If the Oedipal patient suffers from anxieties of castration, the
48 A. Ehrenberg
narcissistic patient is affected by anxieties of loss. The shift from Oedipus to

Narcissus corresponds to the confrontation of psychoanalysis with autonomy.
Cognitive neuroscience developed in a context where the shift from Oedipus to
Narcissus had already occurred, a context where mores had been emancipated from
the old taboos, where flexible work had started to spread, and where workfare was
in the process of replacing welfare. For this reason, cognitive neuroscience is
founded on a slightly different anthropology, an anthropology of the capable indi-
vidual. For cognitive neuroscientists, civilization is derived not from the repression
of drives, but from the expansion of empathy, and related concepts like decision-
making or trust, all concepts which are framed by “theory of mind” and are a stand-
in for social relations.
I’ll end this chapter by presenting cognitive neuroscience as an echo maker of
values and norms of autonomy. Decision making, trust, empathy, cognitive bias,
etc., on which cognitive neuroscience develops its demonstrations in the laboratory
are among the core social concepts of today. Empathy is a necessary attitude in the
flexible workplace where people have to cooperate one with another; this was not
the case in the Fordian workplace. Now, empathy is a skill, not just a moral attitude.
Right decision-making and avoidance of cognitive bias are a huge market for a mul-
titude of personal advisers and coaches who are supposed to help people choose.
Cognitive neuroscience is not in search of mechanisms of obedience, but of decision-
making; anti-social behaviors are defined as wrong decision-making. The brain and
cognitive neuroscience are not pervaded by collective representations of the
mechanical discipline (who is in search of an obedient brain?), but by that of
autonomy.
Of course, this doesn’t mean that cognitive neuroscience can be reduced to a
reproduction of values and norms. I mean something analogous to what Marcel
Mauss said in his famous speech, “A Category of the Human Mind: the Notion of
Person, the Notion of Self” (1938). At the end of the speech, talking about Kant,
Mauss underlined that the
importance of sectarian movements during the seventeenth and eighteenth centuries on the
formation of philosophical and political thought. It is there that the issues of individual
liberty, of individual consciousness, of the right to communicate directly with God, of being
one’s own priest, of having an inner God were raised. The notions promoted by the Morave
Brothers, Puritans, Wesleyans, Pietists were those which formed the basis on which the
notion [of person] was established: person = self; self = consciousness, and consciousness is
the key category. […] It is only with Kant that it has taken an accurate form. Kant was a
Pietist […]. The indivisible ego, he found it around him [my emphasis].1 (Mauss 1950/1968,
360–361)
Mauss underlines the social origins of Kant’s thought, but of course this doesn’t
mean that Kant’s thought is only a reproduction of ordinary categories. It means that
there is an internal relationship, an interdependent relationship between concepts,
categories, and symbols and the lives of those who use them. In the same manner, I
suggest that cognitive neuroscience is loaded with values and social ideas, with
1
My translation.
collective representations of autonomy that it found around it; it expresses, through

the language of biology, ways of being in society that have spread during the last
third of the twentieth century in terms of autonomy. Social and scientific ideas are
intertwined. According to me, it is of a fundamental importance to acknowledge
that this claim aims to provide a sociological alternative—and more precisely both
a Durkheimian and Wittgensteinian alternative—to naturalistic and post-Foucaldian
approaches to these problems.
In most naturalistic approaches, it is science that provides criteria to define
objective reality (for a discussion about science and objective reality, see Winch
1964); more precisely, I should say, the material basis of reality, and in the case of
emotional issues, is the brain. So, real = material = brain.
In the legacy of Foucault, and as a sociological alternative to naturalistic
approaches, many speak of the “objective person”, of “biosociality”, of the “neuro-
chemical self”, etc. They think that there is a paradigm of “brainhood” that is perva-
sive in media. Without going deeper, I will only say that post-Foucaldian approaches
only offer a counter mythology to the new scientific mythology of cognitive neuro-
science. Following Wittgenstein, I want “to understand something which is in plain
view. For this is what we seem in some sense not to understand” (Wittgenstein 1953,
§89). What is in plain view that we don’t see?
The echo maker hypothesis means that cognitive neuroscience is loaded with
values and social ideas, that is, it is pervaded by our current collective representa-
tions, to use a Durkheimian formula. Consequently, we should approach it by think-
ing of its concepts less as criteria defining an objective reality than as the new
language game that has subordinated psychoanalysis to treat the afflictions of
autonomy. With this language game, human beings try to understand their predica-
ment, deal with them, and create a meaningful life in the age of
autonomy-condition.
How do people recognize themselves through their brain and cognitive patterns?
How do they refer to cognition, the brain, etc. in the description of what is going on
for them? How do these references take their place in the tapestry of their lives?
For instance, the trend to merge neuropathology and psychopathology in the
same kind of illness has led people to ask themselves: is it intentional or mechani-
cal? Is it both? How are these two aspects related to one another? Here I’m thinking
of new kinds of narratives that can be called “neuropsychoanalytic”. I’ll mention
one by the composer and pianist Allen Shawn, Wish I Could Be There. Notes from a
Phobic Life (2007), and another by the American novelist Siri Hustvedt, The
Shaking Woman or a History of my Nerves (2009) (for a more detailed analysis see
Ehrenberg 2014). The two narratives are “neuropsychoanalytic” because they
unfold through a tension between neurobiology and psychoanalysis, a tension that
can sometimes transform itself into something more complementary. Research in
neuroscience is necessarily from a mechanical perspective: scholars are in search of
causes. But in real life, people are looking for a global understanding of their situa-
tion and of themselves. Consequently, they need causes and reasons, they need to
understand if there is something intentional in their symptoms (an unconscious
intention, for instance), but also if they are produced by a dysfunctional mechanism;
50 A. Ehrenberg
they need to know if it is either/or (either intentional/or mechanical), if it is of bit of

each, and so on. In real life, causes and reasons are not separate entities; they are
mainly practical distinctions between which there are tensions, intricacy, and
uncertainty.
Being neuropsychoanalytic, these narratives try to make allowances for both the
hidden intentionality of the symptom and the involuntary movement of the neuro-
logical disorder. The shaking of Siri Hustvedt seems to be a manifestation of a
mysterious relationship with her father. In Allen Shawn’s life there is the “missing
part” of his autistic twin sister whose absence, since she was put into an institution
when they turned eight, was progressively replaced by his main symptom, that is,
agoraphobia; he wrote a sequel devoted to this relationship, Twins: a memoir (2011).
Hustvedt and Shawn appear as individuals having subordinated their patient
statuses. The story of her nerves and the story of his agoraphobia are those of the
subordination of their tremors and phobia to their own individuality—their own
self— thanks to an elaboration enabling them to create something singular in
lieu of being subjected to a disability. Of course, Hutsvedt is a writer and Shawn
a composer, but today this new individualism is part and parcel of the life of
masses of people subjected to various chronic conditions (with autism, with
schizophrenia, etc.). Before defining it, one has to say something about the con-
text, which is the following: these people (again, those with autism, schizophre-
nia, etc.), who half a century ago were into closed and total institutions, now live
in the community; therefore, they need the various skills necessary to live a “nor-
mal” life, be it with drugs, psychosocial rehabilitation, cognitive behavior ther-
apy, self-help and coach support, etc., which compensate for their handicaps. In
this new context, the new individualism goes a step further: the condition is sub-
ordinated to a creation of a personal attitude which is not conceived of in terms
of adaptation, but of a different style of life. Here autonomy is shaped in relation
to the idea that there is a creative aspect in a long term or chronic illness—this
subject is the connecting thread of the popular narratives by Oliver Sacks (1995).
I earlier mentioned the topic of strengths about the psychiatric patient. This
notion has recently gained a new meaning: the meaning of a different cognitive
style related to or implying a different form of life. This is a new collective or
common meaning.
This implies a context in which illness is not only approached as a handicap
or a disability, but as a constraint from which you can create something—which
was also a stance claimed by writer Georges Perec and the OULIPO movement
in the French literature half a century ago. It makes a creative aspect of the ill-
ness stand out. Think of neurodiversity for people affected by autism or Voice
Hearers for schizophrenia. Instead of deficient lives, which were lived in closed
institutions, new forms of life are developing in the new context of a community.
Today, there is an extension to other conditions, like ADHD or dyslexia, as hav-
ing strengths or advantages.2 The multiplication of different forms of life is a
2
A recent example among many: “In recent years, however, dyslexia research has taken a surpris-
ing turn: identifying the ways in which people with dyslexia have skills that are superior to those
strong trend: it is an expression of values of choice, self-ownership, and initia-

tive, in the constraint of the disease. It is a style of being affected, a style of living
the illness in a certain way.
These narratives can be linked up to the tradition of German individualism,
which is, as Georg Simmel wrote, an individualism of uniqueness, a singularity for
which Gœthe is the figurehead and Bildung (a rich German word, coming from
German Enlightment and Romanticism, which means literally “education” in the
sense of an education of the inner self that links together the processes of education,
edification, and culture) (Dumont 1994) the form this singularity has adopted. This
is what is in “plain view” (ordinary practices with new objects).
The aim of Peter Winch’s work was “to suggest that the concept of learning from
which is involved in the study of other cultures is closely linked with the concept of
wisdom. We are confronted not just with different techniques, but with new possi-
bilities of good and evil, in relations to which men come to terms with life”. This
wisdom is about what Winch calls “limiting notions”—birth, death, sexuality—
“which give shape to what we understand by ‘human life’” (Winch 1964, 322). We
can add long term and chronic illnesses to these three limited notions. These ill-
nesses, because they’re chronic, are accompanied by a certain suffering and confu-
sion. Considering one’s own life as a whole from the perspective of its limitations
and, eventually, living a different form of life which can be fulfilling, this is what
these narratives are about. In this sense, they express an individualistic attitude
toward adversity—an attitude unimaginable at the time of the “total institution”
(Goffman 1961). This is what we are in search of when we read these narratives, as
when we study other cultures, and to follow Winch, “we may learn different possi-
bilities of making sense in human life” (Winch 1964, 321). These autobiographies
of psychiatric, neurologic, or neuropsychiatric patients do a similar work in show-
ing how to live, sometimes a rewarding life, despite the evil to which these people
are subjected. The patient appears mainly as an individual having subordinated his
patient status, because he extricates himself from the disease with his or her strength
of singular creativity. He has subordinated the disease to his own individuality by
shaping it with a personal style enabling him to create something. We might increase
the possibility to live singular lives.
of typical readers. The latest findings on dyslexia are leading to a new way of looking at the condi-
tion: not just as an impediment, but as an advantage, especially in certain artistic and scientific
fields.” A. M. Paul, The Upside of Dyslexia, The New York Times, February 4th, 2012. One week
later, John Tierney published a “What’s New? Exuberance for Novelty Has Benefits”, The
New York Times, February 13th, 2012: “Those are the kinds of questions used to measure novelty-
seeking, a personality trait long associated with trouble. As researchers analyzed its genetic roots
and relations to the brain’s dopamine system, they linked this trait with problems like attention
deficit disorder, compulsive spending and gambling, alcoholism, drug abuse and criminal behavior.
Now, though, after extensively tracking novelty-seekers, researchers are seeing the upside. In the
right combination with other traits, it’s a crucial predictor of well-being.” “It can lead to antisocial
behavior,” declares a psychiatrist, “but if you combine this adventurousness and curiosity with
persistence and a sense that it’s not all about you, then you get the kind of creativity that benefits
society as a whole .”
52 A. Ehrenberg
Conclusion
There is an apparent paradox of autonomy: the diminishing social value of guilt

has been replaced by a situation where issues of emotional and drive control
seem much more decisive than when autonomy was a secondary value. This
paradox is resolved when we situate it in our current relationship to time. Here,
we have to follow Norbert Elias: “To assert oneself as an adult in society struc-
tured like ours […] demands a high level of anticipation and of self-control of
intermittent impulses in order to reach long run goals and to accomplish one own
desires. The level of constraint demanded corresponds to the length of interde-
pendent chains one forms, as individuals, with other persons. In other words, to
assert oneself as an adult in our society requires a high degree of self-control of
one’s own drives and affects”. (Elias 1980/2010, 99). The more social complex-
ity increases, notably the uncertainty of the future and the length of interdepen-
dent chains (of a now global society), the more our concern for self-control rises.
But this concern rises, as I already underscored it, as a skill. Actually, this is a
utilitarian idea of morality, that of Bentham and Mill: as skills needed to accom-
plish a good life, their lack is a consequence of lack of character that is to the
disadvantage of the subject who lacks of them. The form of life of the capable
individual is much more consequentialist than the one of the guilty individual for
which Kantian moral philosophy fits best.
Mental health and psychic suffering are connected to the autonomy-based sys-
tem as follows: changes in our ways of acting in society, symbolized by the notion
of autonomy, correspond to changes in our ways of being affected symbolized by the
notion of psychic suffering—a notion which is everywhere today through the rich
vocabulary of mental health. Autonomy consists of an emphasis on the activity of
the individual, but, at the same time, it is something to which one is subjected,
which one has to put up with: affect, affection, passion, passivity, all of these words
are about being subjected to or affected by something.
The value granted today to mental health, psychic suffering, affect and emotions
is the fruit of a context through which injustice, failure, deviance, dissatisfaction,
etc., tend to be appraised according to their impact on individual subjectivity, and
the capacity to lead an autonomous life. In the mental health field, we find a genuine
individualistic drama where mistakes, failures, misfortune, and illness, all inter-
twined, are represented. Autonomy logically highlights an affective and emotional
dimension, one that used to have a secondary value and occupied a subordinated
place in a disciplined-based system. In this sense, mental health is a social form
adopted to deal with passions when norms and value are entirely oriented toward
individual action.
Mental health, then, is more than the antonym of mental illness. It is an equiva-
lent of good socialization because being in good mental health is to be able to act by
oneself in an appropriate manner in most situations in life. In other words, it is to be
able to self-activate in displaying enough emotional self-control. In a style of social
life which confronts the individual less with the drama of desire than with the trag-
edy of self-esteem, mental health appears as an ensemble of practices aiming to

render the individual able to control his emotional functioning and whose behavior
is regulated by technique resorting to autonomy.
It is thus possible now that a good life might be defined by the best score on the
Global Assessment of Functioning (GAF) of axis 5 of the DSM-IV: “91–100. No
symptoms. Superior functioning in a wide range of activities, life’s problems never
seem to get out of hand, is sought out by others because of his or her many positive
qualities.”
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Depression as a Problem of Labor: Japanese
Debates About Work, Stress, and a New
Therapeutic Ethos
Junko Kitanaka
Abstract The global rise of depression is often linked to the spread of neoliberal-
ism, which urges workers to constantly design and (re)make themselves in order to
advance their careers through their ever-widening social networks. Depression can
be read as both the pathological breakdown of this self-production and an adaptive
response against the increasing demand for affective communication. The funda-
mentally social nature of depression has been heatedly debated in Japan, where,
since the 1990s, it has surfaced as a “national disease” that disrupts the workplace.
Many workers are said to have become depressed as a result of their traditional work
ethic, notable for its loyalty and diligence, which is less valued in a neoliberal econ-
omy. Using this argument, a workers’ movement has successfully established
depression as an illness of work stress, thereby winning economic compensation
and long-term sick leave for afflicted workers. Yet, this radical reconceptualization
of depression as socially produced has also created an impetus to collectively man-
age workers’ mental health, with the government’s much-disputed plan to impose
“stress checks” on all workers in order to screen out the vulnerable. The emerging
psychiatric science of work also questions the traditional clinical approach to
depression that emphasizes “natural” recovery through rest; instead, it is cultivating
modes of restoring health in ways that render workers more efficient and productive
for business. This paper examines Japanese debates about the nature of workers’
psychopathology, their vulnerabilities, and their recovery – or even their potential
for further transformation – against the backdrop of the new therapeutic ethos.
Depression as a Problem of Labor
In a teachers’ strike in Chicago in 2012, American workers debated whether they

should join a “wellness plan” that would enable employers to observe and intervene
in the realm of workers’ physical health (Finamore 2012). In Japan, where workers
J. Kitanaka, Ph.D. (*)

Department of Human Sciences, Faculty of Letters, Keio University, Tokyo, Japan

DOI 10.1007/978-94-017-7423-9_5
56 J. Kitanaka
have long accepted annual physical health checks as a routine matter, they are now
debating who has the right to intervene into workers’ mental health. This question
has become imminent over the last decade, as Japan has witnessed an “epidemic” of
depression (with its patient number exceeding a million) and a surge in national
suicide rate (hitting historical highs of more than 30,000 per year for fourteen con-
secutive years), both of which are seen as related to the long-lasting recession
(Cabinet Office 2014). Depression, which has been labeled by the World Health
Organization as an important part of the “global burden of disease” impeding pro-
ductivity (WHO 2002), seems to be afflicting Japanese workers on a massive scale.
As many in Japan are said to have become depressed and even suicidal from exces-
sive work stress, the government recently announced a plan to introduce stress
checks on all workers across the nation (Asahi 2010). This has stirred up heated
opposition from workers, psychiatrists, and occupational doctors (Asahi 2014),
many of whom argue that such a move is an insidious form of psychiatric surveil-
lance and a sign of the neoliberal order that puts a new demand of responsibility on
individuals for their own health.
What is ironic about this national call for stress checks, however, is that it is
partly a product of a hugely successful workers’ movement. Since the 1990s, left-
wing lawyers, doctors, workers, and their families have been engaged in legal bat-
tles concerning what they call “overwork suicide” and “overwork depression”,
whereby workers have allegedly been driven to depression and/or suicide from
excessive work stress (Kawahito 1998). With the 2000 Supreme Court verdict that
held a company liable for a worker’s suicide and ordered the highest amount of
compensation ever paid for a worker’s death in Japan, the government has begun to
discuss mental health as a matter of social responsibility (Kuroki 2002). This is a
significant change, as depression had long been regarded in Japan as a constitution-
ally determined, biological disease, and, moreover, a private matter. Recognizing
how excessive fatigue, stress, and sleep deprivation can destroy a healthy mind, the
government has created Stress Evaluation Tables, which lists 31 typically stressful
work events, including demotion, relocation, and harassment, along with standard-
ized scores, to aid Labor Standards Offices to objectively measure workers’ stress
levels and provide worker’s compensation for stress-induced psychopathology
(Okamura 2002). Reconceptualizing the workplace as a potential psychological
minefield, the government has also begun to implement other policy changes,
including the revision of the Labor Safety Law and the creation of the Suicide
Prevention Law, thereby acknowledging the responsibility of the state and corpora-
tions for keeping workers mentally healthy (Asahi 2005; Kōsei Rōdōshō 2001). In
this context, the government’s latest call for stress checks might even seem like an
inevitable evolution of its Durkheimian stance, which regards psychiatric break-
down and the increased number of suicides as a product of society.
Yet, the government’s stance is also conflicted, insofar as it encompasses two
perspectives on depression as a problem of labor – that is, as an impediment to work
and a product of work itself. This also points to the inherent tension in today’s
global discourse about depression, that is, as an illness of productivity in the way it
involves competing politics of causality (cf. Young 1995; Martin 2007). The first
Depression as a Problem of Labor: Japanese Debates About Work, Stress, and a New… 57
perspective sees depression mainly as a biological anomaly, to be detected and

located within the individual, who then becomes primarily responsible for ensuring
his or her own mental health. The second regards depression as a kind of normal
response to a pathogenic work environment, for which the employer and the govern-
ment become accountable. While the lawyers and doctors in Japan involved in the
workers’ movement concerning suicides related to workplace-induced stress and
depression are strongly committed to the latter perspective, they have also grappled
with the fact that suicide, at its core, is an agentive act, and they realize they cannot
completely disregard the role that workers – including their subjectivity – play in
the development of depression (Okamura 2002). Particularly in cases where work-
ers appear as if they have driven themselves to pathogenic overwork, those involved
in the movement have had to ask about workers’ agency and their self-subjugation –
that is, how they become complicit in structuring a pathogenic situation (Kawahito
1998). As such concerns are increasingly voiced in Japan by those outside the work-
er’s movement, I want to examine what political consequences are brought about by
the understanding of depression as a problem of labor. More specifically, I want to
explore how the shift in the conceptualization of depression from a “private matter”
to a “public illness” has come to make individual workers responsible for both their
physical and psychological health, thereby recreating the realm of the psychological
as a new object of self-governance and public surveillance.1
A Brief History of Depression as an Illness of Fatigue
While the legal conceptualization of depression as an illness of labor is a product of

the recent workers’ movement, Japanese psychiatrists have long explored the link
between work, fatigue, and depression. Fatigue had initially emerged as an impor-
tant object of investigation for nineteenth century European scholars of the “science
of work”, who saw it as an indication of the utmost limits of production (Rabinbach
1990). While some of these scholars searched for ways to cultivate “bodies without
fatigue,” other, more socially oriented scholars began to examine fatigue as an
innate defense mechanism that would protect people “against the danger of a work
pursued to the extreme” (Rabinbach 1990, 141). Joining this line of inquiry at the
turn of the twentieth century, Japanese psychiatrists also scrutinized illnesses of
1
My analysis of the rise of depression in Japan is based upon anthropological research that
stretches from 1998 to 2012, a period that covers before and after the onset of the medicalization.
This included two years of intensive ethnographic fieldwork conducted at three psychiatric institu-
tions, observing the proceedings of several overwork death/overwork suicide court cases at the
Tokyo District Court, and attending conferences and a series of study groups held by the lawyers
and psychiatrists involved in such cases. For archival research, I examined the Japanese Journal of
Psychiatry and Neurology from its first issue in 1902 to the present as well as a number of popular
journals and a few of national newspapers from the 1870s to the 2000s. I also used Japanese legal
journals such as Jurist and Hanrei Times in order to investigate the legal discourses regarding
overwork depression and overwork suicide.
58 J. Kitanaka
fatigue such as neurasthenia, which was said to be affecting elites at the forefront of
modernity. As neurasthenia became discredited as a legitimate disease category and
came to be seen as a sign of psychological weakness, some Japanese psychiatrists
turned their attention to investigating depression, which they regarded as a real
biological disease, affecting, in particular, hardworking men in their prime years
(Kitanaka 2008). Prominent psychiatrist Mitsuzō Shimoda elaborated on how these
people – who exhibited a strong sense of responsibility, diligence, and thorough-
ness – seemed constitutionally unable to sense their fatigue and pushed themselves
beyond their limits, only to collapse at the height of exhaustion. In his view, depres-
sion functions like an internal thermostat built into a machine that, when overheated,
shuts down the system so as to protect itself. Thus depression, for Shimoda, is a
“biological response for self-preservation”, a protective mechanism of adaptation
(Shimoda 1950, 2; 1941). The depressed were thus conceptualized in terms of the
body-as-machine and as a product of their inherent constitution, with little agency
or power to enact personal change.
While this early twentieth century theory of depression as an illness of fatigue
had a strong flavor of biological determinism, later Japanese theorists – many of
whom were influenced by the vehement antipsychiatry movement from the 1960s –
began to offer an alternative interpretation. As they witnessed the discovery of anti-
depressants and a surge in the number of depressed persons in the community, they
began to ask why so many seemingly normal, even “ideal” workers were suddenly
driven to this affliction. Recalling how Shimoda observed the depressed to be
responsible, diligent, and thorough workers, these theorists argued that such a “pre-
morbid melancholic personality” is not only an inborn constitution but also a latent
product of Japanese socialization. This would explain why there seemed to be an
increase in the number of people with depression at a time of social change, when
these people’s core values were no longer as appreciated as before, as the changing
structure of the workplace might have turned their inflexible diligence and blind
loyalty into something maladaptive, or even self-destructive (Hirasawa 1966; Iida
1974). Thus, relocating its cause from biology to psychology and from individual to
society, these psychiatrists portrayed depression as an illness of labor and pathologi-
cal of Japanese work ethic (Nakai 1976). Their argument was later adopted by law-
yers and doctors involved in litigation regarding overwork suicide, through which
they have done much to reconceptualize psychiatric vulnerability from something
inherent, static, and biological to something historical, malleable, and social.
This reconceptualization of depression also raised questions about what psychia-
trists can do to cure socially pervasive, collective vulnerability. Given that the aim of
clinical practice is not to voice social critiques but to provide a remedy for the dis-
ruptions in individuals’ lives, psychiatrists began to ask how they should direct
patients’ awareness about the nature of their affliction. Seeing how antidepressants
alone did not seem to entirely cure depression, some psychiatrists in the 1970s
turned to psychotherapy in order to encourage patients to reflect on the social roots
of their depression and the nature of their self-subjugation (see Hirose 1979). This
was an exceptionally experimental time in Japanese psychiatry, given that Freudian
psychoanalysis – though introduced in 1912 – had never taken root in this country,
and most forms of psychological intervention had generally been “viewed with deep
suspicion” (Lock 1980, 258). Perhaps it is not surprising, then, that these psychia-
trists soon began to observe, in their clinical practice, that not only was such intro-
spection often too threatening for patients but that it left them “worse off” than
before (Iida 1978). Criticizing this as a form of “iatrogenesis” – an illness of doctors’
own making (Iida 1978; Yoshimatsu 1987) – and suggesting how this form of con-
fessional technology might be too alien, destabilizing, and even intrusive for many
Japanese patients (cf. Doi 1972; Kandabashi 1974/1988), prominent experts began
to caution against intervening into the intimate realm of psychology. They empha-
sized how depressed persons tend to eventually recover, with medication and ample
rest. Their recommended approach was instead to let patients disconnect from the
pathogenic relations in the workplace, and to retreat into a space of their own inner
freedom (Kasahara 1978, 1989; Yokoyama and Iida 1998). As they intentionally left
the question of patients’ agency unexplored, insight-inducing psychotherapy became
a matter of interdiction for most Japanese psychiatrists for decades to come.
Problematizing Workers’ Psychology
In the current medicalization of depression, there has been a renewed interest in

workers’ psychology, a concern that has emerged from legal, governmental, indus-
trial, and popular discourses. This was first articulated through legal disputes, particu-
larly in the 2003 Toyota case involving the suicide of an employee who was, by all
accounts, an ideal “Toyota Man”. Emphasizing how this man’s objective stress level
(as indicated by the recorded hours of overtime) was not necessarily more than that of
his peers, the defense argued that the worker’s alleged depression was caused by his
own vulnerability (i.e., melancholic premorbid personality), which they argued must
have driven him to take on more tasks than he was able to accomplish. The plaintiff,
while emphasizing how this man was respected for his good leadership and a strong
sense of responsibility and was driven to suicide by impossible work demands,
asserted that what should matter is not the “objective” level of stress but rather how
the worker himself experienced the stress. The judges accepted the latter argument
that it is not the quantity but rather the quality of work that should be considered. The
judges even went so far as to declare that the standards for work conditions should not
be set to accommodate the “average” worker – as the government’s guidelines state –
but rather to those who are “most vulnerable to stress” (that is, as long as their person-
alities remain within an acceptable range found among the workers doing the same
kind of job and having a similar age and experience (Asahi 2003; Daily Yomiuri
2004). While this radical “subjectivist” stance, which challenged the government’s
approach, was reported as another “victory for the weak” (Asahi 2001), it may have
also provoked the government’s interest in the realm of workers’ psychology.
The growing interest in workers’ psychology has also come from industry, which
is bound by the system of lifetime employment and thus faced with the high costs of
depressed workers on extended sick leave. This concern has been shared by some
60 J. Kitanaka
psychiatrists and occupational doctors involved in the field of “psychiatric science

of work,” who, since the mid-2000s, have questioned the idea that initially made
depression a common illness category in Japan – namely, that depression is an ill-
ness of fatigue and stress. Pointing out that there is in fact no definitive scientific
evidence that demonstrates the causal link between stress and depression (see a sys-
tematic review by Fujino et al. 2006), they have emphasized instead how depression
is a product of the interaction between the environment and individuals, and the fact
that how individuals experience and interpret the stress plays an equally important
role (e.g., Onishi and Kondō 2008). To further question the medico-legal discourse
that had shifted responsibility from depressed persons by promoting a “blame-free
self of the therapeutic model” (Douglas 1992, 230), these doctors have instead prob-
lematized workers’ agency by redefining depression as not only a product of stress
but also a form of risk that every worker is subjected to (see the report by Nihon
Sangyō Seishin Hoken Gakkai or the Japan Society for Occupational Mental Health
2006). Depression, defined in this way, becomes something preventable by rational
management both at collective and individual levels – an idea that is becoming more
emblematic of the stance of the government and corporations as they search for
effective means of dealing with the rapid increase in the number of depressed work-
ers. Industry has also begun to find ways to assess and manage workers’ recovery,
not in terms of infinitely malleable and unpredictable clinical time, but rather in
terms of standardized and more strictly controlled industrial time with the hope of
more speedily restoring workers’ health as well as productivity. As both personnel
staff and workers are coming under increasing pressure to return the afflicted to a
healthy state, they have to negotiate the ideals of clinical time that prioritizes a “nat-
ural’ recovery and the demands of industrial time that constantly seeks, even for a
therapeutic process, the principle of efficacy. The new demand for workers’ indi-
vidual “self care” has also served to blur the distinction between “private illness” –
which is dealt with as a personal and family problem – and “public illness” (Nomura
et al. 2003), calling for social responsibility as well as surveillance in Japan.
These legal, governmental, and industrial concerns have also resonated with the
changing tone of the popular discourse about depression through the 2000s, when
the initial hype around new antidepressants quickly waned and was replaced by a
growing sense of disillusionment with psychiatric care (Yomiuri 2010). Particularly
after the mid-2000s, the media began to problematize the rapidly growing number
of depressed patients – many of whom seemed to be developing the problem chroni-
cally, and remaining on sick leave, sometimes for years – as a social problem (e.g.,
NHK 2009). Critics of psychiatry (many of whom are themselves psychiatrists)
pointed out how ambiguous a psychiatric diagnosis can be, and how lay people
seemed all too willing to embrace a diagnosis of depression without fully realizing
what physiological, psychological, social, and economic consequences it might
bring (e.g., Kayama 2008). Indeed, social scientists have long debated the ill effects
of being labeled as mentally ill, as well as the ways in which a socially stigmatized
identity becomes internalized, even to the point of eroding a person’s core sense of
self (Becker 1960; Goffman 1963).
What the current medicalization of depression has brought seems even more
complex: what Ian Hacking calls a “looping effect”; in this case, where the nature
of “depression” is altered by the way people start to live as (and conform to the idea
of) “depressed patients”. As they do so, these people’s lives also evolve in ways that
alter the classifications, descriptions, and experiences of “depression” itself
(Hacking 1999). For instance, some of the depressed persons I met in Tokyo in 2008
and 2009 had been diagnosed as “depressed” and given antidepressants by doctors
who likely would have been more cautious with such a diagnosis 10 years prior.
Despite the fact that some of these patients initially felt uncertain about the diagno-
sis, they continued to take antidepressants, even when they felt the pills were not
helping, but rather aggravating, their condition. Remaining uncured and home-
bound, some of them eventually became part of the growing number of “intracta-
ble” patients, for whom a traditional treatment of antidepressants and ample rest
was apparently ineffective. As psychiatrists were confronted with these “new types“
of patients (or what Hacking would call “moving targets”: Hacking 1999), they
began to discuss the limits of conceptualizing depressed patients as mere victims of
biological and social forces, and to increasingly problematize patients’
psychology.
A New Therapeutic Ethos
While most psychiatrists have remained hesitant to get involved beyond prescribing
antidepressants, in part because they know that past psychotherapeutic attempts
with the depressed have a bad track record, others, who work more closely with
industry, have begun to criticize the traditional psychiatric approaches. Arguing
how the traditional rest cure, which often results in long-term sick leave, may have
adverse effects on patients and emphasizing that the “workplace is no place for
rehabilitation” (Onishi and Kondō 2008), they have devised a more aggressive
treatment program called Rework, which rapidly is becoming, in many companies,
a prerequisite for depressed persons to return to work (Utsubyō Riwaku Kenkyukai
2009). In contrast to the legal conceptualization of depressed persons as passive
victims, driven to depression by stressful social relations, Rework borrows from
cognitive therapy and re-defines patients as active agents who drove themselves to
depression through distorted interpretations of stressful social relations. For
instance, at a leading center of Rework in Tokyo, patients are first urged to manage
their depression by closely keeping track of their bio-rhythms and affective changes.
Second, they are placed with other patients in a mock-office environment and given
communal tasks in order to analyze and correct the patterns of their miscommunica-
tion and distorted cognition. Third, patients are re-trained in affective labor through
group therapy, where they are encouraged to try alternative communication skills
and learn how to control their emotions. Through these daily activities, therapists
carefully control the level of stress that patients are exposed to, and they gradually
increase its level to see how much stronger and healthier patients have become.
They also closely monitor the patients’ biological, cognitive, and affective changes
62 J. Kitanaka
in order to decide when patients are ready to return to their own workplace (Utsubyō
Riwaku Kenkyukai 2009, 2011).
As Rework urges patients to heal themselves by being re-immersed in the thick
of social relations, it clearly departs from the traditional psychiatric approach that
emphasizes therapeutic isolation. Particularly in the way it tries to get inside the
patients’ minds and reshape them as more productive workers, Rework might also
be accused of operating as a “factory of correction” (cf. Scull 1979) that seeks to
instill a new form of self-governance. Such accusations are rarely heard, however,
even among leftwing doctors involved in the workers’ movement. This is partly
because psychiatrists have been pressed to respond to growing criticism of thera-
peutic ineffectiveness, and to adopt a seemingly scientific, managerial program to
restore workers’ health. But more importantly, it may also be a result of Rework
beginning to serve as a place for patients to voice their dissent. As a medical anthro-
pologist, I conducted interviews with patients and doctors in 2000–2003 and 2008–
2009, and found that, despite Rework’s explicit emphasis on distorted cognition, the
numerous testimonies of illness-inducing workplaces across industries that both
therapists and patients encounter serve to undermine the assumption that the prob-
lem mainly lies with individual workers. With its own introspective technology
turned on its head, Rework’s therapeutic aim is constantly destabilized by those
who ask what may lie beneath what appears to be socially induced vulnerability.
In the process, Rework seems to provide patients with an opportunity to critically
examine the nature of their self-subjugation and ask if their relentless pursuit of
personal advancement through the current system is really the way to pursue happi-
ness. In fact, some of their reflections seem to parallel the narratives of depressed
workers I met in a self-help depression group during 2000–2003, many of who told
me how they had reached, through bitter struggles with depression, a sense of libera-
tion in embracing their vulnerabilities, reexamining their worldly obsessions, and
relinquishing their desire to be in control. Yet, a key difference is also apparent, as
patients today no longer seem able to afford the kind of quiet resignation and detach-
ment that their older counterparts had chosen as a cure for depression; they know all
too well that lifetime employment is crumbling, and that social security, as indicated
by the quickly eroding pension and the national health insurance systems, is disap-
pearing from under their feet. In order to escape unemployment, they need to learn
to mask their vulnerabilities and appear resilient to stress. Thus, while Rework does
not impose on workers a set of ethics one might follow and limits itself in offering
workers a set of standardized skills with which to protect themselves, it does seem
to cultivate in them a belief in resilience as a new kind of morality – even if it is not
at all clear what sense of personal fulfillment, if any, that could ultimately bring.
Changing Forms of Self-Governance
The call for collective and individual management of mental health in Japan sug-
gests changing demands for self-governance. The rising interest in the psychologi-
cal realm has been cited as a hallmark of modernity (Rieff 1966; Giddens 1991) and
a sign of the changing nature of political surveillance and possible forms that agency
can take in contemporary society (Marcuse 1970; Foucault 1975; Rose 1996). This
has been particularly pertinent to societies like the United States, where psycho-
analysis had a strong influence over the course of the twentieth century, and where
organizations like the National Institute of Mental Health (NIMH) have done much
to promote public awareness of psychological health. The rise of Prozac from the
1990s – portrayed as a “happy pill” that would not only cure depression but also
transform people’s personality – was widely seen to be putting an end to the domi-
nance of the psychological. Liberating the meaning of the “biological” in psychiatry
from its old connotation of genetic determinism and instead presenting it as some-
thing infinitely flexible and malleable, Prozac seemed to displace the psychological
from its previous role (see Elliott and Chambers 2004). While some critics have
pointed out how the Prozac narrative insidiously promotes an idealized image of the
neoliberal worker as self-directed, flexible, and productive, its attraction certainly
lay in its celebration of individual autonomy, self-enhancement, infinite growth, and
possibilities of transcending nature by means of neurobiological technology (Elliott
2003). Thus helping redefine the biological as the new location of agency, the
Prozac discourse of the 1990s offered a new vision of biological self-governance.
Yet, despite the concern that the Prozac narrative is sweeping the globe, instilling
a single vision of the “neurochemical self” fit for the new economic order, global
medicalization has instead emerged as a fertile ground for local critiques against the
imposition of a homogenizing view of personhood (Rose 2007; Metzl 2003; Ecks
2005; Kitanaka 2012). In this regard, it is notable how the Japanese discourse about
depression as a work hazard is quickly becoming a part of the global reality as other
nations have begun to suffer the same kind of stagnating recession that Japan has
been affected by for the last few decades. For instance, in France, where Japanese
cases of overwork death were once discussed with a sense of curiosity (Brice 1999),
there have been growing reports of suicides among employees of France Telecom,
attributed to the stress they were under due to the company’s radical restructuring
(BBC News, September 12, 2009). Rising rates of suicide and psychopathology in
the workplace have raised public concern elsewhere in Europe – particularly in
Germany, Italy, and Finland – where these are often discussed as products of the
increasing pressure people face in the new economic order (e.g., Mole 2010). Like
their Japanese counterparts, European commentators tend to emphasize how typical
victims are not “deviants” but people who have led well-adjusted lives, and that
their pathologies should not be explained away by their individual biological/psy-
chological weakness but rather interpreted, a la Durkheim, as social problems, even
forms of social protest (Moerland 2009). By linking depression to the “socials ills”
brought on by neoliberalization –including the perils of privatization, the collapse
of lifetime employment, and the crisis in national health care – people seem to be
addressing their sense of alienation as real and concrete, as something that requires
resolution through political intervention beyond Prozac. Yet, this conceptualization
of depression as an illness of labor has already produced inconsistent effects in
Japan, where workers’ calls for social restructuring seem to have invited a national
64 J. Kitanaka
call for restructuring – even reprogramming2 – of workers themselves. They are now
expected to not only overcome depression but also to transcend their former selves,
to become resilient.
Resilience has become a dominant concept in the recent global mental health
movement partly because of its seemingly “benign” connotation (Howell and
Voronka 2012). Its appeal lies in the fact that it glamorizes the transcendental ability
of the individual even as it serves to mask an underlying economic rationality or the
fact that it has risen in the context of the “retrenchment of state services through
neo-liberal restructuring and cost-cutting measures” (Howell and Voronka 2012, 1).
These politics are clearly embodied in the emerging discourse about stress and resil-
ience in post-9/11 America, where, as Allan Young has shown, the notion of resil-
ience “as something to be achieved with the help of experts” has come to threaten
“to displace effortless ‘normality’ as the default condition of human life” (Young
2012). At this historical moment, Japan’s national call for stress checks might begin
to seem not so much a preventative measure for depression and suicide per se as it
is an ominous sign of a coming era of “positive mental health”, with its infinitely
expansive meanings and growing demands for bio-psychological self-governance.
Note This study is supported by JSPS Grant-in-Aid for Scientific Research (No. 24300293). This
chapter is based on additional empirical material and new theorizing of what was presented in my
2012 book Depression in Japan: Psychiatric Cures for a Society in Distress (Princeton University
Press).
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Darwinian Blues: Evolutionary Psychiatry
and Depression
Luc Faucher
Abstract Psychiatry is in disarray. Case in point: psychiatry’s primary classifica-

tion manual has been under attack almost since the nosological revolution initiated
by the DSM-III. The latest version – the DSM-5 – was not even published when
criticism of it began. From many corners of psychiatry, voices were heard that urged
a reclassification of mental disorders based on research in neuroscience and genet-
ics as a solution to psychiatry’s current situation. A radically different solution has
been proposed to ‘cure’ the DSM of its alleged ailments: to build (or rebuild) it
based on an evolutionary understanding of disorders. Indeed, advocates of evolu-
tionary psychiatry believe that psychiatry could benefit from the adoption of an
evolutionary perspective by providing a new understanding of specific mental ill-
nesses such as schizophrenia, phobia, autism, etc. In this paper, I will focus my
attention on two recent explanations of depression that adopt an evolutionary-style:
Nesse’s, and Andrews and Thomson’s. In this paper, I will present their respective
positions in regards to depression. I will then present some reasons as to why one
should remain unconvinced by these explanations of depression.
Introduction
Psychiatry is in disarray, and things seem unlikely to change anytime soon. Case in
point: psychiatry’s primary classification manual has been under attack almost since
the nosological revolution initiated by the DSM-III (see McReynolds 1979; for
overviews of some problems affecting various DSM editions, see Cooper 2004;
Galatzer-Levy and Galatzer-Levy 2007; Kirk and Kutchins 1992; Mayes and
Horwitz 2005; Tsou 2011). The latest version – the DSM-5 – had not even been
published when criticism began, accusing the new manual of either not departing
radically enough from earlier versions (Frances 2009; Frances and Widiger 2012) or
(and possibly as well as) for a lack of empirical support for some of its reforms
(Widiger 2011). Worst of all, the National Institute for Mental Health (NIMH) seems
L. Faucher (*)
Département de philosophie, Université du Québec à Montréal, Montreal, QC, Canada

DOI 10.1007/978-94-017-7423-9_6
70 L. Faucher
to have completely lost faith in the DSM, launching an initiative called the Research
Domain Criteria (RDoC), whose goal is to propose a reclassification of mental dis-
orders based on research in neuroscience and genetics (Insel et al. 2010; Morris and
Cuthbert 2012). As Steven Hyman puts it: “It now appears that the accreting failures
of the current diagnostic system cannot be addressed simply by revising individual
criterion sets and certainly not by adding more disorders to DSM-5” (2010, 3).
A radically different solution has been proposed to ‘cure’ the DSM of its alleged
ailments: to build (or rebuild) it based on an evolutionary understanding of disorders
(Nesse and Jackson 2011; Nesse and Stein 2012). From the end of the 1970s on, as
Nesse and his colleagues observed, a ‘medical model’ has dominated psychiatry. As
one leading advocate of this model put it, psychiatry has placed “the brain and its
structure and functions in health and illness at the center of interest and study”
(Guze 1992, 54). As a result of this model’s adoption (or at least, of an interpretation
of it; see Murphy 2009), psychiatry has turned to molecular and cellular neurosci-
ences (Kandel 1998; Akil et al. 2010) or cognitive neurosciences (Andreasen 1997)
as the “basic sciences” from which explanations (and category validation) of disor-
ders can be expected (the RDoC initiative is the latest expression of the belief in this
model). However, by focusing almost exclusively on the abnormality of brain struc-
tures, it is argued that psychiatry has relied on a “crude medical model” of mental
disorders (Nesse and Williams 1995, 22), and has neglected to understand the func-
tions of the diverse cognitive components that comprise our minds. As many observ-
ers of psychiatry have noted (see Widiger and Sankis 2000; Murphy 2006),
psychiatry lacks an explicit (and scientific) image of what constitutes the normal
functioning of the mind. Such an image is crucial for the establishment of diagno-
ses, and psychiatry without it is somewhat blind. According to Nesse and Williams,
by providing a framework within which to understand the normal functions of the
mechanisms of the mind, the adoption of an evolutionary approach “… would bring
the study of mental disorders back to the fold of medicine …” (idem, p. 22; see also
Nesse and Stein 2012, 3). For this reason, evolutionary biology should also be con-
sidered as “an essential basic science for understanding mental disorders” (Nesse
2005, 903; my emphasis). This is not to say that genetics and cognitive neurosci-
ences should be tossed away, but that they should be incorporated into a larger
framework, which includes evolutionary theories. As Nesse put it recently in a
paper about depression, “Neuroscience is not enough, evolution is essential” (2009).
What would psychiatry specifically gain by adopting an evolutionary frame-
work? It would gain at least two things, according to the supporters of this approach.
Firstly, considering cognition and affect as being the result of evolutionary pro-
cesses should prove helpful in both defining and providing an enriched general tax-
onomy to categorize mental disorders. For instance, Nesse (2002) posits that one of
the most useful contributions of an evolutionary approach is the emphasis on the
distinction between defects or disorders and “evolved defenses”. According to
Nesse, cases of evolved defenses are sometimes confused with dysfunctions because
they cause pain or discomfort (what he refers to as “the DSM fallacy” [Nesse and
Jackson 2011, 182] because the DSM ignores so blatantly this distinction). As will
be seen in the next few sections of this paper, some behaviors and mental states that
cause pain or discomfort to ourselves or others, and for which help is sought (such
Darwinian Blues: Evolutionary Psychiatry and Depression 71
as depression), can indeed be normal forms of defensive responses to certain types

of situations that reduce our reproductive fitness. In other words, pain and discom-
fort are not good cues of what is dysfunctional and what is not.
Other cases of fully functional mechanisms that are misconceived as defective by
psychiatrists are those where the mechanism has to perform its function in an envi-
ronment that is completely or radically different from the one in which it has been
selected to work. In particular, this is the case in new environments where the cues
that previously indicated fitness benefits no longer indicate them. One example of
such an “environmental mismatch” is drug addiction in which an artificial substance
triggers responses that are usually activated by fitness-related stimuli: like food, sex,
etc. (Nesse and Berrige 1997).
The concepts of “evolved defense” and “environmental mismatch” are just two
examples of theoretical benefits that could be gained by adopting an evolutionary
perspective in relation to mental disorders. Another example of such a benefit is the
explanation of the persistence of certain disorders through the invocation of evolu-
tionary phenomena like pleiotropy or polygenic mutation-selection balance (see
Keller and Miller 2006).
Secondly, advocates of evolutionary psychiatry believe that psychiatry could
benefit from the adoption of an evolutionary perspective by providing a new under-
standing of specific mental illnesses such as schizophrenia, phobia, autism, etc. (see
Burns 2004; Mineka and Öhman 2002; Ploeger and Galis 2011). From among this
group of mental illnesses – as Kennair (2003) noted in a review of the field of evo-
lutionary psychiatry – “[t]he disorder that has received most attention recently from
an evolutionary perspective is depression: most of the key researchers within EPP
[evolutionary psychopathology] are involved in the study of this disorder. Within
the review period covered here, papers on depression stand out as most ground-
breaking and probably provocative …” (693). Though more than a decade has
elapsed since Kennair’s statement, I believe it remains accurate. In the past several
years there has been a flurry of papers from some of the main advocates of evolu-
tionary psychiatry as applied to depression (Allen and Badcock 2006; Andrews and
Thomson 2009; Gilbert 2006; Hagen 2011; Keller and Nesse 2006; Nesse 2009;
Nettle 2004; Price et al. 2007; Sloman 2008; Stein et al. 2006). These papers echoed
a growing preoccupation in certain circles concerning the recent and sudden increase
in the number of cases of depression in the general population. Indeed, many authors
have questioned the ability of current diagnostic criteria as found in the DSM-5 to
distinguish the normal from the abnormal, and consider this the source of the
depressionepidemic (Horwitz 2011; Horwitz and Wakefield 2007; Mulder 2008;
Parker 2005).1 For instance, Mulder maintains that “[t]he DSM criteria define a
heterogeneous group ranging from individuals whose symptoms are dysfunctional,
1
The authors listed here have focused on DSM-IV and DSM–IV TR, but their point carries over to
the new version of the DSM. Indeed, according to the APA website of the DSM-5 (www.dsm5.org)
there is no notable changes in the core criterion symptoms or in the duration of major depression
from DSM-IV to DSM-5. The only major change concerns the omission of the bereavement exclu-
sion from the new version of the DSM. This change will only exacerbate the problem noticed by
the authors aforementioned who would rather prefer the exclusion clause to be extended to other
kinds of loss than eliminated (see for instance Wakefield et al. 2007; Wakefield and First 2012).
72 L. Faucher
serious and ongoing to those whose symptoms are fleeting and related to social
circumstances” (2008, 241). It is precisely the distinction between different groups
that evolutionary psychiatry seeks to establish on firmer ground.
In what follows, I will focus my attention on two recent papers about depression
that adopt an evolutionary-style explanation: Nesse (2009) “Explaining Depression:
Neuroscience is Not Enough, Evolution is Essential” and Andrews and Thomson
(2009) “The Bright Side of Being Blue: Depression as an Adaptation for Analysing
Complex Problems”. My reason for selecting these two papers is the following:
despite sharing a common general framework (the evolutionary theory), evolution-
ary psychiatrists who attempt to explain depression can be divided by the positions
they take about the adaptative character of depression, and about the evolved domain
of mechanisms involved in depression. Nesse and Andrews and Thomson have dif-
fered on both accounts. Nesse considers major depression as the result of dysfunc-
tional adaptive mechanisms, while Andrews and Thomson consider it to be an
adaptative response to some varieties of problem.2Nesse considers the domain of
depression (or of the adaptive mechanisms that break in depression) as general (it is
a response to the loss of adaptative resources), while Andrews and Thomson con-
sider the domain of depression as essentially social.
In what follows, I will present their respective positions with regards to depres-
sion (section “Evolutionary explanation of depression”). I will then (section
“Remarks and problems with evolutionary models of depression”) present some
reasons as to why I am unconvinced by these explanations of depression.
Evolutionary Explanation of Depression
As stated in the previous section, evolutionary explanations of depression can be

divided along at least two axes: functionality and domain. Evolutionary psychia-
trists interested in depression have explored all possible options following this
delineation. Though I will briefly recount other positions, in this section I will focus
on two particular ways to think about depression along those axes. The first holds
that depression is a dysfunction and that it is the result of the malfunctioning of a
mechanism that is non-essentially social in nature; the second holds that depression
is functional and that its domain is essentially social.
2
In a brief, general-public oriented presentation of their theory, they wrote: “We believe that
depression is in fact an adaptation […]” (Andrews and Thomson 2010, 57). Later in the same paper
(as well as in a subsequent paper [2011]), they recognized that depression also exists as a disorder
(2010, 61). For instance, they write: “In our article, we argued that while depressive disorder is
probably over-diagnosed, it must exist because all body systems are susceptible to malfunction-
ing” (Andrews and Thomson 2011, 3). This concession would seem to collapse the distinction I am
trying to draw with Nesse concerning the dysfunctional aspect of depression. If such was Andrews
and Thomson’s position after all, it would differ from Nesse’s only by the kind of problems depres-
sion is designed to deal with. But even if this was the case, the two theories still are different
enough in their content to justify to study them both in this paper.
Nesse: Low Mood and Depression
In his “Explaining Depression: Neuroscience is not Enough, Evolution is Essential”

(2009), Nesse argues that “… serious depressionis not an adaptation shaped by
natural selection. It has no evolutionary explanation. However, we do need an evo-
lutionary explanation for why natural selection left us so vulnerable to a disease as
common and devastating as depression. Some abnormal depression is related to
normal low mood, so explaining the origins and functions of mood is an essential
foundation for understanding depression…” (my emphasis; 21). Thus, an evolution-
ary perspective does not commit one to assuming that depression is an adaptation;
in this case, it instead highlights the necessity of explaining why we are vulnerable
to it. It grounds this explanation in the dysfunction of an otherwise functional mech-
anism, a mechanism in charge of what Nesse calls “low mood”. Since low mood is
crucial to the explanation of depression, let’s say a few words about it.
Nesse’s theory of mood is based on a functional theory of moods and emotions
(for a statement of his position, see Nesse 1990; more recently Nesse 2006; Nesse
and Ellsworth 2009). According to Nesse, emotions and moods are organized adap-
tative responses to recurrent problems in our ancestral environment.3 Negative emo-
tions and moods are responses to threatening or loss-type situations, or situations
where costs and risks are greater than benefits. More precisely, low mood is elicited
by cues indicating loss of resources of adaptative significance: “The losses that
cause sadness are losses of reproductive resources […] A loss signals that you
may have been doing something maladaptive” (Nesse and Williams 1997, 9).
Reproductive resources could be “somatic” (personal health, attractiveness and
ability, and material resources), “reproductive” (a mate or an offspring), or “social”
(allies and status; Nesse 2009, 27). For example, low mood can be triggered by the
sudden loss of a pension fund, parental death, a lost love following departure or
rupture, a lost friendship, loss of social status, etc. The patterns of behavior and
cognitive characteristics associated with low mood (prostration, lack of motivation,
etc.) are consistent with the idea that it is a functional response to problematic fea-
tures of the evolutionary environment. Following Klinger’s (1975) seminal work,
Nesse proposes that low mood functions in two stages: “When efforts to reach a
goal are failing, low mood motivates pulling back to conserve resources and recon-
sider options. If conditions do not improve and no other strategy is viable, low mood
disengages motivation from the unreachable goal so efforts can be turned to more
productive activities. If the individual persists in pursuing an unreachable goal, ordi-
nary negative affect can escalate into pathological depression” (2009, 23). Note that
in this theory, low mood is not typically caused by stress or anxiety,4 but by the
inability to disengage from an unreachable goal (for instance, trying to find happi-
ness in an unhealthy relationship). In other words, stress or anxiety is produced by
the low-mood mechanism; it is not the cause of low mood.
3
In this context, “[m]ood regulates patterns of resource investment as a function of propitiousness”
(Nesse 2009, 24).
4
Though Nesse sometimes mentions the fact that exposure to repeated episodes of stress might
lower the threshold of low mood until it becomes pathological.
74 L. Faucher
A few years ago, Nesse and Keller (Keller and Nesse 2005, 2006; see also Keller
et al. 2007) have suggested that selection might have shaped different subtypes of
depression to address different types of problems. This prediction was the result of
the “situation-symptom congruence hypothesis”, according to which symptoms
should be adapted to deal with adaptative challenges characteristic of different types
of situations. According to the studies that Nesse and Keller conducted, bereave-
ment and romantic rupture would be associated with symptoms differing from those
of chronic stress and failures (sadness, anhedonia, appetite loss and guilt in bereave-
ment and fatigue and hypersomnia in romantic rupture).5
Now that we understand Nesse’s hypothesis about low-mood, we can return to
the issue of depression as such. According to Nesse, many cases of what is diag-
nosed as depression by the DSM are actually cases of low mood – that is, totally
normal responses to a loss of resources, which are roughly the equivalent of pain
responses to tissue damage. Pain is a defensive response, as is low mood. Pain
becomes a pathology when the response is disproportionate to its cause, or when it
appears without cause. Similarly, low mood becomes a pathology when it is dispro-
portionate or without cause. In these cases, it indicates that something is wrong with
the low mood mechanism.
One consequence of Nesse’s position concerning low mood and depression –
which I think will be received gladly by some clinicians – is that in order to be able
to distinguish between the two, one will have to look past the symptoms (which
might well be identical in the two cases) and the brain centers (which also might be
identical in the two cases) and look instead at life circumstances and judge if the
patient’s response is appropriate or proportional as it relates to them. Thus, it means
that clinicians should be attentive to context. This is in opposition to the DSM,
where a diagnosis is completed only on the basis of the presence or absence of spe-
cific signs and symptoms. For instance, a diagnosis of major depression is given to
a patient if they have five of nine symptoms for at least two weeks, independently of
the context or the precipitating events that took place before the episode. For this
reason, Nesse and Jackson argue “DSM-5 should incorporate life events and life
situations into main diagnostic categories, where their role as elicitors of emotions
will be clearer” (2011, 192). Such a reform (which was not retained by those who
worked on DSM-5) would clearly lead to a decrease in diagnostic reliability due to
the variability of interpretations of the appropriateness of reactions to circum-
stances, but according to Nesse et al, it would increase diagnostic validity by elimi-
nating numerous false positives.
Finally, as mentioned earlier, the adoption of evolutionary perspectives is not
only motivated by the new testable hypotheses that one can derive from them, but
also by the possibility of explaining general vulnerability as well as individual vul-
nerability. At present, there is no accepted explanation of general vulnerability:
Nesse mentions the possibility that we might live in a “depressogenic” world where
5
Other subtypes might include seasonal affective disorder (SAD) which is a recurrent type of
depression associated with the winter season, and that is characterized by fatigue, increased appe-
tite, sleeping and carbohydrate craving.
goals are often time unrealistic, or that new physical factors like artificial light, lack
of exercise, or changes of diet might influence the brain mechanisms responsible for
depression (Nesse 2006, 2009). If this were the case, part of the explanation of the
depression epidemic would be a mismatched environmental explanation where the
low mood mechanism is activated overtime in the contemporary environment.6 As
for individual vulnerability, evolutionary explanations might refer to the fact that
traits such as low mood tend to have a high variance between individuals, so much
so that some individuals might be at the pathological extreme of the low-mood
spectrum and thus more vulnerable to the development of depressive disorder.
Research suggests that there is a genetic polymorphism on the 5-HTT gene that
increases the risk of depression (Caspi et al. 2003). Though there is no current
hypothesis concerning the possible benefits of having this variant of the 5-HTT
gene, an evolutionary perspective suggests that there might be benefits linked to
certain circumstances, thus motivating the research in that direction.
To summarize, this position states that the depression epidemic can be explained
by the fact that the DSM cannot distinguish between low mood and dysfunctional
depression. Low mood might be on the rise because of differences between ances-
tral environments and present environments, or it might be more frequent in certain
individuals because of balanced selection. Real depression is thus less common than
thought and is produced by a dysfunction of the low mood mechanism.
Andrews and Thomson: Rumination and Motivation
In “The Bright Side of Feeling Blue” (2009), Andrews and Thomson proposed what
they call a “social navigation hypothesis of depression”. Their hypothesis belongs
to a family of models that asserts the role of depression in social relationships as
well as its functional nature. (I am not arguing here that every social theory of
depression also advocates for an adaptative view of depression; see for instance
Allen and Badcock 2006). Before turning to their model, we will quickly present
some of the other models belonging to this family, which can assist in understanding
Andrews and Thomson’s highly original proposal.
Previous Models of Depression as Strategy in Social Competition
The first model is the “social competition” or “social rank” theory of depression.
Price et al. (1997) advocated this position, suggesting that depression is an “invol-
untary subordinate strategy” (sometimes also called “involuntary defeat strategy”
[Sloman 2008] or “social defeat hypothesis” [Gilbert 2006]), which evolved from
6
Note that it is unclear if this explains “real cases of depression” as opposed to what Nesse consid-
ers false-positives (i.e. low mood).
76 L. Faucher
mechanisms mediating ranking behavior.7 According to these authors, depression

has three functions: (1) preventing a costly attempted ‘come-back’ of an individual
whose defeat in a hierarchical struggle is inevitable; (2) sending a “no threat signal”
to dominant individuals; (3) putting the individual in a defeated state which encour-
ages the acceptance of an outcome. As Sloman puts it, depression “[...] is exqui-
sitely designed to influence the individual to give up certain aspirations such as
winning the affection of a possible mate, or to end a confrontation. It can lead to
submission, the development of more realistic goals, and a redirection of energy
towards more productive pursuits” (2008, 221; my emphasis). This hypothesis is
supported by studies from Raleigh and McGuire who observed that in vervet mon-
keys, the highest-ranking males (alpha) had serotonin levels twice as high as other
males. When an alpha male lost his position, his serotonin levels fell immediately
and he huddled and rocked, refusing food – behaviors characteristic of depression
in humans. They also found that, if the alpha male was removed from the rest of the
group and a randomly chosen male was given anti-depressants, that individual male
became the alpha male in every instance (see also, McGuire et al. 1997).
A second model of depression is the “bargaining model” proposed by Hagen
(1999, 2002, 2003; Hagen and Barrett 2007). In this model, depression is seen as a
sort of strike, i.e. a way for an individual to say that he or she no longer accepts the
terms of a relationship, and that he or she demands better treatment. As Hagen puts
it: “When simple defection from a costly cooperative venture is socially constrained
because, for example, each participant has a monopoly on essential resources or can
impose costs on defection, individuals suffering net costs from their participation
may benefit by withholding the benefits they are providing until better terms are
offered, that is, they may benefit by bargaining or ‘going on strike’” (2002, 324).8
Depression is seen essentially as an unconscious strategy to redress the loss of valu-
able social assets and elicit help or concern. This strategy works if it results in the
modification of the “social environment” (increase in solicitous behavior or parental
investment from those whom the strike targets, for instance). Just as some strikes
might be disturbing and experienced negatively by those at whom they are targeted,
depression might also be experienced negatively by those who are socially close to
depressives (and met with indifference or less concern by those who are less close
and thus less dependent on the resources they are ‘deprived of’ by the strike).
7
Note that for advocates of this position, depression is not always adaptative (one wonders if these
researchers should not have distinguished low mood from clinical depression, as Nesse has done).
As Sloman recently stated: “In general, depression and anxiety are adaptative when they are
switched off early before they become too intense. Because a mechanism that is proving ineffec-
tive in coping with agonistic conflict tends to become more entrenched which makes it more dif-
ficult to switch it off and the continued action of the mechanism may lead to a maladaptative cycle
of escalating depression or anxiety” (2008, 222).
8
In this model, psychic pain “should function to inform individuals that life circumstances … are
imposing a biological fitness cost, motivate individuals to cease activities contributing to the fitness
cost, and condition them to avoid similar circumstances in the future” (Hagen and Barrett 2007,
24). Because of the role of psychic pain in depression, Hagen sometimes calls his theory an “evo-
lutionary theory of psychic pain”.
Hagen (1999, 2002) has tested his theory using postpartum depression (PPD) as
a model for depression in general, which enabled him to make a number of specific
predictions and test for them. Among them were: (1) individuals with no other chil-
dren and few future chances to invest in offspring (those who have everything to
lose) should have lower levels of PPD; (2) individuals who, for social reasons (social
norms related to abortion, for instance), are forced to have unwanted children should
experience higher levels of PPD (new costs are imposed on the individual who may
want to renegotiate her current arrangement); (3) PPD in one spouse should be asso-
ciated with increased parental childcare investment by the other spouse. According
to Hagen, all these predictions were confirmed; additionally, there are preliminary
indications that they might be valid cross-culturally (Hagen and Barrett 2007).
Andrews and Thomson’s Theory of Depression
Andrews and Thomson’s theory has a resemblance to Hagen’s; like the latter, they
see depression as a type of strategy to extort increased investment from others. Their
theory also tries to explain the cognitive features of depression, which Hagen’s the-
ory leaves unexplained (Watson and Andrews 2002, 3). Using both Andrews and
Thomson’s recent paper and Watson and Andrews’ (2002) earlier statement of their
position, I will present their explanation of these cognitive features, after which I
will return to the social motivational features of depression.
According to Andrews and Thomson, depression is “an evolved stress response
mechanism” (Andrews and Thomson 2009, 621). More precisely, its function is to
address two classes of problem: social dilemmas and avoidable stressors.9 The
authors state that these problems are complex and must be dealt with in an analytical
fashion, in that they have to be broken down in smaller pieces to be resolved.10 Thus,
if depression is designed to help solve these types of problem, it must “promote an
analytical reasoning style in which greater attention is paid to detail and information
is processed more slowly, methodically, thoroughly, and in smaller chunks” (idem,
622); this is exactly what most features of depression can be seen as doing.
According to these authors, the central designed feature of depression is rumina-
tion, which can be conceptualized as an analytical and methodological way of con-
sidering complex problems whose goal is to generate and evaluate possible solutions
to these problems. This is consistent with studies that demonstrate that depressive
thinking is more analytical in nature and focused on “regretful thoughts”, i.e. under-
9
Note that this is a move from Andrews’ previous theory, in which he stated that “[t]he functional
domain of depression may be social complexity” (Watson and Andrews 2002, 4), in that depression
is now not only exclusively devoted to solving social problems. In their more recent paper, they
assert: “complex social problems may be the primary evolutionarily relevant trigger of depression
in human beings” (Andrews and Thomson 2009, 626; my emphasis).
10
The authors suggest that their position implies the existence of a mechanism that distinguishes
simple from complex problems (Andrews and Thomson 2009, 625). The way such a mechanism
would work is not explained by them, nor is there any evidence that such a mechanism exists in
non-human animals or in humans.
78 L. Faucher
standing why an episode happened and what could had been done to prevent it
(Andrews and Thomson call this ‘upward counterfactual thinking’). Other features
of depression should be understood in the same fashion, such as:
• The depressed tend to attribute more of their failures to their lack of ability and
more of their successes to chance, while non-depressive individuals display the
inverse pattern. Due to this, some cite a ‘depressive attributional style’ (Andrews
and Thomson 2009, 636). This attributional style would help individuals focus
on their possible shortcomings.
• “Depressed people may also seek information that helps them understand why
avoidable problems occurred. For instance, relative to non-depressed people,
depressed people prefer to interact with people who give them negative evalua-
tions of their personalities. […] Depressed people’s preference for negative eval-
uations may be an important mechanism for gaining information that helps them
understand why they are facing a problem and helps them identify what difficult
behavioral changes they may need to make to solve it. Indeed, the depressed are
more interested in negative evaluations because they are believed to be more
accurate” (ibid.).
• Negative mood also seems to lead to more accurate decisions with regard to com-
plex situations and to conservative implementation strategies for these decisions.
• In certain complex situations, depressed individuals are more competent than
non-depressed individuals at estimating the control they exert over a situation
(idem, 639).
• “… depressed people are more sensitive to costs of cooperating than non-
depressed people and are more likely to defect when it is costly to cooperate”
(idem, 634).
• The depressed are less prone to the fundamental attribution error. This error con-
sists of inferring an actor’s internal state despite the fact that this inference is not
warranted (for instance, to infer that those who are asked in an experiment set-
ting to write a paper defending evolutionary psychiatry really believe that evolu-
tionary psychiatry is true or useful). Watson and Andrews (2002) assert that
because the depressed are more socially dependent, they put more effort into
making logically correct inferences about other people’s beliefs or desires. In
supporting this claim, they note that people make fewer errors when their own
outcomes depend on being accurate, and that people in more interdependent
societies commit this error less frequently.
The other features generally associated with depression (such as anhedonia and
psychomotor changes, sleep and eating dysfunctions) are mechanisms that contrib-
ute to ensuring undisturbed rumination. For instance, anhedonia would assist rumi-
nation by rendering individuals indifferent to pleasures that could distract them
from solving their problems. Preference for solitude (a psychomotor change) would
allow the individual to avoid social contact that can be cognitively demanding. This
account predicts a relationship between rumination and anhedonia such that a need
for increased rumination should produce a more intense anhedonia. In the case of
psychomotor changes, it predicts that if an environment is conducive to rumination,
lethargy will work to keep the individual in that environment; but if the environment
is not conducive to rumination, the individual will be motivated to seek out an envi-
ronment that supports it (which can lead to agitation). This makes sense of the fact
that depression can be characterized by psychomotor retardation or by agitation.
What makes their “analytical rumination hypothesis” (ARH; Andrews and
Thomson 2009, 623) particularly interesting is the idea that since most cognitive
resources are devoted to solving the complex problem(s) that triggered depression,
there are none left for other unrelated tasks. This would explain the poor results of
depressive individuals on laboratory tasks. Indeed, when distracted from thinking
about their problems, depressives’ performances on memory tasks or executive control
tasks are similar to non-depressives, whether or not they are otherwise impaired.
Contrary to what has been traditionally proposed on the basis of laboratory task results,
a depressive individual’s cognition is not dysfunctional. Rather, it is perfectly tailored
to solving a specific kind of problem. For instance, analyzing problems requires the
use of working memory (WM). Since depressive individuals consider their problems
to be serious, all resources should be devoted to these problems. Thus, irrelevant tasks
that would tap WM show poorer results. Yet these poorer results are not explained by
a dysfunctional WM, but rather by the fact that this structure has limited resources and
is impervious to disruptive conditions — in other words, it is “distraction resistant”
(this state may be achieved through attention control structures, as suggested by
increased activity in the left VLPFC in people suffering from depression).
So ARH makes four claims:
1. Complex problems (the primary evolutionarily relevant kinds being social) trig-
ger a depressed affect;
2. Depression coordinates changes in body and brain systems that promote sus-
tained analysis of the triggering problem;
3. Depressive rumination often helps people solve the triggering problem;
4. Depression reduces performance on laboratory tasks because depressive rumina-
tion takes up limited processing resources.
Let’s now turn to the motivational aspect of depression. We have previously seen
that authors such as Sloman, Gilbert and McGuire believe that the function of
depression is to send a “no threat” message to social dominants. The function of this
message is to reduce aggression towards the depressive individual. Andrews and
Thomson make a different claim; consistent with Hagen’s position, they claim that
depression is used as a means to gather social support either by honestly signalling
need11 or by motivating fitness extortion (by demonstrating that one is ready to inflict
11
In this framework, suicidality can be seen as adaptative: a way of signaling the seriousness of
intent, or the individuals’ level of need. As per Hagen: “Suicide threats are … threats to impose
substantial costs on group members and can be viewed as a means to signal cheaply and efficiently
to a large social group that it may suffer such costs if assistance or change is not forthcoming”
(2003, 112). Supporting the idea that suicidality is a form of gamble is the fact that most depres-
sives warn others about their intentions, and frequently choose methods known to be unreliable:
“Important for this hypothesis, most suicide attempts fail: globally, there are more than 14 attempts
for every completion; for young adult US women, there are more than 100 attempts” (Hagen 2011,
722). As the editors of this volume pointed out to me, psychiatrists typically distinguish two situa-
tions: suicidality with a warning to others about suicidal intentions; and suicidality without warn-
ing to others. The second kind of situations results in successful suicide more often then the first
80 L. Faucher
costs on themselves and others in order to gain additional support or a new social
role). A prediction that follows from this model is that depression should end when
support is gathered.12 It also predicts that depression should generate more support
from closer social partners than from distant ones, as one does not have the same
bargaining leverage with people for whom you are not a resource. Finally, because
of the two preceding predictions, it follows that depression should get more intense
when one is removed from one’s social milieu (for instance, by being hospitalized).
Since depression is conceived as an adaptation to solve a specific kind of prob-
lem, “… performance on the triggering problem [should be considered] as a crucial
metric for evaluating depressive cognition. … the conclusion that depression
impairs social skills depends on accepting the notion that some behaviors, such as
friendliness and cooperation, are always better for social problem solving, regard-
less of the situation or context. A more direct definition of social competence is
simply the ability to achieve social goals, especially in situations of social conflict.”
(Andrews and Thomson 2009, 637). In other words, what appear to be cognitive and
social malfunctions because of its disvalued effects might actually be a functional
way to achieve adaptative goals.
The previous theory has consequences for the way therapy should be conducted.
Firstly, therapies whose effects are longer lasting should be those that encourage
rumination and help to solve social dilemmas or stressful, complex problems.
Secondly – this being corollary to the first remark – trying to bypass rumination via
antidepressant medications (or otherwise) should not lead to long-lasting changes.
Thirdly, isolating an individual from their social milieu risks the exacerbation of
depressive symptoms.
Finally, in their paper, Andrews and Thomson do not provide an explanation of
depression’s prevalence, but in Watson and Andrews it is suggested that
[t]oday’s social environments differ from ancestral ones in ways that could affect the preva-
lence and intensity of depression. Modern social complexity and dynamism probably
increases the context for ruminative and motivational depression, because people face an
ever-changing array of fitness enhancing opportunities, but are blocked from or do not
understand how to access them. Moreover, people tend to have a greater number of positive
fitness partners in modern societies and this could increase the incidence of depression. At
the same time, these partners become more replaceable and so the average fitness interest
amongst them is lower. Reduced fitness interests amongst partners may increase the inten-
sity of depression needed to motivate partners to help (2002, 2).
So depression is not dysfunctional, but the actual prevalence of depression is

explained by the fact that we nowadays live in a more “depressogenic” environment
(once again, it is a mismatch environment case).13
kind. Hagen’s remarks are directed to the first kind of situations and he has nothing to say about
the second one.
12
“Recovery from depression is hastened by improvements in social relationships and strong social
support.” (Watson and Andrews 2002, 4).
13
Hagen explains the biased sex-ratio of depression through the fact that women more often
conflict with powerful others (2003, 115).
Remarks and Problems with Evolutionary Models

of Depression
In this section, I will comment on and formulate a few critiques about what has been
written thus far. Before going any further, a word about how one should evaluate an
evolutionary hypothesis. It seems to me that there are two constraints that such an
explanation needs to meet:
1. If one considers a known trait as an adaptation, an evolutionary explanation
should assess the central design features of that trait in light of its hypothesized
function(s). That is, one should try to explain the multiple features of a given
trait (at least its most central and costliest features) as complex and coordinated
ways of dealing with a (set of) specific challenge(s) faced by our ancestors in
their environment. If one can demonstrate that a trait has these complex and
coordinated features and that in virtue of having them it can provide a solution to
an adaptive problem this would be evidence (though a rather weak one) that one
has identified an adaptation.14
2. An evolutionary explanation should be consistent with knowledge in other disci-
plines (in our case, with knowledge in psychology, neuroscience, ethology, etc.).
That is, at minimum, it should not contradict established knowledge in other
disciplines (in the event that it does, it should demonstrate that what we believe
is firm and established knowledge is indeed false).
Now that we have set our constraints, let us see if the evolutionary models of
depression respect them; I will posit seven reasons why it might not.
1. The problem with the various etiological pathways leading to depression:
Kendler’s work (see Kendler et al. 2006) suggests that there are at least three major
pathways that lead to depression: internalizing symptoms, externalizing symptoms,
and adversity and interpersonal difficulty. Many of these pathways include events
that took place in childhood (sexual abuse, dysfunctional family, a depressed
mother, public humiliation, etc.).15 Moreover, in a recent paper, Kendler and his col-
leagues (2009) present studies on twin pairs of subjects who suffered from depres-
sion, and identified two genetic pathways to major depression: one pathway has
been identified among those subjects who had an early age onset of depression
14
It is with this constraint in mind that evolutionary psychiatrists make claims such as: depression
is “exquisitely designed” for a certain purpose (Sloman 2008, 221); or that certain results “ … sug-
gest that symptoms are a functional response to particular social problems” (my emphasis; Hagen
and Barrett 2007, 24); or that depression is an “orderly” syndrome (“there is a neurological order-
liness that appears to specifically and proficiently promote analysis in depressive rumination and
is not likely to have evolved by chance”; Andrews and Thomson 2009, 622). This ‘orderliness’ of
the syndrome is taken as evidence of special design (Andrews 2007, 49; see also Andrews and
Thomson 2010, 58; Durrant and Heig 2001, 362).
15
The mechanism through which depression is thought to develop in these cases is believed to
involve the “programming” of the responsiveness of the hypothalamic-pituitary-adrenal (HPA)
axis (see Hyman 2009; Krishnan and Nestler 2008; Pariante and Lightman 2008).
82 L. Faucher
(AAO) and one among individuals who had vascular disease (VD). The members of
the latter group have a late AAO, thought to be due to ischemic brain lesions.
Neither depression rooted in childhood events nor depression caused by vascular
disease (or for that matter, by other physical illness via the inflammatory effects of
cytokines on hippocampal cells) strongly supports the idea that depression is the
result of a mechanism in charge of disengagement, or that it is in charge of solving
complex social problems.
This is not much of a concern for Nesse, who admits that depression is not always
adaptative and that it takes many forms. The problem for Nesse is that if many or
most cases of depression are explained by either dysfunctional development envi-
ronments, or by cerebral accidents or infection, he still has to provide us with an
“evolutionary explanation of depression” (in other words, there would be a great
number of cases of depression that are not explained evolutionarily). As for Andrews
and Thomson’s theory, it does not fit well with that kind of data, since in these cases,
depression is apparently not an adaptation nor necessarily (or primarily) caused by
complex social problems.
2. The problem with proportionality and understandability: Nesse wants us to
consider as “normal” episodes of depression that are “proportional” to their trigger-
ing events (the same point is made by numerous people, among them, Horwitz and
Wakefield 2007). One obvious problem with proportionality is the fact that the
determination of what is proportional is rather subjective (it depends on a general
and non-scientific conception of human nature). That situation can be fixed by pro-
viding a detailed empirical (and maybe an evolutionary) theory of emotions which
would describe their normal range. For the moment, though, such a theory is lacking
and we are left without empirical grounds to make our judgments.
Moreover (and this is related the previous point, according to which some epi-
sodes of depression might have no external trigger), one should avoid committing
what some have called the “fallacy of misplaced empathy”, i.e. the “well-intentioned
clinicians [who are] missing the diagnosis of MDD because [they] can ‘understand’
that ‘anybody’ undergoing a serious life stressor – whether becoming disabled,
impoverished, terminally ill, humiliated, or bereaved – might be distraught and
upset” (Lamb et al. 2010, 20). Indeed, it does not follow that if one can understand
someone’s reaction to an event, that the reaction is not pathological (this can be
understood as a precautionary principle; it should not be understood as saying that
proportionality can or should not be used, but rather that one should be careful not
to apply it blindly16). As Maj also notes, a number of factors favor being mindful of
identifying “presumed” triggering events: for instance, “… the presence itself of a
16
Though I will not argue for this, I think that part of what lead to the elimination of the bereave-
ment exclusion clause is linked with the fear of false negatives (i.e. the fear of overlooking people
who are really suffering from major depression and who might need treatment or might commit
suicide). It is disputable that the elimination of the clause was really the solution to that problem
or even if there was a problem in the first place with the clause as such (by contrast as with the use
of the clause by psychiatrists; see on this Wakefield and First 2012; Wakefield and Schmitz 2014).
depressive state may affect the individual’s accuracy in reporting life events” (2012,
222). Finally, as it became clear in recent debate about the validity of the bereave-
ment exclusion for a diagnosis of major depression, patients with different levels of
psychosocial adversity experienced prior to the episode of depression do not differ
significantly on several variables (Lamb et al. 2010, 22; for critical comments on the
Lamb et al. paper, see Wakefield and First 2012), and their response to anti-
depressants is unrelated to the presence or absence of such an event (so much the
worse, then, for proportionality as an important factor to identify pathological
depression).
Where proportionality might not be a good indicator of depression, some have
argued that phenomenology might be a better indicator of differences in underlying
mental conditions (Maj 2012). It is believed that the phenomenology of “ordinary
sadness” and depression are quite different (Lamb et al. 2010; it seems that this was
recognized by the DSM in its bereavement exclusion clause which mentioned that
the sadness experienced after the death of a loved one does not have all the features
of major depression; for instance, it has no severe psychomotor retardation, no
morbid preoccupation with his or her worthlessness, no impairment in overall func-
tion, etc.). In ordinary sadness related to death, the emotional connection with sig-
nificant others is not severed as it is in depression; dysphoria is experienced in
waves rather than being omnipresent; self-esteem and personal potency are not
affected, etc.
One might argue that the distinctive phenomenological experiences of normal
sadness and depression are caused by different underlying neural mechanisms. If
such is the case, it is not at all clear that the two are related. In depression, motiva-
tional mechanisms might be impeded, where in normal sadness they are not – it is
just the case that one simply does not know what to do.
3. The problem with the idea that neuroscience neglects the role of life events:
Contrary to what Nesse says about neuroscience, it is untrue that “it neglects the role
of life events and other causal factors that interact with brain variation to cause most
depression” (2009, 22). True, neuroscientists have not been interested in providing
a precise description of the nature of events that trigger depression17 as they have
tried to provide an explanation in molecular and neural terms of “how adversity gets
under the skin” (to use the title of Steven Hyman’s 2009 paper). But, as epidemio-
logic studies have shown, genes alone are insufficient for depression, and environ-
ment in one form or another has to play a role (Caspi et al. 2003; Kendler et al. 2005;
Hariri et al. 2005).
Nesse is also wrong to suggest that adopting a brain perspective “encourages
studying major depression as if it is one condition with one etiology” (2009, 22). A
quick glance at the literature on depression in neuroscience provides reasons to
reject Nesse’s statement. For instance, one of the primary investigators in the
17
What counts as a stressors is often undefined, though not always, see, Hill et al. 2001; Goodman
et al. 2011.
84 L. Faucher
Research Domain Criteria of the NIMH, Bruce Cuthbert, says that “… the problem
with the DSM disorders is that they are very heterogeneous and may involve mul-
tiple brain systems.” (quoted by Miller 2010, 1437). Similarly, Krishnan and Nestler
conclude their review paper by stating “[…] researchers and clinicians must embrace
the polysyndromic nature of depression and use a multidisciplinary approach to
explore the neurobiological bases for depression’s many subtypes” (Krishnan and
Nestler 2008, 901). Lee and colleagues (2010) explain the absence of a simple rela-
tionship between biogenic amines and depression by saying that “… depression is a
group of disorders with several underlying pathologies” (1); while Lilienfeld
reminds neuroscientists that “they are not dealing with one disorder, but with mul-
tiple phenocopies that stem from diverse causes” (2007, 268). In light of this,
Nesse’s suggestion appears to mischaracterize neuroscientists’ attitudes toward
depression.
However, what Nesse is right about is that neuroscience does not typically con-
sider the possibility that people with genetic or brain variations might actually be
advantaged in certain environments – in other words, that variation itself might be
adaptative, or that it may reflect a frequence-dependent adaptation. Such a possibil-
ity is considered by Nettle (2004) who proposes that increasing neuroticism (a per-
sonality factor linked with increased chance of depression) might have been selected
for its beneficial effects. Nesse might also be right about the fact that the focus on
depression as a pathological state has taken attention away from studying the func-
tion of low mood (this is a sociological and historical claim that could be studied
empirically), and from considering some individuals who present behavioral or
physiological symptoms of depression as healthy.
4. The problem with the symptoms left unexplained: As mentioned at the begin-
ning of this section, one constraint that satisfying evolutionary explanations should
meet is that they should explain how a condition’s symptoms are responses to par-
ticular problems. It should not select only certain symptoms that it can explain well
and leave unexplained certain central symptoms of a condition. Unfortunately, this
is what happens in Nesse’s case.
Many symptoms of major depression are left unexplained by Nesse’s theory:
sexual dysfunction, physical pain, sleep issues, and increased suicide risk are hardly
addressed (Varga 2012, 49). Moreover, Nesse’s explanation of certain symptoms is
not at all obvious. For example, as Murphy (2006) remarks, why should the break-
down of the low mood mechanism generate loss of sleep or inability to make
decisions or concentrate? Further, why is the disengagement mechanism not accom-
panied by a positive affect or a motivational structure of some sort that would cause
behavior to change? This idea has precedent in the literature: for instance, animals
experiencing severe food restriction will increase – not decrease – their energy
expenditure and increase risk-taking behavior. In a recent paper, Nettle (2009) used
optimal-foraging models and suggested that Nesse is at least partially correct:
“when things are going quite badly, it is not time to take risks, but as things improve,
greater experimentation is warranted” (3). However, the models also predicts that
“… there comes a dire point beyond which it is maladaptative to avoid risks and
conserve energy: the situation is already too dangerous for that. Instead, the indi-
vidual should be highly motivated to take risks and try new solutions; to do anything
that has any chance of returning her to the acceptable range of states” (ibid., 3).
Nettle notes that this state might be found in patients classified as depressive because
of their negative affective tone, but whose symptoms include locomotor accelera-
tion and restlessness, and a feeling of speeding and a desire to follow risky, pleasur-
able impulses (perhaps thought of as a form of “dysphoric mania”). What Nettle
proposes is a further refinement of functional theories of the kind defended by
Nesse. According to Nettle, adaptative responses in the case of loss of resources
would be different as a function of the individual’s evaluation of the condition’s
severity. As he states, “[t]he mood responses to different types of situations will
show different suites of design features that represent adaptative strategies in that
context [...] Thus, a mood representing a response to dire circumstances could
involve simultaneous activation of negative emotion systems [...] and behavior
approach systems. Such a mood state would be like depression, in its negativity, but
also like positive mood, in its energy and risk-proneness”. (ibid., 4)
5. The problem with the lack of consistency with other findings from basic sci-
ences: Andrews and Thomson’s theory fares better in terms of the first constraint
because it tries to incorporate all features associated with depression and explain
that they are part of coordinated responses to a specific kind of problem.18 Their
notion that features of rumination might be adaptive, and their notion that cognitive
resource allocation to social problems might impede non-relevant laboratory tasks
are both worth exploring. Yet Andrews and Thomson don’t fare as well with the
second constraint.
Firstly, it is unclear that the rumination of depressive individuals targets the reso-
lution of a problem. Repeatedly thinking: “I am worthless”, “I am a failure”,
“nobody really likes me”, etc. hardly seems like problem-solving. Moreover, stud-
ies on depressive subjects show that “rumination prompts them to appraise their
problems as overwhelming and unsolvable and to fail to come up with effective
problem solutions” (Nolen-Hoeksema et al. 2008, 400–1). Secondly, rumination is
thought to help solve the problems that triggered the depressive episode, but, as
Varga (2012) points out, there is not much support for this notion. Instead, the evi-
dence points to the idea that rumination enhances the effects of depressed mood on
thinking. Indeed, Andrews and Thomson’s support for their idea comes from a
study from Hayes and colleagues (2005) which, as Varga observes, concludes some-
thing different, which is that the “important tasks in treating depression are to reduce
patterns of avoidance and rumination and to facilitate processing” (my emphasis;
112, quoted by Varga 2012, 49). Thirdly, Andrews and Thomson also argue that the
depressed have cognitive features that facilitate the resolution of social problems.
However, it is not at all obvious that more rapid or more rational (from a game-
theoretical perspective) solutions to social dilemma help to resolve social problems,
rather than generating more of them. Moreover, as Nettle (2004) points out, the
18
Though I have not presented it in section “Andrews and Thomson: Rumination and motivation”,
their theory also explains why (and predicts in which situations, see 2009, 645) people will attempt
to escape pain generated by depression or try to commit suicide, for example.
86 L. Faucher
depressed also have cognitive features that might handicap them in this task: they
are slower and less accurate than control subjects at reading non-verbal social cues;
they show impaired social skills; they seem more realistic than others only when the
normal population is unrealistically positive (and depressive individuals are unreal-
istic when the normal population is reasonably accurate) and “… depressives per-
form worse than controls on tasks designed to tap inter-personal problem solving
skills” (96).19 Finally, it is not at all clear that rumination enables individuals to
escape their condition, or that it helps them gather social support. In regards to the
former, Varga notes: “Because the ruminating person will be focused on her depres-
sive symptoms, which typically involves negative self-ascriptions, the conclusion
will often be that he/she lacks the capacity to engage in constructive activities.
Ruminating depressives will lack confidence in their solutions that might be the
reason why they often do not pursue them … Studies reveal that even if the rumina-
tor acknowledges that a certain activity would have an effect, they have trouble in
motivating themselves to actually engage in these activities” (2012, 49).20 With
regard to the latter, if it is true that ruminators are more likely to look for social
support and sometimes receive it, they also are more prone to aggressive behavior
and are often criticized for their inability to cope, as others become frustrated with
their continued need to discuss their loss or problems (Nolen-Hoeksema et al. 2008,
403 and 408; see also Coyne 1976).
Another issue with Andrews and Thomson’s proposal is that they assume that
depression triggers are social or predominantly social in nature. Here, one wonders
about the direction of causality: is depression caused by social problems or are
social problems caused by depression? Depression can cause marital problems, lack
of social support, or the defection of social partners – all of which are also identified
as factors in depression. And if depression is caused by social problems, does it
allow people suffering from it to acquire more support or new deals with coopera-
tive partners? Hagen has provided data for PPD, but no such data are available for
depression in general.
Moreover, if depression is adaptative and is designed to solve social problems,
why is it that Keller et al. (1992) found 70 % of those who suffer major depression
will have at least one other episode and 20 % will develop it as a chronic condition
(rate of continuous freedom from illness is very low – 11 % over 25 years; Nettle
2004, 95)? What these numbers suggest is, as Murphy notes, “if depression is an
adaptation designed to make them [the depressive] function better in society, it is
not working” (295). Indeed, once depression has achieved its function, should it not
19
As Allen and Badcock observe: “… although some recent studies have shown that mild depressed
states facilitate both social reasoning and performance on theory of mind tasks, other studies using
the same assessment procedures have found that in clinical populations, these advantages are
absent or even reversed” (2006, 822).
20
As Nolen-Hoeksema and colleagues note “… rumination leads people to see obstacles to the
implementation of solutions, to be less willing to commit to implementing the solutions they gen-
erate, and to be more likely to disengage from real-life problems than to continue trying to solve
them ” (2008, 408).
disappear? Why, then, does it become chronic in 20 % of cases?21 If one accepts

Andrews and Thomson’s theory, this means that for some individuals, having an
episode of depression makes them more likely to reencounter a similar kind of prob-
lem – this is hardly progress!22
One last problem with their account is, as Nettle points out, if “all normal human
beings have the capacity to feel physical pain … there is no evidence that all indi-
viduals have the capacity to become clinically depressed. Rather, it seems likely that
most depression is the result of an inherited diathesis borne by a minority of the
population” (2004, 93). Indeed, according to him, there is no support for the idea
that depression is a universal adaptation.23
6. The problem of comorbidity: It is widely known that there is an important
comorbidity between anxiety and depression. For instance, among patients in the
general population who meet criteria for major depression, approximately 50 %
also suffer from anxiety disorder (Hirschfeld 2001; Sandi and Richter-Levin
2009). An evolutionary explanation of depression should be able to explain why
this is the case. Nesse (2009) explains this by positing that the problems that trig-
ger depression sometimes also demand greater vigilance, thus also triggers threat
systems. The question then becomes “Why do these two systems break down, and
why do they so often break down together?” Nesse has no response to this
question. Likewise, Andrews and Thomson do not provide an explanation of the
21
Worse, as Nettle (2004) and Nesse (2000) observe, as depressive episodes continue (for third and
subsequent episodes of endogeneous depression), the triggers required to produce depression
become smaller and less related to life events.
22
As an editor of this volume observed, “design does not imply success”: for instance, the evolu-
tionary function of spermatozoids is to fertilized egg cells, even if most of them will never achieved
this feat. There are two problems with this remark in the context of the discussion of Andrews and
Thomson’s theory. First, remember that they claim that “performance on the triggering problem
[should be considered] as a crucial metric for evaluating depressive cognition” (2009, 637). If most
depressions fail to solve triggering problems and are followed by other episodes of depression,
then depressive cognition does not seem to be very efficient at this task. Second, if most cases of
depression are not adaptive (that is, they failed to provide a solution to the problem that triggered
them), the usefulness of an evolutionary theory of depression for psychiatry is questionable. We
are left with people who suffer, who have problems that they cannot solve themselves: knowing
that their problems are the result of an evolutionary mechanism which failed to accomplish its
function is not of a great practical help. As to recurrence, it is possible that the initial loss that
provoked the depression is typically followed later by other losses. The problem would be with the
life of the depressives, not with the depressives themselves. I do not want to deny this possibility,
but it seems to me that more empirical works need to be done on this: first, to substantiate the
claim; and second, to show that these losses are not caused by the very mechanism that is supposed
to fix the situation, i.e. depression.
23
This last point has been contested lately. Some authors (Moffit et al. 2010; Rohde et al. 2013)
have been arguing that the low rate of depression found in epidemiological survey is an artifact of
the retrospective method used in those surveys (in which respondents are asked to retrospect over
the past years to recall episode of depression). The use of a prospective method (basically, longitu-
dinal studies) gives much higher rates of depression in the general population (with rates of 40–50
% of the sample having had an experience of depression compared to 12–17 % with retrospective
studies).
88 L. Faucher
comorbidity of anxiety and depression, nor for that matter, of the comorbidity of
depression and hypomania.
Neuroscience seems better equipped to explain such comorbidity. According to
Sandi and Richter-Levin (2009), there is good reason to think that high-anxiety
traits (or neuroticism) play a crucial role in explanation of depression. In their
paper, they describe “the dysfunctional neurocognitive cascade” that leads indi-
viduals with hyperactive amygdala to develop depression. A hyper-reactivity of the
amygdala, coupled with impaired prefrontal cortex ability to control the activation
of the amygdala, makes individuals more prone to experience fear and stress. This
leads to an enhanced activation of the HPA axis, which is known to increase the
activation of neurons in the basolateral amygdala, which activate the production
and release of CRF (corticotropin-releasing factor) in the central nucleus of the
amygdala and prefrontal cortex. Higher activity of the amygdala combined with
phasic release of CRF produce emotional potentiation for memory (“increased
storage of both fear association and of negative emotional episodic memory”
(2009, 316) and impair memory retrieval and working memory. The resulting sys-
tem is, as Sandi and Richter-Levin put it, a “sensitized systems” with an exagger-
ated focus on the negative side of events. Confrontation with stressful events will
increase amygdala and HPA axis activation, which translates into greater attention
to negative events, and recall of negative memory. It will also translate into further
dysfunction (and structural changes) to the hippocampus and prefrontal cortex,
which will render individuals ineffective at certain cognitive tasks, which in turn
will increase their feelings of hopelessness. Thus here, one is tempted to say that,
contrary to Nesse’s claim, “evolutionary theory is not enough, neuroscience is
essential”.
7. The problem with the interpretation of treatment efficacy: The last point is
related to the previous two points, and relates to the remission of symptoms. In his
“Reconstructing the Evolution of the Mind is Depressingly Difficult”, Andrews
claims that one way to identify the problems that depression has evolved to solve is
by assessing treatment efficacy. As he puts it: “Although antidepressants alleviate
acute depression, they do not prevent relapse, whereas talking therapies do.
Moreover, talking therapies that attempt to address social problems [...] are often the
most effective. Because treating the cause should be more effective than treating the
symptom, the fact that social interventions are better than medications at preventing
relapse suggests that the cause of depression resides more in the social environment
than in a malfunctioning nervous system” (2007, 49). As was shown earlier, one
consequence of Andrews and Thompson’s theory is that only therapies encouraging
rumination should have long-lasting effects.
There are many problems with this view, of which I will only address two. As
was emphasized by Adolph Grünbaum (1984), the success of a therapy does not
constitute proof of truth of the principles it postulates as causally efficacious. Anti-
depressants might not be a very effective cure for depression (Andrews et al. 2011),
or they may even be harmful (Andrews et al. 2012), but because some kind of cure
is working does not mean that it works as a result of its having identified the true
causes of depression. However, for our present purposes, let’s pretend it does. Let’s
pretend that the causes of depression are indeed social, and that we have to treat
them in order to get better. Even if such is the case, it is not clear that therapies per-
mitting rumination would work better than others that do not. Nolen-Hoeksema and
her colleagues argue that
Inducing dysphoric or depressed participants to distract from their moods and ruminations
for just 8 min leads them to generate solutions to problems that are just as effective as non-
depressed participants’ solutions and significantly more effective than those generated by
dysphoric participants induced to ruminate. The short distraction induction also leads dys-
phoric and depressed participants to express more control and self-efficacy, to appraise the
causes of problems more optimistically, and to have more confidence in their ability to
overcome their problems than do dysphoric people induced to ruminate [...] These results
suggest that attempts to resolve self-discrepancies will be more successful and less likely to
devolve into persevarations about problems if individuals are either in a neutral or positive
mood or if they first use neutral or positive distractions to lift their moods and interrupt
ongoing rumination (Nolen-Hoeksema et al. 2008, 415).
This brings me to the second problem, which is related to the first. Contrary to
depression therapies based on content (for instance, Beck’s cognitive therapy or
CT24), Bar (2009) proposes a “content-less” therapy. Like Andrews and Thomson,
he focuses on one symptomatic characteristic of depressive individuals, their ten-
dency for rumination. For Bar, rumination implicates the fact that thinking revolves
around the same negative ideas. Rumination can be opposed to broad associative
thinking, i.e. thinking which involves thought processes that advance smoothly
from one context to the other. Bar’s rather bold hypothesis rests on the observation
that positive mood promotes associative thinking (an idea developed and explored
by Isen et al., 1985), and inversely, that associative thinking promotes positive
mood. Observing that the contextual associations network in the brain functions
abnormally in depressive subjects, and that chemical and electrical stimulation ther-
apies work on parts of the contextual associative network, Bar suggests that rumina-
tion might be caused by over-inhibition of MTL (medial temporal lobe) by MPFC
(medial prefrontal cortex) and neighboring anterior cingulated cortex. Given the
link between association and positive mood, Bar then proposes that therapies should
promote the “acquisition of mental habits of broad associative activation and a
cognitive-driven reconstruction of the underlying cortical network” (2009, 460).
This is how Hayes et al. are interpreting the success of their writing therapy: it
works by avoiding patterns of rumination and facilitates processing.
If Andrews and Thomson’s theory is right, this would suggest that Bar’s propos-
als about using associations to create good mood would produce long-term detri-
24
Beck’s CT is “… a structured, skill-based psychotherapy that focuses on modifying the faulty
thoughts, evaluations, attributions, beliefs and processing biases that characterized anxiety and
depression. It is assumed that CT results in significant reduction of symptoms by weakening or
deactivating disorder-related maladaptative schemas and strengthening alternative, more positive
modes of thinking. Patients are taught to identify their maladaptative thinking, evaluate its accu-
racy, generate more adaptative and realistic perspectives and test-out the utility of their new per-
spective through structured behavioural homework assignments” (Clark and Beck 2009, 420).
Note that this kind of therapy, which is known to be quite successful, seems to be focused on get-
ting rid of the cognitive features that are deemed to be essential by Andrews and Thomson to solve
the depressives’ problems.
90 L. Faucher
mental effects and would likely create further depressive states. The latter requires
testing. For the moment, Bar’s explanation is more consistent with the reason why
deep electric stimulation and other means to cure depression are working.
Conclusion
My conclusion is concise: this paper examined two recent proposals from leading
evolutionary psychiatrists concerning depression. I have shown that these proposals
have different, important problems: they either leave aside (unexplained) certain
central and costly traits of depression, or they are inconsistent with current estab-
lished knowledge about depression. As such, one should not forget the status of
these proposals – they are speculations. For this reason, one should not base actions
(for instance, therapy) on them yet (which is not to say that we should reject all
evolutionary explanations of depression. I have been pointing to the weaknesses of
current evolutionary explanations of depression; I did not formulate an overall argu-
ment against them!).
I opened this paper by rehashing evolutionary psychiatrists’ positions concern-
ing the potential role of evolutionary considerations in psychiatry. It is clear that at
this time (and for years to come), the momentum of depression research comes from
genetics, genomics, or the brain sciences. This is clearly where institutions such as
the NIMH are putting their money, with projects like RDoC initiative (for a descrip-
tion and criticism of that very project, see Faucher and Goyer 2015). Even if I have
been very critical of evolutionary approaches to different mental disorders and to
psychiatry in general (see for instance, Faucher 2012; Faucher and Blanchette
2011), I do not think it should be completely ignored either – even if it might not
deserve the status of “basic science” for psychiatry that Nesse advocates. At pres-
ent, evolutionary psychiatrists can’t offer well-confirmed theories; they might never
be able to produce such theories. Yet, their proposals can play a heuristic function
by changing the focus of current brain sciences, and questioning traditional posi-
tions in this field (for instance, trying to explain the depression epidemic by the fact
that current diagnostic criteria capture natural reactions to losses). If only for those
reasons, we should keep an attentive – yet critical – ear to what evolutionary
psychiatrists have to say.
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Is an Anatomy of Melancholia Possible? Brain
Processes, Depression, and Mood Regulation
Denis Forest
Abstract Neurobiological models of depression aim to explain its conditions

through a description of the underlying neurocircuitry. The present paper analyses
the skeptical doubts that may be raised in response to neurobiological accounts of
depression and the conditions under which these models may shed some light on the
corresponding phenomena. Far from excluding other kinds of enquiries, neurobio-
logical models may greatly benefit from a philosophical enquiry on our affective
life, and especially from closer attention paid to ill-defined phenomena like moods.
I suggest that what is crucial to depression is defective affective regulation, and that
it is with this perspective that we may make sense of neurophysiological data.
Introduction
The central problem of a philosophy of psychiatry today is not difficult to grasp:

everything is plausible and you can argue in favor of almost anything. What I mean
is that there is no conception of mental disorders that cannot be defended. The risk,
then, is that any attempt to argue in favor of a thesis may lead us in a circle: first, you
pick up your favorite view of the world; then, you spend enough time to find in the
available literature innumerable reasons to believe it is true; lastly, you are even
more convinced that your first intuitions were sound.
Take, for instance, depression. If you favor naturalism, you will find what you are
looking for in the expanding body of discoveries concerning the neural correlates of
depressive states (Drevets 1998; Fitzgerald et al. 2008), in the development of ani-
mal models of mood disorders (Overstreet 2012), and in a wide range of specula-
I would like to thank Jerome Wakefield and Steeves Demazeux for their feedback on the draft of
this paper, Samuel Lepine for his comments on an earlier version, and Larry Dewaële for his care-
ful reading of the final version.
D. Forest (*)
Department of Philosophy, Université Paris Ouest Nanterre, Nanterre, France
Institute d’Histoire et de Philosophie des sciences et des techniques, Paris, France

DOI 10.1007/978-94-017-7423-9_7
96 D. Forest
tions about the evolutionary history of affective mechanisms (Nettle 2004). You will
end up with the very biological view of depression that was your starting point.
However, the philosopher who has little sympathy for a naturalistic ontology, or for
evolutionary explanations of our mental features, will remain remarkably unim-
pressed. Thinking that depressive states are the states of the mind of a person, and
not of his or her brain, he has at his disposal causal models of depression as they
have been formulated by sociologists (Brown and Harris 1978), ethnographic enqui-
ries offering evidence that culture and context matter in the development and symp-
tomatology of mental disorders in general (Kleinman 1988) and of depression in
particular (Kleinman 1986; Kitanaka 2011, 2016), and analysis of the consequences
of a shift from a professional culture of responsibility to a culture of initiative and
performance (Ehrenberg 2009, 2016). If he has a constructivist or a Foucauldian
turn of mind, and if he is ready to challenge psychiatry as a form of so-called “bio-
power” and as an agent of normalization of conducts, the philosopher also may also
take advantage of the growing literature about what is now called the medicalization
of ordinary life (Conrad 2007), a chief example of which is the unmotivated diagno-
sis of depression (Horwitz and Wakefield 2007). All of this may lead to endless
clashes, to a pessimistic, Weberian view of the disunity of knowledge, where differ-
ences of methodology and perspective lead to attitudes that cannot be reconciled. It
may result in awkward attempts of reconciliation, or more radically, in a robust form
of skepticism for which no treatment is currently available.
In the present article, I shall review first the reasons why a neuroscientific
approach of depression may be judged unsatisfactory and then consider how we
could defend it. What I call a neuroscientific approach is a view in which depression
is seen as an impairment of the joint activity of crucial brain regions, as the product
of a “depressive neural network”. This view can be understood as a development of
the neuroscientific tradition of symptom localization (Mayberg 2009) and of the
mechanistic decomposition of the mind-brain in key processes and components
(Bechtel and Richardson 2010). It is worth noting that this view may be challenged
on grounds other than an anti-naturalistic stance: in particular, the idea that some
kind of chemical imbalance is the origin of depression (for an historical perspective:
see Healy 1997, Chapter 5) may suit advocates of reductionism (Bickle 2003),
according to whom we should focus directly on the lower-level components and
activities that are studied by molecular neuroscience, such as serotonin reuptake.
But even if we leave aside theoretical alternatives to a reductionist view of explana-
tion in neuroscience (Craver 2007), it is striking that progress in antidepressant
pharmacological treatment is often judged “limited” (Holtzheimer and Mayberg
2011). Moreover, depressive relapse following the end of such treatment along with
the high number of patients who do not respond to antidepressant drugs remain
major medical problems. In this context, it is no coincidence that new neurobiologi-
cal models of depression with innovative therapeutic implications are proposed
(Mayberg 1997; Drevets et al. 2008) and updated (Mayberg 2009). My own view
will be, first, that these recent circuit models of depression are not idle theoretical
constructs, but that their significance depends ultimately on a correct understanding
of what corresponding physiological mechanisms are for. Second, I shall argue that
Is an Anatomy of Melancholia Possible? Brain Processes, Depression, and Mood… 97
to develop a neurobiology of depression, a prior analysis of mood and affective

states may be useful where we try to identify which questions are worth asking.
Consequently, I suggest that philosophy of psychiatry and philosophy of mind
become closely related.
The title of this paper is intended as a reference to the 1621 classic work by
Burton, The Anatomy of melancholy (Burton 1621), but also to the title of the pio-
neering PET scan study of Bench and colleagues “The anatomy of melancholia:
focal abnormalities of cerebral blood flow in major depression” (Bench et al. 1992)
and to the subtitle of an article by Wayne C. Drevets, who has made a significant
contribution to the development of fMRI studies of depression: “Functional
Neuroimaging studies of depression: the anatomy of melancholia” (Drevets 1998).
Melancholia is here seen as the affective side of depressive disorders in general, not
as a distinct clinical entity. The debate about whether or not we should consider
melancholia (or ‘endogenous depression’) as a mood disorder distinct from major
depression has not been settled yet and has even become more intense during the
preparation of the DSM-5 (Parker et al. 2010; Healy 2013). The present paper does
not take sides in this controversy. The key issue here is not classification based on
clinical and biological features. It is how (and under which conditions) neurosci-
ence fits in the broad explanatory project of psychiatry. In this case, the target of the
explanation is the pattern of recurrent, harmful disturbances of affective life that is
typically shared by depressive disorders.
Depression and the Brain: The Skeptical View
There are at least three kinds of reasons why findings about the brains of patients
suffering from depression could be welcomed with caution. The first kind has to do
with the central role of neuroimaging methods in investigations that focus on the
depressive brain (Gotlib and Hamilton 2008). The conclusions of these investiga-
tions have suggested crucial roles for structures like the amygdala, parts of the ante-
rior cingulate cortex and dorsolateral prefrontal cortex. Meanwhile, working models
like the model of limbic-cortical dysregulation (Mayberg 1997), where increased
subgenual cingulate activity and decreased dorsolateral prefrontal activity are cor-
related, have been proposed. We could, for one, remain skeptical about the signifi-
cance of neuroimaging studies of depression, as they have been conducted since the
1990s, on general methodological grounds. As they reveal differences in regional
blood flow related to neural activity, and not neural activity itself, it may be that
imaging techniques do not provide us with a picture of regional brain activity as
accurate as it is supposed to be. Stressing that this point does not imply, in itself, that
depression has no biological dimension, or that research about brain states in the
context of depression, is by itself misguided. Pointing out that we don’t know
enough about x because of the intrinsic limitations of a given technique (which is
supposed to give us access to x) is not claiming that x does not exist or that x has no
intrinsic significance. But it is clear that there is an ongoing debate about brain
98 D. Forest
imaging techniques (Logothetis 2008; Roskies 2008; Forest 2014). In principle, one
may believe that depression has a biological nature and hold, however, that to get a
picture of a given pattern of regional blood flow is far from enough to understand
the corresponding brain activity (Hardcastle and Stewart 2002). Secondly, we can
also doubt that images of the brain are by themselves revelatory in the context of
depression because of the ambiguous relation between what is shown by a given
picture of the brain and the corresponding depressive state. According to Kessler
and his colleagues (Kessler et al. 2011), images do reveal differences between the
brain of patients suffering from depression and the brain of control subjects, but the
special features of the depressed brain may be understood (a) as neural predisposi-
tions (non sufficient conditions), (b) as genuine etiological factors, (c) as mere con-
sequences of episodes of depression, or (d) as compensatory brain mechanisms.
Reduction of hippocampal volume, for instance, may be a consequence of depres-
sion, and decreased amygdala-frontal connectivity, a factor of susceptibility. As a
consequence, it is not impossible that explanatory models of depression based on
fMRI studies often count as genuine etiological factors that should be considered as
predispositions, mere consequences of depression or byproducts of the disorder
with or without a compensatory role. Accordingly, it is plausible that many neural
correlates of depression have no explanatory relevance (Craver 2007) because they
have no causal role in the production of a given psychological or behavioral feature
of depression. It is legitimate to question our current ability to disentangle these
different factors.
The second kind of reason has to do with the relation between psychological and
neurobiological levels of analysis. In standard medical practice, the presence of
depression is defined by diagnostic criteria, and it may be tempting to think that we
could substitute a brain-based approach for this symptom-based approach. If depres-
sion is a well-defined medical category, and if neuroscience is able to identify the
neural signature of depression (or what the philosopher Robert C. Roberts would
call its “neurological map”), one can think that brain research will be able to address
two key issues: knowing what depression is, and knowing who is (really) depressed.
Knowledge of deep neurobiological causes would supersede knowledge of mere
psychological epiphenomena. But this is also dubious. The first observation we
could make is that neurobiological mechanisms involved in depression may be
mechanisms that are not unique to it; as a consequence, a different basis for diagno-
sis does not mean that we shall be on firmer ground when we speak of depression,
but rather that we may adopt a revisionary attitude where the very existence of
depression as a legitimate medical entity would be challenged. A new entity would
be, for instance, disorders of the neurobiological system that has the function to
mediate and regulate negative affects. As parts of the medial prefrontal cortex are
components of such a system, and as the altered functioning of these parts has been
implicated both in depression (Drevets 2000) and post-traumatic stress disorder
(Shin et al. 2005), we would have reason to revise or eliminate usual diagnostic
categories, rather than reason to give them a neurobiological basis (Meier, in
Forgeard et al. 2011). What should be noted, however, is that in this case, nothing
tells us that it will be easier to agree on “natural” categories if we try to define them
in terms of neurobiological systems rather than constellations of symptoms: because

of the many causal roles that may be ascribed to the same brain regions, because of
ubiquitous mutual and reentrant connections in the brain, because of the many cri-
teria we could use to define a given neural system, because of the lack of correspon-
dence of such systems with traditional, gross anatomical divisions, we could end up
with as many disputes about the boundaries of a given system (and its pathologies)
as about our current clinical entities.
The second observation we could make is that, whether or not the neurobiologi-
cal enquiry takes this dramatic, revisionary turn, it could be that there is no neuro-
biological knowledge of depression that is not only related to, but also dependent
on, clinical knowledge and psychological analysis. According to Robert C. Roberts
(Roberts 2003), the neurological analysis of emotions is to its conceptual analysis
what a physical analysis of sound patterns are to the corresponding musical analysis
of a work of music. Just as it is only if he has some kind of understanding of musical
concepts that an expert acoustician will be able to make sense of a physical account
of a symphonic piece, it is only because he has an understanding of the psychologi-
cal significance of given neural events that a neuroscientist will be able to make
sense of his discoveries about, for instance, the amygdala. One description is no
substitute for the other, and that would hold for brain knowledge of mood disorders
as well. The psychological lexicon of ordinary descriptions of negative moods, as
well as familiar, narrative explanations of why they occur would be ineliminable:
they would possess, in particular, both the relevant conceptual framework and the
appropriate level of generality.
The third source of reservation about the alleged benefits of the ongoing neuro-
biological enquiry would come from the problem of the boundaries of depression.
Heated recent debates about false positives due to over-inclusive diagnostic criteria,
and about the potential consequences of the removal of the bereavement exclusion
clause in the DSM-5 (Wakefield and First 2012), are testimony enough that this is
not a purely academic and theoretical debate. In their influential book, Horwitz and
Wakefield have argued that symptomatology alone is unable to distinguish between
normal sadness as it is motivated by a loss and depression as a mental disorder
(Horwitz and Wakefield 2007). It is very doubtful, with the current state of our
knowledge of the depressive brain, that pointing to intrinsic neurobiological differ-
ences is in itself sufficient to settle the issue. As it is plausible that brain correlates
of sadness and brain correlates of depression will have much in common (for the
corresponding evidence, see Mayberg et al. 1999), we may have to deal with two
kinds of undesirable but plausible cases. First, if some pattern, which we will refer
to as P1, is understood as suggesting depression, then some may argue that P1
includes only non-essential differences from normal brain functioning. Second, if
another pattern, P2, is understood as suggesting normal sadness, it is also possible
that others will claim that it is only because, for instance, the level of activation in
key region R that is considered sufficient to reveal some dysregulation is far too
high; the consequence being that P2 is in fact the sign of a marked disruption of
affective brain systems that remains ignored because of a flawed interpretation of
data. Brain science, then, if symptomatology is ambiguous, may fail to effectively
100 D. Forest
solve the demarcation problem. In these dubious cases, even equipped with the
most-advanced technology, we would be back to the solution of Horwitz and
Wakefield: only the context of the emergence of symptoms, and how they evolve
with time, will allow us to make a well-motivated distinction between normal sad-
ness and depression.
Beyond Mere Correlates
Confronted with the results of fMRI studies of depression, the skeptic is ready to
point out (a) that there is only a “limited overlap” between regions that have been
identified by different neuroimaging studies of depression (Fitzgerald et al. 2008),
and (b) that the status of these alleged “neural correlates” of the disorder remains
ambiguous. However, differences in experimental techniques and populations of
patients may explain why only a few regions are consistently identified by different
types of studies. Second, conclusions of such studies should not be considered apart
from evidence coming from other kinds of research. Moreover, it would be unfair to
judge the evidential base of brain-working models of depression on the conclusions
of PET and fMRI studies alone. Let’s consider, for instance, reports made about the
consequences of brain lesions. Neuroimaging studies have suggested that abnormal
patterns of activation of parts of the prefrontal cortex (PFC) play a role in the patho-
genesis of depression. To support the view that ventromedial PFC hyperactivity and
dorsolateral PFC hypoactivity do play such a role, it is possible to consider the con-
sequences of strokes and injuries that impair the functioning of these regions. A
study by Koenigs and colleagues (Koenigs 2008) suggests that bilateral lesions in the
dorsolateral PFC cortex confer increased vulnerability to depression, while bilateral
lesions in the ventromedial PFC are associated with low levels of depression. Even if
inferences from local lesions to functional specialization are always dubious because
of the complexity of the functional architecture of the brain (Sporns et al. 2000), this
kind of study adds support to causal interpretations of fMRI results, if we adopt a
view of causal relations where A is causally related to B if and only if an intervention
on A modifies B (Woodward 2003). Local lesions play the role of “natural interven-
tions” and even if we take into account possible side effects of focal lesions, it is
reasonable to think that this kind of study may help disambiguate fMRI results.
Even more interesting are the reasons offered by Mayberg (Mayberg 2009) to
ascribe a critical role to a specific brain component, the subcallosal cingulate gyrus
(SCC, Brodmann area 25, with parts of areas 24 and 32) in the complex neural net-
work involved in depression.
1. SCC activity has been repeatedly observed as a correlate of acute negative affec-
tive states;
2. SCC is one of the regions where metabolic effects can be identified in a context
of clinical improvement due to antidepressant treatment, while hyperactivity in
SCC is characteristic of treatment-resistant patients;
3. Cellular abnormalities have been observed in the subgenual region in patients

suffering from mood disorders: in particular, a reduced number of glial cells,
which are cells that play a crucial role in physiological processes essential to
normal neural activity (Ongür et al. 1998);
4. There are efferent and afferent connexions of the SCC with regions like the
insula, brainstem and hypothalamus, suggesting a regulatory role for SCC in
physiological activities responsible for circadian rhythm and appetite;
5. Deep brain stimulation targeting directly the SCC has yielded marked effects, in
contrast with regions that are anatomically close to it.
Ascribing a crucial role to the SCC region in an extended neural network, then,
is trying to make sense of a large body of data, as much as it is a part of a therapeutic
strategy. Making sense of a large body of data aims in particular at finding a solution
to the problem of the co-occurrence of apparently unrelated symptoms. This is an
intended, general benefit of working models: for instance, on the one hand, the
association between sad moods and impaired attention is well documented in the
clinical literature; on the other hand, the increased activity in depression of the sub-
genual cingulate region, characteristic of the experience of sadness, seems to deac-
tivate regions known for their involvement in attentional processes (Mayberg et al.
1999). A functional model, then, has two closely related motivations: explaining
why we have a given clinical profile, and making sense of the corresponding pattern
of brain activation.
In a sense, a “circuit model” of depression is parasitic on a model of correspond-
ing physiological functioning, as, for instance, it is only because SCC is connected
to regions already known for their involvement in mood monitoring and mood regu-
lation that we can expect, or understand why, its stimulation may have distinctive
effects in these domains. But as it is in the context of research on depression that the
physiological meaning of the SCC region begins to be understood, models of
depression, in turn, help us to update and complete the description of mechanisms
involved in the genesis and regulation of affective states. Accordingly, in agreement
with what has been suggested by Moghaddam-Taaheri through her “broken-normal
view” (Moghaddam-Taaheri 2011), progress in our understanding of pathological
mechanisms of depression and of affective mechanisms are tightly linked. And to
use a notion introduced by Kitcher (Kitcher 2003), as the research is moved by both
epistemic and practical interests, the discovery of the role of the SCC region gets its
“scientific significance” from both kinds of context.
On Moods and Mood Regulation
Problems of the second and the third kind listed above (the relation between symp-
toms and brain mechanisms, the role of brain knowledge in the definition of the
disorder) are probably deeper and more specific to depression research. The second
suggestion I want to make is that recognizing the importance of the neuroscientific
102 D. Forest
view of depression does not preclude that we need not only a psychological
investigation, but also a prior conceptual analysis of affective states. I would even
suggest that it is only if we have a better understanding of what affective states are
that we can hope to shed some light on neural mechanisms that play a role in depres-
sion, and on the proper domain of affective disorders.
Oddly, philosophy of psychiatry is often divorced from the literature in philoso-
phy of mind and moral philosophy about emotional states. However, it seems diffi-
cult to consider “emotion”, “sadness”, or “depression” as unproblematic terms
associated with notions that would not be worth enquiring about. For instance, cen-
tral to Horwitz and Wakelfield’s view of depression is a certain idea of what sadness
is as an emotion. The depressed individual would be depressed because what he
experiences is similar to a normal (or proportionate) response to circumstances that
usually yield sadness and grief, although his experience is due to the internal failure
of the corresponding affective mechanisms. In this case, being authentically sad is
being in a state (a) that has the appropriate relation to circumstances that justify it
(the individual has reasons to be sad); (b) that is the product of affective mecha-
nisms that have the function to detect negative events and to adjust one’s emotional
response to them. The understanding of depression, then, is subordinate to an under-
standing of emotional life.1 But we should note several things. First, depression is
usually considered a mood disorder, rather than an emotional disorder. When a
Capgras patient is not emotionally aroused by the presence of a person he is close
to, one can think that there is some kind of underlying disturbance of emotional
mechanisms: the symptoms have to do with the appraisal of a given, specific situa-
tion, while depression has an intrinsic dimension of generality. Moreover, direct
lesions to brain parts that are essential to emotional mechanisms do not typically
lead to depressive states (Mayberg 2003). Perhaps, then, sadness and emotional
responses to specific events are not the most appropriate starting point when we
consider depression as affective state, whereof we would like to give a proper and
independent description.
Second, philosophers have made efforts to distinguish moods from emotions by
using criteria that are less trivial and vague than duration. One of them is that emo-
tions have a given intentional dimension, a proper object, while the same is not
obviously true or paradigmatically true of moods. This has led to several sugges-
tions: moods are objectless, they are identified by the way we feel, not by reference
to a specific object or collection of objects (Armon-Jones 1991); moods are there to
tell us about our situation in general, rather than to detect a given change in our
environment, as it is the case with emotions (Prinz 2004); when depression is an
1
To say that depression should not be confused with experiences of intense sadness (due for
instance, to a loss) does not mean that the fact that MDD is usually adversity-triggered is ignored.
As Jerome Wakefield has convincingly shown (Wakefield 2015), in no way does the “bereavement
exclusion” necessitate that grieving people cannot be diagnosed with depression. But to define
tests in order to draw the line correctly between normal sadness and depression may be problem-
atic: for instance, impairment in role functioning or even a feeling of worthlessness, if temporary,
may not be a clear sign of a depressive, pathological state. This is why, to define depression, we
may focus on the recurrence of the symptoms rather than on their specificity.
emotion, rather than a mere mood, it has something to do with the way we view our
own future, being linked to “poor prospects” (Roberts 2003). Another distinction
would be that emotions have reasons while moods may have mere causes (Roberts
2003): X may view his future in terms of poor prospects because he is tired, or
because he is already in a melancholy mood, and he may rationalize his mood in
terms of upcoming failure while the view of an upcoming failure is a mere conse-
quence of his internal disposition, not a cause for it. Being in a negative affective
state without a proper reason is no sign of disorder by itself, as it may be a conse-
quence of the normal variability of our affective dispositions, and a sign of our
sensitivity to external events, like bad weather, internal events, and exhaustion.
Starting with an analysis of mood, rather than a reference to sadness, could lead us
to a different view of depression.
Another interesting feature of moods is that they have the ability to alter one’s
disposition and one’s answer to external events. This is what Griffiths has expressed
in asserting “they cause global changes in propensities to occupy other states and to
respond to stimuli” (Griffiths 1997); this could be understood, at the neurobiologi-
cal level, in terms of modification of the “the probability of transitions between a
given input, internal states, and output” (ibid., p. 255). Moods usually persist, per-
vade our mental life, and have non-specific causal powers such as when they modu-
late our emotional response to environmental changes. For instance, were I not in
the mood in which I am now, I would not respond to somebody’s demand as I do
(Roberts 2003, pp. 114–115). The association of negative moods with mood-
congruent representations in working-memory is a phenomenon well known to psy-
chologists (Siemer 2005). To sum up, I would define melancholy as the combination
of two features: it is a state of mind with a character similar to sadness that may
persist without reason, and it is a kind of disposition to negative appraisals of events
and stimuli.
One source of confusion in the literature is that depression, as we have just seen,
may be considered in some cases as an emotion, rather than a mood; and second,
that usually philosophers of mind are not concerned with the question of what is
pathological and what is not when they deal with emotions and moods. But these
confusions are not inevitable. We can distinguish between (a) depression as an emo-
tional state, the consequence of the negative appraisal of a given event to which I am
not indifferent (I am depressed about something and I have good reasons to be so),
(b) melancholy, as the mood that we have defined above, with no intrinsic patho-
logical character, and (c) melancholia as the harmful propensity to remain in such a
mood or to return to it, a propensity that is typical of depressive disorders. This
would be, I think, in full agreement with the recent proposal of Holtzheimer and
Mayberg: “We […] propose that the primary abnormality of depression is not the
depressive state itself, but rather the inability to appropriately regulate that state”
(Holtzheimer and Mayberg 2011). The dimension of disorder does not come, then,
from an additional qualitative character of symptoms, or from a lack of reasons to
be sad. It comes from a “recycling” of negative thought in rumination, rather than
from the negative content per se. In line with Griffiths’ suggestion, this can be
understood as a modified probability of transition between states, where the
104 D. Forest
individual becomes unable to alter his mood, to regain his concentration or his appe-
tite, or to escape anhedonia and find new sources of pleasure. The failure of many
antidepressant treatments would come from the fact that they are able to “shift a
patient out of the depressive state without preventing reentry into that state”
(Holtzheimer and Mayberg 2011). But then we need to know much more about
what affective regulation consists in and how we could analyze it in cognitive terms.
If (or when) inhibition of irrelevant processes and contents is crucial, depression
may be understood in reference to executive (dys)function, and disorders of selec-
tive attention. If (or when) depression results from diminished reappraisal of nega-
tive emotions, this may be conceived in reference to metacognition (X is unable to
form second-order thoughts about his negative feelings that would help him to regu-
late his mood), and therapies aiming at the development of metacognitive abilities
of patients may be promising (Segal et al. 2006). It is possible that there is some
room for variability here, and that, if affective regulation may follow more than one
path, this could lead to different styles of depressive thought.
Moreover, this analysis of moods and mood regulation may suggest interesting
questions for neuroscience, or help us to select the most interesting studies or the
most promising lines of research from the trove of current literature. Instead of
looking for neural correlates of intense sadness, or dark moods, or specific symp-
toms, we may look for neural systems involved in affect regulation, reappraisal,
selective attention, and inhibition of negative thoughts. For instance, why we have
reasons to care about the neural correlates of the inhibition of negative stimuli, like
the increased activation of the rostral anterior cingulate cortex –rACC, in depressive
patients (Eugène et al. 2010), is because psychological investigation suggests that
what is essential to depression in many cases is not an initial orientation towards
negative stimuli, but the difficulty to disengage one’s attention from them (Joormann
and Gotlib 2010).
Conceptual analysis, then, may help us determine relevant questions neurosci-
ence can address and how we should characterize the corresponding mechanisms.
Neural correlates of depression are only intelligible if they are the harmful alteration
of mechanisms of which we understand the usual output and purpose; and there is
no interesting characterization of such an output that is not at least compatible, if not
derived from, our understanding of our emotional life. If depression is a vicious
circle, it is not emotion, but reappraisal, not mood itself, but affective regulation, of
which it is important to discover and understand the specific neural conditions. The
idea would be of a mutual benefit: on the one hand, conceptual analysis of our men-
tal life may help us to single out the most interesting questions – what is worth being
investigated, like reappraisal and affect regulation – and on the other hand, finding
which neural circuits are involved in the pathogenesis of depression will constrain
our analysis of what goes wrong in depression at a psychological level.
Lastly, it may be possible to articulate different kinds of explanations: for
instance, social sciences may identify environmental conditions that heighten the
frequency of melancholy moods; moral philosophy can add to our understanding of
the link between our moods and our concerns or prospects; and the most decisive
contribution of neuroscience would be to explain how these moods supersede other
kinds of affective states and where the powerlessness of the individual (in terms of
mood regulation) may come from. Social sciences would deal with kinds of risk
exposure, moral philosophy with the relations between self-perception and affective
life, neurobiology with the vicious circle in which the individual is trapped in
depression.
Conclusion: Acoustics and Musical Thought
A neuroscientific model of depression like the one offered by Mayberg may appear
unappealing, or irrelevant, for two main reasons. The first is that depression is no
ordinary pathology: there is something deeply unbelievable, or even offensive, in
the idea that things as intimate as negative mood and anhedonia may have some-
thing to do with the relations between the anterior insula, the dorsomedial thalamus
and the midbrain ventral tegmental area, as they are pictured on a diagram: in these
matters, detail, and neuroscientific jargon seem only to make things worse. As a
patient says (quoted by Kleinman 1988, 87): “Depression may be the disease, but
it’s not the problem. The problem is my life”. However, when a life is plagued by
depression, it may be because of a downward spiral whereof a neuroscientific
description may be both relevant and useful. The second reason is that for a philoso-
pher it may seem reasonable to think that either neuroscience is an optional comple-
ment to our understanding of affective life, or if it has to be taken more seriously, it
is only in the context of a kind of radical eliminativism where hard science will
supersede the concepts of folk psychology. But, to use Roberts’ metaphor already
mentioned above, if the science of acoustics does not eliminate musical aesthetics,
it does not mean that the two have to remain forever on two different levels, that the
science of sounds does not contribute anything substantial to music as an art. Recent
history tells us that composers who have learned about the properties of sound
waves are able to rethink musical composition and conceive new kinds of musical
patterns, as has been the case with spectral music. In a similar way, it is not impos-
sible that, in addition to its current and future therapeutic applications, a neurosci-
entific account of depression may stimulate philosophical thought about our
affective life and expand our understanding of ourselves.
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Woodward, J. (2003). Making things happen. Oxford: Oxford University Press.
Loss, Bereavement, Mourning,
and Melancholia: A Conceptual Sketch,
in Defence of Some Psychoanalytic Views
Pierre-Henri Castel
Abstract Today, arguing in favor of the psychoanalytic view of depressive states is

likely to be hopeless, not so much for epistemological reasons, but because most
contemporary clinicians (including many psychodynamically-oriented therapists)
have lost sight of the intuitions at the core of the Freudian and post-Freudian visions
of mourning and bereavement. This paper, through a close reading of one of Henry
James’s most praised short stories, almost a contemporary of Freud’s work on mel-
ancholia, offers a detour back to the origin of this misunderstanding. It is a plea for
the aesthetic, philosophical, and anthropological re-education of therapists,
upstream from the conceptual quandaries that have plagued an ill-founded refuta-
tion of psychoanalytic views on depression.
When it comes to defending psychoanalytic views, the danger of misunderstanding

is always great. But it does not so much arise because of their conceptual articula-
tion, or of their empirical content; rather, it originates from the unavailability, for
contemporary clinicians, of the “form of life,” as Wittgenstein would have put it,
within which the psychoanalytically relevant grammatical rules and factual regu-
larities are smoothly interwoven, and provide a type of emotional and linguistic
evidence which cannot be reached otherwise. So it should not come as a surprise if
my point of departure is a literary one. For in what kind of world could Freudian
views be better appraised than in the very world, and at the very time, they were
designed and offered to the general debate?
In one of his most praised short stories, first published in 1895, “The Altar of the
Dead,” Henry James (1895/1984) presents two strikingly evocative characters.
Stransom has lost his spouse-to-be, Mary Antrim, an undetermined number of years
I am especially grateful to Louis A. Sass, who revised the first draft of this paper, and helped me
to overcome my reluctance to write about psychoanalysis in English. I also thank Steeves
Demazeux and Jerry Wakefield for their precious comments.
P.-H. Castel (*)
Centre National de la Recherche Scientifique (CNRS), Ecole des Hautes Etudes en Sciences
Sociales (EHESS), Paris, France

DOI 10.1007/978-94-017-7423-9_8
110 P.-H. Castel
before the plot unfolds. To the disconsolate memory of her, and for the needs of his
private cult, he erects a magnificent shrine of light and tapers, in a church lost in a
remote London neighbourhood: the altar of the Dead. There, one sad and gloomy
evening, he meets a “nameless lady,” not too much younger than himself, and “in
mourning unrelieved,” as James depicts her. The reader is at first struck by the close
analogy of their predicaments, both spiritual and physical. Both exhibit the same
moral pain in their bereavement, including enduring and pervasive sadness and
world-weariness; both are bereft of all intimacy with friends and family; they show
the same fidelity to their dear lost ones; they follow the same rites of mourning,
speaking half-jokingly about their odd “community of service”; and they both inex-
orably age, barely coping with the dark prospect of their own termination.
The plot thickens as they unexpectedly realize, after years spent in prayer at the
altar of the Dead, that one and only one man is the shared object of their most poi-
gnant ambivalence. His name is Acton Hague. A friend of Stransom, turned secret
foe for reasons James artfully keeps in a hazy background, he appears to have been
the mourning niece’s lover, and the most distressful deception of her life—once
again, we do not know why. As this paper is not intended to be a spoiler, I will say
no more. Suffice it to say that François Truffaut made use of James’ short story for
the scenario of his 1978 film, The Green Chamber, and that Stransom comes to a
tragic end, in an arch-typical melancholic abandonment of his own life, at the very
minute the mourning niece finds her final relief, and opens her heart again, though
rather unconsciously, to the possibility of life.
Here is the typically psychoanalytic question I will now try to articulate: why do
most human beings, when bereaved, painfully learn to live with their loss, whereas
a few others, who display the same behaviour, and who ache from the same depres-
sive mood, slowly die with their dead?
A brief observation, made in passing in “The Altar of the Dead,” will be my
thread. Uncovering the abyss of their mutual misunderstanding, the mourning niece
ponders: “We simply had different intentions”. In other words, whatever may be the
behavioural similarities, and the purely quantitative variations between depressive
states lumped together for statistical purposes, we are still in need of an explanation
for such dissimilar outcomes in bereavement. The underlying intentional structure
of loss and bereavement endows them with an unmistakable clinical specificity. And
this structure likely accounts for the subjective fate, in the long run, of these painful
experiences. My first endeavour will be to make a bit more explicit what such an
intentional analysis of loss and bereavement might be. For it somehow blurs the
alleged clinical differences between “normal” and “pathological mourning,” or
between “major depressive disorder” with or without “psychotic features” and
“melancholic features”—all classifications that take into account only observable
and behavioural characteristics of depressive states. Conversely, such an intentional
analysis of loss and bereavement might establish the grounds for a more psycho-
logically significant difference between all these conditions.
The two fates of Stransom and “the mourning niece” are but an introduction to
Freud’s “Mourning and melancholia”. Actually, I aim to show that some Freudian
and post-Freudian views on these two conditions are best understood in the light of
an intentional analysis of loss and bereavement. This entails a number of
Loss, Bereavement, Mourning, and Melancholia: A Conceptual Sketch, in Defence… 111
consequences, not for the pharmacological management of depressive states (once

more, their purely behavioural components are similar all along), but for its rela-
tional and inter-subjective dimensions.
So which are the grounds for an intentional description of depressive states in
psychoanalysis?
Abraham’s 1912 View on Melancholia
There is a constant that runs through all psychoanalytic theories of depression:

depression is seen as a form of (forbidden) hate towards some external object, which
backfires onto the self in a punitive way. I contend that this process makes sense
only if its inherent intentionality is taken into account. Intentionality, here, does not
refer to “intending to do something,” wilfully, and with a goal; rather, it is the more
abstract and more mental “aboutness” we find in the relation of a mind to its objects.
Karl Abraham’s 1912 framing of that idea was the following (Abraham 1953):
Melancholics cannot repress their hostile impulses, so projection is their last line of
defence. But they cannot keep their hate at bay through projection—that is, fix it for
good in the external world, according to the classic paranoid pattern of persecutors,
who, however, usually guess as if “from within” what the patient is about to do in
order to escape the persecutors’ evil intents. That is the reason why these aggressive
motions backfire onto the self, inducing the typical feeling of being justly punished
even for non-existent or trivial misdeeds. In this way, Abraham envisioned melan-
cholia as paranoia in reverse, as a self-persecution. And melancholics do look oddly
shameless in their self-reproach—until you realize who else they are actually attack-
ing under the cover of self-accusation. But why such a reversal of paranoia? Because
the roots of melancholia are to be found in the subject’s “ambivalence”. The hated
object is also (and remains) a loved object. Hence, the weight of hatred must ulti-
mately fall back upon that loving self, who cannot cope with the negative side of his
or her ambivalence through repression, and who must therefore be punished for it.
This is just what happens to Stransom with respect to his former friend Hague.
Grammatical and Psychological Coordinates of Intentionality
Beyond the literary or clinical context, the idea that depressive feelings are but
“inverted” aggressive impulses emerges in various ways. Both in French and in
English, one can provide good examples of this reversal. For example, the English
“grief”, means “grievance” in French.
This is not a mere coincidence. To borrow philosopher John L. Austin’s distinc-
tion, the illocutionary content of aggressive utterances is usually replete with perlo-
cutionary effects of the depressive kind, and vice versa. For, whatever we intend to
convey, the very fact of saying “You make me sad” to somebody often expresses not
so much sadness as anger and resentment. Reciprocally, we may cry out of moral
112 P.-H. Castel
pain when shouting, “I hate you so much” to a loved one. From a more psychologi-
cal standpoint, sadness is often consciously experienced as an inward rage barred
from public display; anger, similarly, when not fully acted out, commonly reverts to
grief and feelings of helplessness. Finally, children (and dominated people as well)
appear to be highly sensitive to the actual possibility of openly displaying either
their resentment or their moral pain. The opposition of inward vs. outward feelings
will often reflect socially coded constraints on the legitimacy of the public exhibi-
tion of affective states. Agitated and violent children may actually be sad, while
passive or submissive women, internally consummated with rage.
But there is more to the matter, as Abraham suggested. And this will help us to
understand the intentional aspect of this projective reversal of aggression into self-
aggression (with depression as self-punishment). In fact, this reversal does not
imply a fuzzy affective transmutation of outward hate into inner depressive feelings,
but, rather, two distinct processes:
1. A semantic reversal of “to love” into “to hate”
2. A grammatical permutation of the subject and the object of the verb.
In this process, “I love you” first turns into “I hate you” (ambivalence), and then
(via projection), “I hate you” turns into “You hate me” (and hence, I feel dejected,
valueless, saddened, and the like).
But what exactly is this double process meant to explain? Following Abraham, it
explains why self-persecution is so intense and perspicuous in melancholia. The
subject “knows” all too well which secret aggressive impulses he or she should not
have even conceived of, which were addressed to whom, and why they were ulti-
mately returned upon him. Even if he is not conscious of all this, the stringent,
inescapable, and torturing directedness of self-reproach makes it unmistakable in
itself.
To this extent, the biology of mood disorders cannot be the end of the story. If,
on the one hand, we suspect a grammatically ordered transformation of sadness into
aggression, and, on the other hand, have some ground to connect it to the social
context of our moral life, we need nothing more to suggest the possibility that our
affective states may well follow some intentional patterns as well as causal neuro-
biological laws.
Affective vs. Epistemic Intentionality
But what kind of “aboutness” is this? Or, in philosophical parlance, what kind of
object-directedness or intentionality does it demonstrate?
Certainly not epistemic intentionality, such as the one linking, for instance, a
belief to the state of affairs being believed. In epistemic intentionality, the object
must precede the intention directed to it. One cannot believe in a state of affairs
one knows for sure to be false. To believe something is to believe that something
is true—objectively true. The intentionality I am referring to, by contrast, is an
affective intentionality. But as we know, being desirable, lovable, hateful, is nei-
ther an intrinsic nor an objective property of anything. Desirability originates from

the subjective desire that aims at or targets the desired thing. So when one consid-
ers whether one “truly” wishes anything, one does not look at the desired object,
but at oneself. By contrast, when one checks whether one “truly” believes in
something or not, one pays attention to its objective properties. Thus, if holding-
for-true requires objective grounds, holding-for-good originates from our subjec-
tive intent.
More: our wish to believe usually prevails over belief. This is wishful thinking:
if we cannot believe in something because it is false or because it does not exist, we
hallucinate it. We just create out of nothing, or rather, out of ourselves (projec-
tively), the missing content of a representation, and this plays the same role in our
thinking processes that a well-grounded referential picture of reality would nor-
mally play.
Freud: A Two-Level Model of the Mourning Self
Here enters the bizarre and seductive idea put forth both by Freud and Abraham: not
only do we hallucinate what we wish to believe, but, through projection, we even
substitute ourselves for the non-existent object of our projection. The hallucinating
subject, at the culmination of the projective process, somehow becomes the halluci-
nated object. And the less we have on the object’s side, the more the subject is
doomed to provide of its own substance as a compensation for the non-existence, or
paucity, of its objective counterpart. In other words, as soon as we accept the ulti-
mate affective privacy of bereavement, there is no limit to the inner closeness of the
lost loved object we wishfully hope to still exist. That is, when the object is forever
lost, we tend to identify ourselves with it, and we incorporate it so as to make it live
and exist out of our own flesh and blood. But this implies that there will always be
a slippery slope from:
1. Becoming in the name of love the lost object, in order to keep it within us and;
2. Losing ourselves within the lost object, out of love for it.
Once again, such formulas ought not to be taken as the descriptions of a psycho-
logical mechanism—even though Abraham drew a nightmarish picture of such a
mechanism, in which the mourner “eats” its object, or, conversely, is “eaten” by it,
and feels himself “excreted” by it (or dejected). More simply, the formulas specify
within which logical boundaries affective states can transform into each other. They
preserve the aboutness of these transformations (the specificity of their intentional
objects) even as the mode (with what sort of mental attitude or direction of
relationship the objects are related to) changes. And finally, they capture some poi-
gnant elements apropos of what we feel in grief, with a quite interesting nuance: if
losing ourselves in merger with the lost object is an intrinsic possibility of our life,
then, beyond sadness, a deep-seated anxiety also looms on the outer limits of true
bereavement.
114 P.-H. Castel
Freud’s “Mourning and Melancholia” (1915–1917/1957) takes for granted:

1. Abraham’s grammatical analysis of projection;
2. The parallel between mourning and melancholia, with two caveats, (a) the idea
that in usual mourning, what we lost is obvious whereas outbreaks of melancho-
lia are much more enigmatic, and (b) the fact that melancholia, unlike mourning,
implies a strong ambivalence to the lost object;
3. Melancholia as paranoia in reverse.
But Freud goes much deeper than Abraham when he brings in his notion of nar-
cissism, for he implies two distinct levels of subject-object intentional relationship.
At the first level, the ego of the mourner develops its identification with the lost
object—tainted with hallucinatory elements, of course, but still preserving a clear
distinction between the ego and its loved object. The point is that, in Freud’s view,
the desperate need to save, at all cost, one’s relationship to the love object, entails
trespassing the clear distinction between the bereaved subject and its object. At some
point, both collapse into one subject-object (“The shadow of the object fell upon the
ego”). That new subject-object becomes, in turn, at the second level, the object of a
certain valuation from another instance: the one responsible for moral conscience in
everyday life, and which is in clinical accounts of guilt nothing but the super-ego.
Freud is eager to improve the plausibility of his view with a clinical parallel. He
insists that in obsessional neurosis, the super-ego makes itself felt as the moral agent
judging and condemning the relations between the subject and its desired objects,
and calling for their repression. Here, the super-ego no longer condemns a relation-
ship. It targets the very identity of the subject to its (lost) object, or the product of
the so-called “narcissistic identification” of the mourner with its object.
Consequently, when its dejection has reached its climax, the self really ejects itself
as “one” (ego and super-ego together) in a frightening acting out. This ejection is
often to be taken literally (think of the typical suicide of melancholics jumping out
of a window without warning). In James’ short story, Stransom identifies with the
“one” taper missing from the array of the altar of the Dead, the one that could have
stood for Hague. It would have been the only one taper meaningful to his fellow
mourner. But so far, he had always denied it to her. Surrendering at last, he instantly
follows Hague into death, to the niece’s disbelief.
Hence Freud’s construct makes room for a more complex view of depressive
states than does the strictly behavioural approach. Depressive states may not differ
merely in degree of intensity, for there may be qualitative and structural differences
between major depressive states, and melancholia proper. Freud’s construct also
leaves open the question as to what exactly “self-esteem” and its loss in depression
consist in. In my loss of self-esteem, do I mourn some obscure ideal trait of the lost
love object I identified with? Or, rather, do I despise myself, and feel radically
ashamed of the very fact of remaining still alive, whilst other valued people have
died? Of course, we cannot answer such questions with a scale of psychomotor
retardation; or by objectively assessing whether the supposed closeness of the lost
object was delusional or not. We have to pay attention to the intentionality of loss.
This is the rule of thumb of clinical sense and sensibility, and the only alternative to
the “flight to objectivity” in mental matters.
Melanie Klein’s Critique of Freud
Freud’s sketch also drew a set of critics from other psychoanalysts. Perhaps most
prominent in this regard is Melanie Klein, with her reappraisal of Freudian mourn-
ing, through her use of her notion of the “depressive position” (Klein 1940; Leader
2008). Because of her idea of a “depressive position”, which is in fact no pathology,
but, on the contrary, a necessary step in all psycho-therapeutic transformation,
Melanie Klein remains, without doubt, the most influential writer in the field of
depression and psychoanalysis. Let me list a few of her objections to Freud:
1. Freud himself acknowledges that normal mourners always “rebel” against the
mourning process. It is, after all, a highly paradoxical process, that must achieve
detachment and renunciation to the lost object through a systematic and exhaus-
tive re-investment of past memories (usually through idealization) in the process
of their ultimate “de-cathexis”. Yet, the more we think of our lost love ones, the
less we want to let them part from us! Or, maybe, we just wish, at times, that we
could expel the dead from our living mind. This is hard to see as a mere instance
of a conflict between reality-testing and wishful thinking. Ambivalence obvi-
ously exists not only in melancholia, but in normal mourning as well. In James’s
story, the niece is clearly “ambivalent” with respect to her lost lover, Hague.
2. Is it so clear that in mourning, we know what we have lost, whereas in melancho-
lia, the triggering factors remain hidden? Freud himself was not so sure. For it is
unclear what exactly we mourn when we mourn somebody; at the same time,
many melancholia outbreaks are easy to trace back to some manifest disillusion
or moral wound.
3. Finally, Freud was compelled to admit to a normal form of “narcissistic identifi-
cation”. Before reaching the developmental level at which the ego enjoys a full-
fledged capacity for loss, identifying with the lost object (orally absorbing it, in
dream-like parlance) was, in fact, its only available coping mechanism. But this
implies that what can be deemed a “regression” in melancholia was once a nec-
essary ingredient of our psychic growth. And as infants, we had no other option.
The fruitful way to proceed is to envision the Kleinian development as a concep-
tual extension of Freud’s ideas. In this respect, Melanie Klein put forward a number
of important aspects, not previously mentioned by Freud, of bereavement and
mourning:
1. First, she clearly envisioned that the template of “moral conscience” upon which
Freud devised his version of the super-ego falls short of what his concept of
narcissistic identification should have hinted to him. For if we are such stuff as
narcissistic identifications are made on, our super-ego is formed much earlier
than any moral conscience. The instance that either lauds or deprecates the
mourning ego is nothing but the memory of past and insurmountable identifica-
tions with our first love objects (namely, the Oedipal ones, particularly for our
arch-object, the first care-giver, the Mother).
116 P.-H. Castel
2. This implies that, instead of one moral conscience, we have a whole internal
world of past identifications and fantasied objects that serve as the very ideals for
narcissistic identifications. This, of course, is but James’s altar of the Dead itself:
a beautiful presentation of all our lost “Others”, as he literally puts it. But what
does this imply? Mourning is no longer, as in Freud, a desperately private trial.
Confronting our losses, we call out for help to our Oedipal figures, who mourn
with us and within us. Our fantasized parents share our burden of grief, and they
recall their past love to our bereaved self. Note that the dream language in which
all this is expressed now incorporates the reassuring voice and the amicable gaze
of our first love objects. At the climax of the short story, and before its final tragic
turn, Mary Antrim’s uncanny descent, as a radiant ghost, almost saved Stransom.
But he could not take hold of this motherly and celestial hand, and instead
slipped into death.
Losing someone, to sum up, is no longer a private experience turned in upon
itself. It conjures up an “inner world” of identifications, or of fantasied lost love
objects that have silently become parts of our selves, but which emerge and speak
out when we are torn apart in bereavement. More precisely, the feeling of being
locked into one’s grief, as a desperately lonely mourner, is true melancholia. Normal
mourning implies just the opposite: recalling a host of vivid self-memories. This is
why Melanie Klein reads Freud’s famous motto, “in mourning, the world is empty,
in melancholia, the ego itself is deserted”, precisely the other way round. “In mel-
ancholia”, Melanie Klein might suggest, “our inner world shrinks down like a
shagreen (think of the French “peau de chagrin”, and of Balzac’s 1831 short story),
while in normal mourning, the ego copes with the loss of its object thanks to the
strength and vividness of its deeper narcissistic base”.
One crucial consequence is the following: depressive states are to be evaluated in
light of their intentional content (what is lost to whom?). But they are also endowed
with an intrinsic therapeutic quality. For depression goes with integration, and
detachment from love objects with new narcissistic layers of our affective self,
much deeper than what our ego is aware of. So loss in the outer realm implies re-
creation within the inner self. The “depressive position” is born out of this dynamic
process. It follows that the true psychotic depression which melancholia is can be
defined not as the failure of ordinary mourning, but as the failure to process our
ambivalence (or our anxiety about attacking the good object), through what Melanie
Klein called the “depressive position”.
Lacan and Anxiety in Mourning
One psychoanalyst specifically emphasized the role of anxiety in mourning: Lacan

(1962–1963/2004).
His starting point is the claim that mourning is not only the loss of a love object,
but the loss of someone to whom we were, or fantasized ourselves to be (no differ-
ence, here), a love object. As Stransom put it: “Mine are only the Dead who died
possessed of me” [my emphasis]. Mourning reveals the true dependence of human
beings on each other: our love objects are subjects, and those whom we miss are
themselves subjects whom we experience as missing us. It is important to recognize
the reciprocity of loss. For among the torturing questions we raise in mourning are
surely these: “What would the dead person have thought of this? What would he or
she have liked me to do?” What we were for the dead, and the plain fact that such a
question is now forever without an answer, instills anxiety in mourning. Conversely,
a sign that mourning is over, and loss consummated, is the moment when we realize
how strange, and even how alien to us, was the very person we loved, and whom we
thought of as loving us. We lived by him or her, and we never understood how
poorly we knew him, what he actually wanted of us. At this turning point, we know
that we have parted from that person for good. Sadness is gone, and with it, all the
anxiety attached to what the lost person may have thought and wished about us, and
which could have been a source of guilt and resentment towards him. The niece’s
salvation relies upon this, in James’ tale. At the very last, she sees that Hague was
not the “One” she must love better than her own living love. Freed of anxiety to
disappoint her lost lover, she breathes again, alas, at the very moment Stransom suc-
cumbs to what Henry James calls his “malady of life.”
Being a human being and living in a symbolic order, Lacan suggests, means that
we cannot separate what the “Others”, be they dead or alive, are to us, from what we
are to them. Hence, our Oedipal identifications depend on kinship, and on what it
prescribes, both emotionally and in terms of social subordination. What may seem
an oddity, the bi-directionality of loss in mourning, actually manifests the way the
individual’s mental and affective life is woven into social networks that extend far
beyond what we are consciously aware of. This is why, to our amazement, we may
feel more anxious than sad in mourning. And it may even be the case, even more
counter-intuitively, when the lost person is not one we loved, but one whose putative
desires and expectations were much more meaningful to us than what we ever
thought.
Lacan’s view of anxiety in mourning, to this extent, radicalizes the Kleinian
stance. For the Kleinian “inner world” of past projective/narcissistic identifications
is better understood as a “symbolic world”, a world of enduring social re-creation of
what we mean to each other. Going all the way through the paradoxical mourning
process, namely, painfully re-investing all our memories of the lost object so that at
the end we can detach ourselves from it, finally turns up as a cultural task. We must
erect an “altar” in our memory, a monument that both enshrines the lost object as
“good”, and forgiven, and that marks an impassable frontier between it and us, a line
which prevents it from eliciting our regrets any further. Our individualistic societies
are perhaps not the best place to understand this, for we usually collapse the time for
private grief and mourning, and the time for the collective rites of funerals. But what
are funerals in societies that celebrate them at a distinct moment of time, namely, as
a closing chapter of the mourning period? It is the time when the Dead are ascribed
to their symbolic place, whence they shall never return. Thus funerals are intended
to soothe not grief, but anxiety about intentions of the Dead. They relieve the
haunted mourner, not his sadness. And this, once again, is a social process. It is not
the kind of process Freud or Melanie Klein would have conceived of, but only
118 P.-H. Castel
Lacan, who regarded the Unconscious as the “Other’s discourse” rather that existing
within a private psyche, and who thought of symbols as elements of language and
shared collective representations to which, as subjects, we are all “subjected”.
Concluding Remarks
Let me sum up my argument about the irreducibility of intentionality in mourning

and in melancholia, for it epitomizes the contribution of psychoanalysis to the issue
of depression.
1. If we rely on solely behavioural criteria, there is no way to make the crucial dis-
tinction between two distinct meanings and psychological experiences of depres-
sive states: one which is to painfully learn to live with our loss (normal mourning),
and the other, which is to let oneself die with the dead (melancholia as psycho-
sis). Henry James’s Stransom, on the one hand, and the “unnamed lady”, on the
other hand, typify both the behavioral indiscernibility of these two conditions,
and their dramatically divergent outcomes.
2. Not only do we have to read loss as an intentional concept (focusing on its
“aboutness”), as a loss “of x”, as a loss “for me”, but even as a loss of “the X (a
subject) who lacks me”. I suggest that a logico-grammatical analysis of loss and
bereavement coincides, at least to some extent, with certain psychological traits
of mourning (e.g. to its paradoxical process, its possible derailment in psychosis,
its link to anxiety beyond sadness).
The Freudian challenge to contemporary treatments of depression (namely,
cognitive-behavioral therapies) should now appear self-evident:
1. Psychoanalysis implies that there cannot be any “mourning work” in a melan-
cholic patient; indeed, the impossibility of it is what rigorously defines this con-
dition. This is paradoxical, for it is not literally Freudian, but rather Kleinian and
Lacanian. Prodding such a patient into remembering his loss, with the goal of his
finally overcoming it, will ultimately fail because such a patient lacks the full
ability to maintain within himself what James called the “altar of the Dead”. Any
such reinforcement of his memories will entice him all the more into following
his lost object into death—far from helping him to identify with the many affec-
tive links which connected him to it, as is the case with a maturing sense of self
in normal mourning.
2. Instead of indiscriminately addressing “negative cognitions” and an over-
simplified “loss of self-esteem”, therapists should pay attention to their design.
For instance, I would consider it significant to scrutinize the exact nature of
negative cognitions about one’s own negative cognitions. Which self, moreover,
identified to what kind of inner objects, and sustained by which past narcissistic
identifications, do we suppose in the background of the mourning process?
3. Far from regarding the culture of mourner as peripheral information, therapists
should recognize that to mourn is an attempt to re-create a livable symbolic
world, a world that must survive the disappearance of an object intimately con-
nected to a host of other lost emotional objects. It is not a brain-centered, nor an
individual-centered process. For we are “ritual animals”, as Wittgenstein aptly
remarked, and we must be treated as such.
4. Last but not least, we should learn from the melancholy geniuses of art what the
consummation of loss actually consists in. Neither in the vanishing of sadness
nor in its forceful voiding, but rather in the artful creation of an intrinsically
artificial device: a symbolic hole within which a whole world can be both lost,
and yet, somehow, survive.
References
Abraham, K. (1912/1953). Notes on the psychoanalytical investigation and treatment of manic–

depressive insanity and allied conditions. In Selected papers on psychoanalysis (Vol. I,
pp. 137–156). New York: Basic Books.
Freud, S. (1915–1917/1957). Mourning and melancholia. In The standard edition of the complete
psychological works of Sigmund Freud (Vol. XIV). London: Hogarth Press.
James, H. (1895/1984). The altar of the dead. In E. Wagenknecht (Ed.), The tales of Henry James.
New York: Frederick Ungar Publishing Company.
Klein, M. (1940). Mourning and its relation to manic-depressive states. International Journal of
Psychoanalysis, 21, 125–153.
Lacan, J. (1962–1963/2004). Le Séminaire, livre X: L’angoisse. Paris: Seuil. English edition:
Lacan, J. (2014). Anxiety: The seminar of Jacques Lacan, book X (C. Gallagher, Trans.).
Oxford: Polity.
Leader, D. (2008). The new black: Mourning, melancholia, and depression. London: Hamish
Hamilton.
Suffering, Meaning and Hope: Shifting
the Focus from Depression in Primary Care
Christopher Dowrick
Abstract The diagnosis of depression is not fit for the purposes of primary care. It
is inherently problematic, with regard to both validity and utility, and can be chal-
lenged on ethical and evolutionary grounds. It has iatrogenic effects, including
reducing the sense of personal agency. These effects are exacerbated by GPs’ deter-
ministic explanatory metaphors, and aggravated in cross-cultural consultations
which attempt to integrate experiences of traumatized self-identity within routine
technical practices.
We need a theory of the person based not on medical assumptions of passivity
but on awareness of personal agency. Two key concepts are coherence and engage-
ment. Coherence involves an understanding of ourselves as consistent beings, per-
sons with the capacity to lead our own lives. We make sense of ourselves in terms
of our engagement with the world around us: this is crucial in creating and sustain-
ing our sense of identity and well-being.
To provide high quality primary care for depressive feelings, we cannot limit
ourselves to individualized biomedical perspectives. In our clinical encounters we
do well to see depressive feelings through our patients’ eyes. We should acknowl-
edge suffering, explore meaning and offer hope. We need to incorporate concepts of
agency and coherence within our dialogues with patients, expand social understand-
ings of distress and encourage engagement at the community level.
The Problem of Depression
Depression is commonly diagnosed in primary care. In a major international study

on mental illness in general health care involving 15 centres across the world, the
overall prevalence of current depression, using criteria of ICD-10, was estimated to
be 10.4 % (Goldberg and Lecrubier 1995). In a study of general practice attenders
in Montpellier, in France, 16.5 % met DSM-IV criteria for depressive disorders
(Norton et al. 2009). Compared with standardised diagnostic criteria such as these,
C. Dowrick, M.D., FRCGP (*)

University of Liverpool, Liverpool, UK

DOI 10.1007/978-94-017-7423-9_9
122 C. Dowrick
general practitioners (GPs) are more likely to over-diagnose than under-diagnose

depression: for every 100 unselected cases seen in primary care, a meta-analysis of
reported studies (Mitchell et al. 2009) estimates that GPs make 15 false positives
diagnoses, miss 10 cases and identify 10 cases of depression.
There are apparent benefits in making the diagnosis of depression in primary
care. Its existence enables researchers to generate epidemiological information
about the prevalence and trajectory of the disorder. It provides clinicians with a
basis for discriminating between different treatment options, and hence generating
guidelines regarding clinical care (NICE 2009). It offers distressed people the pos-
sibility of exculpation, insofar as the diagnosis of a disease implies that symptoms
are not the fault of the person suffering from them; and carries with it the implica-
tion that the medical profession will take responsibility for providing treatment and
care (Killingsworth et al. 2010).
But the diagnosis of depression is inherently problematic with regard both to its
validity, the extent to which it can be seen as a discrete entity with natural boundar-
ies, and utility, the extent to which it reliably informs treatment decisions (Kendell
and Jablensky 2003). It can be challenged on ethical and evolutionary grounds, and
has potentially noxious effects.
Problems of Validity
Genetic Bases
The validity of the diagnosis cannot be predicated on a firm genetic basis, since
evidence in this field is equivocal. While numerous studies indicate an interaction
between genes (most commonly the 5-HTT gene) and environment in increasing
the risk of depressive disorders (Caspi et al. 2003; Uher and McGuffin 2008), there
is a need for caution in interpreting these findings (Munafò et al. 2009). Only a
handful of specific genes have been identified, and further advances will require the
analysis of hundreds of affected individuals and their families (Cowan et al. 2002).
The effects of the 5-HTT gene are far from clear. Positive linkage of effects tends
to be over-reported in small samples, and the combined analyses of multiple datas-
ets, including a larger number of candidate genes and polymorphisms, will be nec-
essary for an adequate assessment of the presence and impact of depression
susceptibility genes (Levinson 2006). Genetic studies have not yet proved useful as
a basis for disease biomarkers or approved diagnostic tests (Miller and O’Callaghan
2013).
Genetic variations are more related to generic than specific vulnerability.
Associations have been found, for example, between short variations of the 5-HTT
gene and predisposition to alcohol disorders (Pinto et al. 2008) and schizophrenia
(Sáiz et al. 2007), while there is accumulating evidence for an overlap in genetic
susceptibility across the traditional classification systems that divide schizophrenia
from mood disorders (Craddock and Forty 2006).
Suffering, Meaning and Hope: Shifting the Focus from Depression in Primary Care 123
All we can safely say at present is that there is some evidence to support the
hypothesis that certain genetic and early environmental factors may predispose cer-
tain people to react more adversely than others to stressful experiences later in life.
This does not give genetic support for a specific diagnosis of depressive disorder.
Border Disputes
The current received wisdom that depression is a unitary concept derives from the
position adopted by Akiskal and McKinney (1975). In a seminal paper they pro-
posed that a large number of disparate conceptual models should be integrated
within a unified framework, with the depressive syndrome ‘conceived as the psy-
chobiological final common pathway’.
However there are at least three current border disputes involving the diagnostic
category of depression. In Beyond Depression (Dowrick 2009) I have characterised
these as anti-imperialist, integrationist and fundamentalist. For the anti-imperialists,
the borders between depression and other mental states are unclear. In consequence
other diagnoses such as adjustment disorder are in serious danger of annexation or
obliteration (Casey et al. 2001). Integrationists see depression’s current borders as
too small, narrow and rigid. They advocate diagnostic amalgamation with other
mental states, arguing for overlap of depressive symptoms with normality, with
anxiety (Shorter and Tyrer 2003), or with the symptoms of physical conditions.
Fundamentalists take the opposite view. For them the state of depression is too large
and unwieldy to be adequately defended. They advocate withdrawal to a safer, cen-
tral heartland and provide evidence for discrete sub-sets of the depressive condition
(Parker 2007a, b).
My own position is closest to the fundamentalists. I see the homogenisation of
depression as a mistake (Dowrick and Frances 2013). I would resurrect the term
melancholia to distinguish rarer and more severe forms of depression from the
increasingly common diagnoses related to reactive distress: not least as an antidote
to DSM-5’s toxic expansion of depressive diagnoses to include grief reactions
(Parker 2013).
Problems of Utility
The utility of the diagnosis is also under threat, with expanding evidence of a sub-
stantial placebo effect of antidepressant medication.
Although published pharmaceutical drug trials usually indicate benefit of
active drug over placebo (Gibbons et al. 2012), we cannot always have confi-
dence in these data. Turner et al. (2008) found evidence of selective publication
bias of clinical trials submitted to the United States’ Food and Drug
Administration (FDA). Trials which showed positive effects of antidepressants
compared with placebo were much more likely to be published than trials
124 C. Dowrick
showing negative or questionable effects. Thirty seven studies viewed by the

FDA as having positive results were published, and only one study viewed as
positive was not published. In contrast 36 studies viewed by the FDA as having
negative or questionable results were either not published at all or else pub-
lished in a way that conveyed a positive outcome. The difference in apparent
effect size of antidepressants between FDA and published data was 32 % in
favour of the published data. Similarly, the balance of risks and benefits of anti-
depressants for children looks very different when unpublished data from phar-
maceutical research are added to results published in peer-reviewed journals
(Whittington et al. 2004).
Kirsch and colleagues have undertaken detailed analyses of the antidepressant
medication data submitted to the FDA. Using Hamilton’s depression rating scale
as their benchmark, they found that the mean overall difference between responses
to antidepressant drugs and placebo in this database was only two points (Kirsch
et al. 2002), well below accepted levels of clinical significance (Löwe et al. 2004).
They subsequently found that drug-placebo differences increase in relation to ini-
tial severity. There is virtually no difference at moderate levels of initial depres-
sion and a relatively small difference for patients with severe depression.
Conventional criteria for clinical significance are reached only for patients at the
upper end of the very severely depressed category (Kirsch et al. 2008). The lack of
evidence for the effectiveness of antidepressant medication for milder depressive
diagnoses has been confirmed by Fournier et al. (2010) and Barbui et al. (2011)
amongst others.
The proportion of people responding to placebo appears to be increasing over
time (Walsh et al. 2002). As treatments for depression have become more widely
available and socially acceptable, it has become easier to recruit members of the
general public to take part in clinical trials, rather than relying on patients referred
from other clinicians. As a result, it is possible that clinically important characteris-
tics of patients taking part in treatment studies may have altered. For example, peo-
ple coming forward from the general public may have less chronic types of
depression, or experience fewer contributory life difficulties, than those recruited
through hospital clinics. There are also some methodological changes in the studies
themselves. The main difference is that the average length of the trials increased
significantly during the 20 years under review. This would give more time for the
cumulative effects of non-specific interventions which are inherent and inevitable in
clinical trials, and – importantly – provides a longer period during which spontane-
ous recovery could be observed.
The evidence for efficacy of psychological interventions such as cognitive behav-
iour therapy is open to equal or even stronger challenge, on the grounds that their
precise modes of action have not been adequately tested. Contextual factors such as
the impact of hope generated by an apparently scientific approach to treatment, the
effects of therapist personality, or the benefits of time spent with a sympathetic pro-
fessional may be equally if not more important than the specific formal components
of a given therapeutic approach (Parker 2007a, b).
Ethical and Evolutionary Perspectives
Jerome Wakefield has offered a conceptual rationale for the decision to award some
negative emotional experiences the status of an illness, by defining them in terms of
harmful dysfunction of our biological mechanisms for responding to loss (Wakefield
1992a, b; Horwitz and Wakefield 2007).
According to Wakefield, harmful is a value term based on social norms. It refers
to something which causes disbenefit under present environmental standards, and
which is socially disvalued according to the standards of a given culture. One exam-
ple would be extreme male aggression, which had Darwinian survival value but is not
seen as useful or generally acceptable in modern western societies. Wakefield sees
dysfunction as a factual, scientific term, referring to the failure of an internal mecha-
nism to perform a natural function for which it was designed by evolution. Function
is based on natural selection, and has at its root the ability to ensure reproductive
success (Wakefield 1992b). He draws explicit parallels between organs such as the
heart and artefacts such as a chair. These have specific functions, and can be defined
as dysfunctional if they cannot perform as they are supposed to perform. In the same
way he argues that mental mechanisms can be seen to either to function effectively,
or not. Both parts of the concept are needed for the definition of disorder.
On this basis Wakefield argues that much of the current conceptualization of
depression as a disorder is invalid, and that the diagnosis should be reserved only for
those relatively few cases where harm and dysfunction are beyond doubt (Wakefield
and Schmitz 2013).
This position is supported within the parameters of evolutionary biology, where
theorists have postulated the functionality of many depressive symptoms in mini-
mising harm in situations where biological fitness is threatened, including social
losses and failure to reach personal goals (Keller and Nesse 2005). In relation to
social competition, depression may be effective as a strategy enabling the individual
to accept defeat in antagonistic encounters and accommodate to what would other-
wise be unacceptably low social rank (Price et al. 1994; Faucher 2016). It may also
be useful as a means of enhancing analytic abilities and encouraging reluctant social
partners to provide help (Watson and Andrews 2002).
More generally, we may not believe that the experiences which form the core of the
depressive syndrome, or their corollaries in terms of action failure, should be nega-
tively evaluated at all. To an orthodox Buddhist, a description of the core of depressive
disorder as the generalisation of hopelessness is strongly reminiscent of the funda-
mental concept of dukkha. The experience of this emotion or mental state, for a
Buddhist, is not necessarily a symptom of a common mental illness: it may simply be
an accurate understanding of the world as it is (Obeyesekere 1985). Then we have Eric
Wilson’s passionate essay Against Happiness, based on his fear that its overemphasis
‘might be dangerous, a wanton forgetting of an essential part of a full life’ (Wilson
2008), and his case for the generative power and deep heart of melancholia, enabling
Keats to appreciate how beauty is enriched by our awareness of life’s transience:
in the very temple of Delight
Veil’d Melancholy has her sovran shrine.
126 C. Dowrick
Iatrogenic Effects
Although some of the more extreme depressive experiences do warrant the label of
a disorder, reaching for a diagnosis of depression can all too often lead to the medi-
calisation of experiences of distress and suffering, which may better be seen as
normal, unavoidable, sometimes even necessary facets of human experience
(Dowrick and Frances 2013).
The diagnosis of depression may simply be unnecessary. For example, Brown
and Harris (1978) have developed a highly sophisticated and influential life span
model of depression, involving a complex interaction of adversity, support and self-
esteem. Although they predicate this on an assumption of depression as a biologi-
cally rooted psychiatric condition, what would happen to the model if the concept
of depression were removed from it? Clearly it would raise some practical difficul-
ties in pursuing a research programme since there would no longer be any specific
criteria by which to judge who should be recruited to their studies. But the key ele-
ments of their model – the range of social and individual factors which predict
whether or not we feel life is going well – would survive quite happily on their own.
These factors and their interactions are a useful guide to all of us in understanding
how our lives are going, regardless of whether or not we consider ourselves to be
depressed.
Diagnosing depression can also have harmful consequences. As Horwitz and
Wakefield (2007) argues, the introduction of routine depression screening in places
like New York represents ‘a new form of social penetration of our private emotions’,
affecting our view of the abnormality of distressing feelings and enhancing the
apparent legitimacy of psychiatric interventions.
Diagnosis can mould the perceptions of doctors and their patients, who come to
see themselves as ‘depressed’ people and are encouraged to take on this mantle
when they next encounter social stresses or emotional difficulties. Ian Hacking uses
the concept of classificatory looping to describe how our methods of classifying
people interact with the people being classified, and ultimately change the nature of
these people. People are aware of being classified, in contrast to quarks, chemical
elements or rock formations. People tend to ‘act under a description’: that is to say
their ways of being ‘are by no means independent of the available descriptions
under which they may act’ (Hacking 1999). Thus when individuals are aware of the
classification they have been awarded, the way they experience themselves changes.
Their feelings and behaviours may evolve because they are so classified.
Alternatively, they may attempt to rid themselves of the classificatory system by
altering their behaviour and feelings. At the same time, those around the classified
individual – members of their immediate family, the wider community and those
professionals and institutions dealing with them – may also react and behave differ-
ently to the individual as a consequence of the classification.
More specifically, while people may value antidepressants insofar as they enable
them to return to normal functioning by reducing symptoms, they may also lose
their sense of being normal, precisely because they are having to rely on external
agents. They may wish to stop taking medication when they feel better, but fear the
consequences of so doing and hence decide to play safe and continue to take them
(Verbeek-Heida and Mathot 2006). If antidepressants are not as useful as is com-
monly supposed, then such loss of personal agency or increase in fearfulness
become important iatrogenic effects.
Negotiating Distress
These iatrogenic tendencies are unwittingly exacerbated by the prevalent metaphors

employed by GPs. We tend to use mechanical metaphors to explain diseases. We
consider patient’s problems as puzzles, and cast ourselves on the role of problem
solvers and controllers of disease. We talk about the body as a system. When talking
about psychological unease, we use words based on the physical metaphors of ten-
sion and relaxation, and speak about ways in which medication such as tranquillis-
ers may ‘affect what is a finely balanced system’ (Skelton et al. 2002). Our
explanatory practices have a strong orientation towards determinism, which is of
limited utility in an arena like depression, where in reality doctors have few answers.
These problems are further aggravated when we attempt to introduce the diagno-
sis of depression within cross-cultural perspectives (see also Kitanaka 2016).
The Cross-Cultural RE-ORDER study is part of a large mixed-method longitudi-
nal study of depression in primary care in Melbourne, Australia. It involved semi-
structured and interpreted interviews with 24 people from Vietnamese and East
Timorese communities, and five GPs (Kokanovic et al. 2010). This study posed a
central dilemma: how to integrate experiences grounded in one social context into the
matrices provided by another? We identified a tremendous collision between migrants,
whose experience was framed by patterns of alienation, traumatized self-identity, and
GPs, for whom cultural differences were seen as technical problems of practice.
Migrants saw their distress as related to housing and finance, familial disintegra-
tion, marital breakdown, intergenerational conflict, immigration issues and cultural
distance:
Oh, my first impression was that it was so cold… It was cold. From Malaysia where it was
hot, we had on only light clothing. So it was terribly cold. It was on a Saturday that we
arrived; there was no one in the city. … I thought how come there were no people in this
country. The streets were deserted. I thought now I was in another country, and I did not
know English, I did not know how I would start a new life. That was my continuing worry.
The GP perspectives focused on patients’ need for pragmatic assistance with

practical life problems:
They quite often present distress in terms of pragmatic issues that are going on like a son is
causing trouble in the family […] or it’s housing problem, or trouble with visa, or some
relational difficulty… They seem to want a pragmatic sort of help… like offering some help
with housing or an offer to see the offending member of the family.
128 C. Dowrick
Our interpretation is that the diagnosis of depression here is not a clinical entity,
but a mechanism of decoupling: it replaces loss with illness, and individualizes
previously social problems.
Changing Discourse
Medicine needs a new perspective, a theory of the person based not on passivity but
on agency and creative capacity. Human beings need a sense of meaning, of pur-
pose, an understanding of the ends of life, a belief in ourselves as valuable and
valued persons. These may be construed by some in lofty, noble and universal terms,
and by others as immediate, pragmatic, and highly personal.
Developing a conceptual framework within which to make sense of what we
know about depression, in Beyond Depression (Dowrick 2009) I propose two prin-
cipal components:
• An understanding of ourselves as coherent beings, neither wholly individualised on
the one hand, nor illusory, fragmented, or role-playing on the other; and within this,
an understanding of ourselves as persons with the capacity to lead our own lives;
• A belief that we make sense of ourselves in terms of our engagement with the
world around us: the context of the history, place or ‘practices’ within which we
find ourselves, and which we have the ability to modify; and within this, a belief
that such engagement – whether construed in political, social or personal terms –
is crucial in creating and sustaining our sense of identity and well-being.1
Within this framework we can begin to think of patients not as passive victims of
circumstance, whether that circumstance be genetic or social, but as persons with
the capacity to lead purposeful lives.
Coherence
The concept of coherence is predicated on the belief that human life has an essential
unity throughout its whole extent. We are fundamentally real and intrinsically valu-
able beings, who have the capacity to change and progress. We are predetermined
neither by our biology nor by our social roles. Coherence contains elements of
desire, memory, imagination and curiosity.
My understanding of desire derives from Spinoza’s conatus: “the endeavour by
which each thing endeavours to preserve in its being is nothing other than the actual
essence of the thing” (Spinoza 2000). It is apparent in literature with the ‘life hungry
1
Although developed independently, these concepts of coherence and engagement have strong
resonance with two bases of personality health - identity cohesion and interpersonal functioning –
in DSM-5’s alternative dimensional approach to personality disorder (American Psychiatric
Association 2013).
stupidity’ of Pi, when faced with the prospect of sharing a lifeboat with a Royal
Bengal tiger (Martel 2002); and in life, with Joe Simpson’s response to falling onto
a precarious ice bridge inside a vast Andean crevasse (Simpson 1997). The conatus
provides a basis for articulating our determination to survive, come what may.
Memories are the principle means by which we can demonstrate our sense of
continuity to ourselves, linking cognition and emotions in a way that produces a
sense of self-coherence (Wollheim 1984). They can be turned into a source of
energy, either by drawing new implications from old memories or else by expan-
sion, incorporating the experiences of others (Zeldin 1994).
Curiosity refers to our eagerness to find out about new things, our inquisitive-
ness, our sense of excitement at finding the unexpected. In 350 BC Aristotle intro-
duced his Metaphysics with the statement ‘All men by nature desire to know’ (Ross
1953). Descartes (1649/1967) agrees: our innate curiosity is an essential means of
increasing knowledge. Zeldin takes this argument a stage further. Reflecting on the
life of Alexander von Humboldt, he concludes that curiosity can be a successful
remedy against sadness and fear. If we use our personal worries as stimuli to explore
the general mystery of the universe ‘the limits of curiosity are at the frontiers of
despair’ (Zeldin 1994).
Imagination is the ability to produce ideas or images of what is not present or has
not been experienced, and the ability to deal resourcefully with unexpected or
unusual problems. The enhancement of memory by imagination can help us
‘through the traffic jams of the brain’ (Zeldin 1994). However imagination is only
liberating when it is constructive, arranging fertile marriages between images and
sensations, recombining obstacles to make them useful, spotting what is both unique
and universal in them.
Our health is related to our sense of coherence (Antonovsky 1987). A strong
sense of coherence has been directly correlated with self-rated health (Eriksson
et al. 2007), while a weak sense of coherence is significantly predictive of the onset
of depressive disorders (Lehtinen et al. 2005) and the onset of diabetes (Kouvonen
et al. 2008). Importantly, our sense of coherence is not a static set of personal attri-
butes. It can change over time, or as the result of therapeutic interventions such as
mind-body therapies (Fernros et al. 2008), and salutogenic group therapy with focus
on personal narratives, health promoting factors and active adaptation (Langeland
et al. 2006).
Engagement
Our sense of identity has important social dimensions. Language and culture are
important in defining and shaping our understanding of emotional states. They are
also highly relevant to understanding ourselves. As the Hegelian French philoso-
pher Paul Ricoeur puts it, our desire has an ‘intersubjective structure’. Our engage-
ment with the world around us is both profound and crucial. We make sense of
ourselves in terms of our engagement with the world around us: the context of the
history, place or ‘practices’ within which we find ourselves, and which we have the
130 C. Dowrick
ability to modify. Such engagement – whether construed in political, social or per-

sonal terms – is crucial in creating and sustaining our sense of identity and
well-being.
Engagement may take the form of participation in practices and moral communi-
ties, in ‘coherent and socially established cooperative human activity’ with inherent
standards of excellence (MacIntyre 1984). Practices involve the use of a set of skills
in a systematic way, with the intention of enriching our lives and the lives of those
around us. They may be self-contained, such as chess, music or sport; or purposive,
such as law and politics.
Engagement more often takes the simpler form, proposed by Charles Taylor, of
the affirmation of ordinary life through investment in our ‘webs of interlocution’:
in the family tree, in social space, in the geography of social statuses and functions, in my
intimate relations to the ones I love, and also crucially in the space of moral and spiritual
orientation within which my most important defining relations are lived out’ (Taylor 1984).
Or it may take the form of engagement with the circumstances in which we find
ourselves, whether they involve cultural alienation or physical illness, and – with
Camus’ Sysiphus, endlessly rolling his rock up the mountain – our determination to
make of them the best we can:
‘La lutte elle-même vers les sommets suffit à remplir un cœur d’homme. Il faut imaginer
Sisyphe heureux’.2 (Camus 1942)
Engagement is good for us. Absorption in pursuits and activities beyond oneself
are central to proposals for a psychology of positive emotions, aimed at understand-
ing and building on our virtues and strengths. Identifying our signature strengths
and using them in new ways can increase our happiness and reduce depressive
symptoms for at least 6 months (Seligman et al. 2005). A sense of engagement also
reduces the likelihood that low income will lead to the development of diabetes
(Tsenkova et al. 2007).
The combination of a sense of personal coherence and an engagement with the
world around us enhances our sense of personal resilience, the capacity to maintain
or regain well-being in the face of adversity (Ryff 2014). Adopting strategies to
enhance personal resilience improves outcomes for people diagnosed with depres-
sive disorders in primary care (Griffiths et al. 2015).
Implications
What we clinicians should do, in our encounters with patients whom we think may
be depressed, is to help generate meaning and purpose out of suffering and distress.
This is the essence of healing.
Scott and colleagues (2008) provide persuasive qualitative evidence that high
quality primary care consultations can enable meaning-making. Trust, hope, and a
2
The struggle itself towards the heights is enough to fill a man’s heart. We should imagine that
Sisyphus is happy.
sense of being known, can be fostered within the clinical encounter, especially if we
value and create a non-judgmental emotional bond with the patient, manage our
power in ways that provide most benefit for the patient, and display a commitment
to caring over time. We are more likely to achieve this if we have self-confidence,
emotional self-management, mindfulness, and knowledge.
At the heart of the healing process lie two assumptions. The first assumption is
that the emergence of meaning, order or form is therapeutic in itself, particularly for
people who are feeling lost, alone, frightened or misunderstood (Gask et al. 2003).
The second assumption is that such emergence is most effective if it is mutual, if we
find ways of engaging with our patient’s conceptual worlds, if understanding of
problems and their solutions are negotiated and agreed by both sides, not just
imposed arbitrarily by the doctor.
The emergence of meaning is an imaginative construction, built by processes
which take the event of a life and mould them into a coherent narrative. The doctor
must be able to use their imagination empathically and thereby enter the patient’s
world. The solution comes in seeking more detail, however small, in the reality of
the patient’s life. Each detail triggers new scope for the imagination, a renewed pos-
sibility of empathy and a much increased chance of the patient feeling heard. Heath
(1999) reminds us that as doctors we have a ‘responsibility to locate hope through
the glimpse of an alternative’.
The diagnosis of depression, as currently deployed, is too rigid and restrictive to
be useful in primary care. We do better with less diagnosis and more understanding,
with fewer prescriptions and more listening; and with a view of our patients not as
machines in need of an overhaul, but as persons leading their lives. We should see
the experience of illness through the patient’s eyes (McWhinney 2000), and focus
with patients on enhancing a sense of coherence and engagement with social roles.
We can usefully build on two key elements of the medical encounter: the acknowl-
edgment of suffering, and the offer of hope.
The adjectives depressing and depressed are generally safer than the noun
depression. Adjectives by definition must be related to a subject other than them-
selves, whereas a noun assumes an independent state, a thing in itself. Saying to
someone ‘you must have found that really depressing’ is powerful for two reasons:
it offers the possibilities of empathy, and indicates that the core problem is outside –
not inside – that person. As a clinician, I am relatively comfortable talking with
patients about ‘feeling depressed’, or ‘having depressed thoughts’ since these
phrases refer to specific sensations and experiences and are not defining of the
patient as a whole. The statement ‘I think you are depressed’ is more troublesome.
Although it allows for several possible interpretations, it is explicitly making a glob-
ally defining statement about the other person, and when made by a doctor to a
patient it is more likely than not to be understood as conferring formal clinical status
on their problems.
To provide high quality care we need to work across biomedical and social per-
spectives, and engage at both individual and community levels (Furler et al. 2010).
We should pay careful attention to our patients’ perspectives on what may be caus-
ing their problems, not least because these may be radically different from our own.
We should be sensitive when elucidating their health beliefs, when enquiring about
132 C. Dowrick
the ways in which they make sense of their experiences. Although patients may
sometimes have clear and consistent explanatory models, they often hold beliefs
about the cause of their problems which are tentative and fluid, sometimes internally
contradictory, and characterised by uncertainty (Kokanovic et al. 2013).
We should look carefully at the ways in which general practice delivers mental
health care, and how this may impact on patients’ illness experience. Many people
with high levels of mental distress are currently disadvantaged: either because they
are unable to access care, or because when they do have access to care it does not
address their needs (Dowrick et al. 2009). We have demonstrated the benefits of a
new multi-faceted model of care with three principal components: increasing com-
munity aweareness that primary care can provide help for common mental health
problems; increasing the competence of primary care teams in understanding and
responding to the differing ways in which people present suffering; and tailoring
psychosocial interventions to meet the needs of people from under-served groups
(Dowrick et al. 2013).
We need to reorient our assumptions about the nature and purpose of the consul-
tation, and revise our understanding of our patients: not as passive victims of dis-
ease or circumstance but as active agents, experts in leading their lives, who
occasionally need some help, some new ways of looking at old ideas, and perhaps
an instillation of hope.
We need to acknowledge and take seriously the misery, suffering, loss and grief
that they bring with them into the consulting room. Empathy is crucial: even in set-
tings of high social deprivation, it increases patients’ sense of enablement and pre-
dicts change in their feeling of well-being (Mercer et al. 2008). So is our ability to
listen, and then listen even more. Ronald Epstein (1999) encourages clinicians to
expand our attentiveness, curiosity and presence. He argues that we should cultivate
habits of mind such as experiencing information as novel, thinking of “facts” as
conditional, seeing situations from multiple perspectives, suspending categorization
and judgment and engaging in self-questioning. Mindful practice is not easy: it
requires mentorship and guidance. But its goal of ‘compassionate informed action
in the world’ is of high intrinsic and instrumental value.
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An Insider View on the Making of the First
French National Information Campaign About
Depression
Xavier Briffault
Abstract The first national public health information campaign on depression –

“Depression, know more about it to get out of it” – was implemented in France in
2007, nearly 20 years after the first campaign on this topic was initiated in the
United States by the NIMH. The chapter is based on an observant participation by
the author, who has been involved in the making of the campaign at all stages and
levels of its design and implementation; it will present the multiple logics that
occurred in shaping the campaign messages for the general public and health
professionals.
The chapter will examine the exchanges and documents (e-mails, meetings,
forums, successive versions of the final documents…) produced by and between the
various stakeholders involved in the design of the campaign during the entire pro-
cess (experts from different backgrounds, professional associations, government
agencies, institutes of quantitative and qualitative surveys, user groups, communica-
tion departments and agencies, designers, health professionals of various types,
depressed people, general public…) and their contributions to the making of the
final content of the campaign.
We will particularly highlight how conflicts are negotiated between apparently
irreconcilable positions of actors whose ideological presuppositions, professional
interests, working methods, and categories of analysis diverge, within a EBM
framework strictly imposed by the public health agency supporting the campaign,
and the constraints that this whole system imposed on the answer that could be
proposed to the original question: “Depression, how to get out of it?”.
X. Briffault (*)
French National Scientific Research Center, Cermes3 (Centre de recherche, médecine,
sciences, santé, santé mentale, société), Paris, France

DOI 10.1007/978-94-017-7423-9_10
138 X. Briffault
Introduction
Information campaigns on public health are not restricted to physical illness or

usual hygienist recommendations (tobacco, alcohol, nutrition, sexual health…).
They also extend to mental health issues. Many public health institutions, including
the WHO, recommend the use of information campaigns in the field of mental dis-
orders, particularly depression (Dumesnil and Verger 2009).
The first French national public health information campaign on depression, “La
dépression, en savoir plus pour en sortir”,1 was implemented in 2007, nearly 20
years after the first campaign on this topic was initiated in the United States by the
NIMH (the DART2 and the NDSD3 projects – see below). This chapter is based on
the author’s participant observation; he was involved in the making of this campaign
at all stages and levels of design and implementation (Briffault et al. 2008; 2010a,
b, c; Briffault and Beck 2009; Beck et al. 2009a, b). This privileged access to inter-
nal communications (minutes of meetings, emails, comments on documents…)
allows for the analysis of the multiple logics involved in shaping the messages of the
campaign for the general public as well as for health professionals. For ethical rea-
sons, only data directly involved in the production of content for the campaign are
used here, and all content is presented anonymously, as well as the name of the
public health organization supporting the campaign (replaced with “the Agency”).
This chapter will specifically focus on how conflicts were negotiated between
apparently irreconcilable positions of actors whose ideological presuppositions,
professional interests, working methods, and categories of analysis were divergent.
These conflicts occurred in an Evidence-Based Medicine (EBM) framework strictly
imposed by the public body supporting the campaign, and within the constraints
imposed on the whole system by the intention to respond to the initial question:
“depression, how to get out of it?”
A Brief History of Information Campaigns About Depression
Since the first national information campaign on depression for the general public,
called the “Depression Awareness, Recognition and Treatment” – DART, USA
(Regier et al. 1988), many others followed in different countries: in 1991, still in the
U.S., the “National Depression Screening Day” (NDSD) – which from this time
became a recurring event (Magruder et al. 1995; Greenfield et al. 1997, 2000); in
1992, in the United Kingdom, the “Defeat Depression Campaign” (Baldwin et al.
1996; Priest et al. 1996; Paykel et al. 1997, 1998; Moncrieff and Moncrieff 1999;
Rix et al. 1999; Paton et al. 2001); in 1997, still in the UK, the campaign Changing
Minds (Crisp et al. 2000, 2005; Benbow 2007); in 2000, in Australia, the campaign
1
Depression, knowing more about it to get out of it.
2
Depression Awareness, Recognition and Treatment.
3
National Depression Screening Day.
An Insider View on the Making of the First French National Information Campaign… 139
Beyond Blue (Ellis and Smith 2002; Parslow and Jorm 2002; Jorm et al. 2005, 2006;
Highet et al. 2006); in 2001, the campaign NAAD (Nuremberg Alliance Against
Depression) (Althaus and Hegerl 2003), followed by the campaign EAAD
(European Alliance Against Depression) (Hegerl et al. 2006, 2007); in 2003, in the
United States, a campaign targeted at men, Real Men, Real Depression (Rochlen
et al. 2005, 2006); in Scotland in 2005, the campaign Doing Well (McCollam et al.
2006); and finally, in 2007 in France, the campaign of the Agency “La dépression,
en savoir plus pour en sortir” (Briffault et al. 2007); for a more detailed review see
(Dumesnil and Verger 2009), and (Quinn et al. 2013) (Kravitz et al. 2013) (Lanfredi
et al. 2013) for the many other campaigns that continued to flourish after 2007.
Internationalized Rhetoric and Categories
Information campaigns on public health are presented as vectors of public informa-

tion on disorders and their treatment and claim to be based on scientific data.
However, these campaigns do not only provide the population supposedly “neutral”
information originating from scientific research; they make choices based on their
objectives, the strategies used to achieve them, the scientific paradigms on which
they are based and the influences of various social actors involved in the design of
messages. In addition, the scientific foundations on which they are based, for exam-
ple the chosen nosographic options, do themselves carry specific orientations that
shape the content that can be produced from the initial rational and axiomatic
(Horwitz and Wakefield 2007; Kirk and Kutchins 1992).
In this, the messages broadcast by the national campaigns are not only informa-
tive, but also, to speak like the philosopher J.L. Austin, “performative”: they estab-
lish, through the legitimacy and communication power of the institutions that
support them, a definition of mental disorders, mental health, and psyche, and they
carry a specific anthropology. If this performative dimension does exist in each kind
of public health communication, it is especially operative in the case of mental
problems. These do indeed rely little or not at all on any identified pathophysiology,
and their definitions – which are not at all consensual – set the boundaries of normal
and pathological as well as (see Horwitz and Wakefield, this volume) or even more
than, they describe them (Kendell and Jablensky 2003). Public communication pro-
vides terms and meaning of terms, conceptual organizations, relational grammars,
forms of organization of social relations (role of patient, role of peers…) that par-
ticipate in the social definition of disorders (Ehrenberg 2006a, 2004b; Jorm 2006).
Initiated by the National Institute For Mental Health (NIMH), the first informa-
tion program on depression in the world, DART, and its successor, NDSD, imple-
mented a rhetorical structure and content that flourished in subsequent campaigns;
these are found almost identically in subsequent campaigns in other countries, as
well as in the French campaign that we are considering here. This rhetorical struc-
ture takes the following form (the details of this analysis are developed in [Briffault
et al. 2010a]): (1) there exists an observable, isolable and characterizable entity,
namely depression; (2) this entity has serious individual and collective conse-
140 X. Briffault
quences; (3) those who are affected are stigmatized, despite the fact that; (4) depres-
sion is a disease; (5) that is very common and can affect anyone at any time; (6) for
which affected people are not responsible; (7) this disease is complex, poorly under-
stood, and has multifactorial origins, without any specific cause that can be identi-
fied; (8) however, there exist effective treatments, pharmacological and
psychotherapeutic; (9) but they are too scarcely used or are too often misused;
(10) and the disease is often incorrectly identified/diagnosed or diagnosed only with
difficulty; finally, (11) the use of services provided by competent professionals
capable of delivering these treatments is too low. To address these shortcomings,
(12) professional and general public information about depression is necessary.
How does this rhetorical structure, based on a set of implicit and explicit set of
theoretical assumptions, happen to be used in the French campaign, and how do the
various stakeholders involved in the design of the campaign fit into it? This what we
will describe in examining from the inside the vicissitudes of the central question of
the definition of depression, its treatment, and its relations to the various profes-
sional jurisdictions (Abbott 1988).
The Institutional Order and How the Campaign Is Made
The report of the first meeting of the group of experts convened by the Agency
(2005b) states that “an information program to inform the general public and gen-
eral practitioners about depressive disorders and possibilities of treatment is in
preparation by the Agency since the spring of 2004”. The “strategic orientation of
the information campaign” has been defined as “a first working group consisting of
the main departments of the Ministry of Health and Solidarity (DGS,4 DGAS,5
DHOS,6 DREES7), HAS,8 AFSSAPS9 and INSERM10 [that] met from September
2004 to May 2005”. This group has produced a draft document: “Depressive disor-
ders: definition and management. Summary of French Recommendations” (Agency
2005e). This campaign is part of the “no. 1 strategic axis of the mental health pro-
gram of the Agency: to inform the general public about depressive disorders,
treatment options and care pathways in France” (Agency 2005d), which is stated to
derive from the objective n°60 of the Law n°2004-806 of 9 August 2004 on public
health policy, which is formulated as follows:
4
Direction Générale de la Santé.
5
Direction Générale de l’Action Sociale.
6
Direction de l’Hospitalisation et de l’Organisation des Soins.
7
Direction de la Recherche, des Etudes, de l’Evaluation et des Statistiques.
8
Haute Autorité de Santé.
9
Agence Française de Sécurité Sanitaire des Produits de Santé.
10
Institut National de la Santé et des Recherches Médicales.
Bipolar, depressive and neurotic disorder: increase by 20 % the number of people suffering
from bipolar, depressive, neurotic and anxious disorders that are treated in accordance with
good practice recommendations. Prior goal: Develop and validate screening instruments.
Indicators: Number of people suffering from depressive, neurotic or anxious disorders that
are treated in accordance with good practice recommendations (Française 2004).
This n°60 objective, as specified for example in the explanations given to com-
munication agencies in charge of the media campaign (TV, radio) (Agency 2005a),
comes from:
The axis 1.1 of the “Psychiatry and Mental Health” plan (2005–2008) of the Ministry of
Health: “Better inform and prevent” which plans to implement several large public com-
munication campaigns between 2006 and 2009 in order to “let the public know main dis-
eases, their causes, symptoms and treatments, in order to change perceptions and improve
in the long term medical monitoring of people with mental disorders” (santé 2004).
It is specified in the plan that “the content of the information will be drawn from
the collective expertise of INSERM, the national and international best practice
recommendations and the latest scientific data in the field” and that “the messages
will be declined in one or more media tailored to different audiences”.
The plan also states that “recommendations have been made by various national
and international organizations including WHO (OMS 2001) and the “International
Consensus Group on Depression and Anxiety” ” (Ballenger et al. 2001) and that “a
number of countries and international organizations have already implemented such
actions (United Kingdom, Canada, USA)”.
It is also asserted, without any bibliographical reference, that “the scientific eval-
uation of these campaigns showed that they had a positive impact on knowledge and
attitudes of people in terms of mental health and care, and that they could also
encourage the use of services”. The work program of the Agency states that “the
information [will be developed according to the guidelines of the plan] and will be
studied with working groups involving the DGS and other departments concerned
(DHOS, DGAS…), different agencies and health institutes (ANAES, AFSSAPS,
Inserm…), professional associations and mental health users and professionals”.
The budget forwarded by the plan for the campaign is € 7 million. The main tool
of the campaign is a paper information booklet (88 pages), of which the campaign
distributed nearly one million copies, accompanied by a website11 that contains con-
tent in a form suitable for use online, and by a major media campaign (TV, radio).
A Redaction Group Mainly Composed of Medically

Oriented Experts
The group of experts involved in the design of the information campaign includes a
sub-group dedicated to the drafting of the final information booklet (Agency 2007)
and presented as “authors,” and a second sub-group dedicated to reviewing and
11
https://www.info-depression.fr/
142 X. Briffault
control, presented under the heading “This guide has been produced with the
assistance of …”.
The first sub-group of authors includes 7 people: a psychologist heading the
“Maison des usagers”12 at Sainte-Anne Hospital (Paris); a representative of the
National Federation of Former Psychiatric Patients (FNAP-PSY); a physician rep-
resenting the national health insurance; a psychiatrist from the hospital of Saint-
Antoine (Paris); a psychiatrist specialized in suicide from the hospital of Lyon I; a
representative of the France Depression Association13; and a social scientist special-
ized in mental health (the author of this chapter). These authors do act intuitu
personae as experts of their respective fields, although the two representatives of
associations also act as representatives of their users and their interests.
The second sub-group – reviewing and control – includes, in addition to the pre-
vious people, some fifteen people: a representative of the French Federation of
Psychiatry (FFP)14; a representative of the general practitioners; a representative of
the French Federation of Psychologists (FFPP)15; a representative of the French
Federation of Psychotherapy (FF2P)16; a representative of the School for Parents
and Educators17; a representative of the National Union for Suicide Prevention18; a
representative of the National Union of Families and Friends of Mentally Ill Persons
(UNAFAM)19; a representative from the collective expertise center of INSERM20
and some representatives of AFSSAPS21 and HAS.22 These experts act as represen-
tatives of their respective professional groups.
The DSM, the Inescapable Frontier between Normal

and Pathological
The design of the campaign takes place in a difficult French context, which differs
from the context encountered in Britain or the United States. The French context is
marked by various controversies occurring in the field of mental health, especially
regarding the effortful development of legislation on the use of the title of psycho-
therapist and the publication by INSERM of two controversial reports (INSERM
12
https://www.ch-sainte-anne.fr/site/centrhosp/usagers/maison.html
13
https://www.france-depression.org/
14
https://psydoc-fr.broca.inserm.fr/
15
https://www.psychologues-psychologie.net/
16
https://www.ff2p.fr/
17
https://www.ecoledesparents.org/
18
https://www.infosuicide.org/
19
https://www.unafam.org/
20
https://www.inserm.fr/qu-est-ce-que-l-inserm/missions-de-l-institut/mission-expertise
21
https://ansm.sante.fr/
22
https://www.has-sante.fr
2004, 2005) that generated important ideological conflicts (Briffault 2009; Thurin
and Briffault 2006; Ehrenberg 2004c, 2006b, 2007; CCNE 2006). In this context,
one of the central concerns of the Agency and group of experts is to avoid raising
new controversies. In particular, great care is taken not to excessively “medicalize”
depressive states, not to suggest that more and more “existential anxiety” will be
included in the jurisdiction of psychiatry, and in particular, not to overly promote
psychopharmacology and give the impression that the pharmaceutical industry is
covertly influencing the campaign. It is thus stated in the literature review given to
the experts by the Agency that:
Mental and behavior disorders are not just variations within the limits of “normal”, but are
clearly abnormal or pathological phenomena. To be considered as such, the anomalies
should be permanent or repeated, and cause distress or disability in one or more than one
areas of everyday life” (WHO, 2001). Periods of sadness, depression or discouragement are
part of the normal human feelings and experiences. These are common reactions encoun-
tered in face of various difficulties of life. They can be linked with personal, relational or
social difficulties or appear without real cause. To talk about depression in terms of pathol-
ogy, it is necessary that a number of criteria (symptoms, severity, duration, psychological
distress, social disabilities) be present (Agency 2005e).
This laudable attempt to not let “normal sadness” (Horwitz and Wakefield 2007)
be lumped into the jurisdiction (Abbott 1988) of psychiatric depressive disorders,
however, faces a problem: as the problem has been formulated in the initial institu-
tional order and review of the literature that has resulted, the reference to the inter-
national DSM and ICD psychiatric nosology for the definition of these pathological
criteria cannot be avoided, since it is explicitly stated that:
These criteria are defined in the manuals of psychiatric diagnoses. The Diagnostic and
Statistical Manual of Mental Disorders (DSM-IV) and the International Classification of
Mental and Behavioural Disorders (ICD-10) present the totality of mental disorders and
behaviors. They list the pathologies, define the various disorders and their symptoms and
enable to formulate psychiatric diagnosis.
Since the campaign is being conducted by a governmental agency of a country

(France) affiliated to the WHO (OMS 1986, 1998, 2005), the reference to the world-
wide organization is mandatory, as well as the use of its particular conception of
mental disorders and their diagnosis:
WHO (2001) states that “the symptoms and signs have been defined with precision to
ensure uniform application”, that “the diagnostic criteria were standardized at international
level” and that “we can now diagnose mental disorders with the same certainty and preci-
sion as most common physical disorders” (Agency 2005c, 2005e).
Thus, it is for reasons of logical articulation of categories and a required compli-

ance with the initial institutional order that the DSM (ICD being, in fact, never actu-
ally used, mainly because most scientific publications about depression use the
DSM criterions) becomes the border guard on the passage from a common “depres-
sive ill-being” to an internationally standardized “depressive pathology”, conceptu-
alized with a logic similar to that used for “common physical disorders”. This is
reflected in the working documents (original format) in which DSM criterions are
used as the dividing line between normal and pathological as follows:
144 X. Briffault
Sub-goals METHODS
1.1 Enable (self) identification of depressed Definition of depressive disorders according to
people in need of care the DSM-IV symptoms, psychological
distress, disability.
Questionnaire (CIDIsf = DSM-IV).
Testimonials
3.1 Enable (self) identification of individuals Presentation of depressive ill-being:
with non-pathological depressive ill-being Differences between normal emotions and
major depressive disorder (DSM-IV,
ICD-10).
Different types of depressive ill-being.
Questionnaire (CIDIsf = DSM-IV).
Testimonies.
Psychoanalytic Clinical Approach against Public Health

Psychiatric Epidemiology
This general orientation of the project initially raises few objections within the
experts group, as well as the first draft of the final booklet written in this general
inspiration, as can be seen in an email from the head of communication service of
the Agency who wrote: “We have sent the booklet to various experts, so far there
have been mostly positive and constructive comments about the booklet”. But things
deteriorate with the comments made23 by the representative of the French Federation
of Psychiatry (FFP), on which we will focus now, since they are particularly repre-
sentative of the violent conflict between the logic of public health mental health
brought by government agencies and the logic supported by a still dominant part of
French psychiatry that reasons from a psychoanalytic clinical point of view
(Jeammet 1996; Effenterre et al. 2012; Gansel 2014; Lézé 2010), and of the present
status of this conflict.
These comments are announced by the head of communication service of the
Agency in a letter to a psychiatrist member of the experts group whom she seeks to
align with the Agency against the criticisms of the FFP:
However we received this morning some extremely aggressive comments from the FPP (see
attached). [The Director of the Agency] and [the Director of Scientific Affairs] will be pres-
ent at the beginning of February 9 meeting to answer the FFP but we know it will be very
useful for us if psychiatrists, other than the representative of the FFP, may be present to
counteract their speech (mail 30/01/2007).24
The head of scientific affairs says in response:
23
Received 29 janvier 2007.
24
All the mails used in this chapter were originally written in french, and translated in english by
the author of this chapter.
How to find an agreement with some psychiatrists who contest the very notion of diagnosis
of depression from a list of criteria (or symptoms) (DSM, CIDI). It seems to me that we are
constrained in such a document to have a public health and epidemiology of mental health
approach and cannot enter into a diagnostic approach such as experienced by clinical spe-
cialists. How to get out of this problem? Moreover, we feel that we will be presented the
usual equations: DSM-IV = anti-psychoanalytic attitude = reducing to symptoms = influence
of Big Pharma (mail 30/01/2007).
As a matter of fact, these “equations” will take place in the comments of the FFP
associated with different elements of the text of the booklet.
Extension of the Depressive Domain
The FFP criticisms written in the document joined to the mail sent by the head of
communication service of the Agency first bear on the indefinite extension of the
depression diagnosis that would result from adopting the DSM-IV criteria used in
the booklet to define depression.
Thus, for the minimum duration of two weeks of symptoms, the experts repre-
senting the FFP affix the following comment to the draft of the booklet: “Two
weeks, even if this is the definition, it is a promotion of depression”.
Regarding the affirmation of the booklet that “the state experienced during
depression is characterized by […] an extraordinary sadness, not a continuum with
normal sadness”: “It is an open door to everything despite the shade”.
On a table that presents two pages of the symptoms of depression, “this is a ‘cata-
logue à la Prévert’, I do not know who would not be depressed”.
Regarding the precision that “postpartum depressive episode (after delivery)
should not be confused with the ‘baby blues,’ that is a transitory depressive state”:
“it does not mean anything and it opens the door to all drift, it is absolutely not suit-
able for the term baby blues”.
Regarding the self-assessment questionnaire of depressive symptoms (CIDI
directly issued from WHO (OMS)), that is still associated to the warning: “This
questionnaire is designed to help you identify the symptoms of depression. It is by
no means a diagnosis. A diagnosis of depression is a complex procedure, which
requires taking into account all of your symptoms, your situation, your background,
your personality…”: “Is this a quiz to promote depression? I think we are going to
prescribe a lot of drugs after the publication of this document, is the pharmaceutical
industry part of sponsors? We should ask them a financial support”.
Regarding the exclusion criteria of the diagnosis of Major Depressive Episode in
a situation of grief formulated as “in the weeks following the loss of a loved one, it
is common to experience depressive symptoms that are part of the normal grieving
process. It is only if these symptoms persist over a long period (over 2 months) or if
they have excessive impact on the person that it is necessary to treat”: “this is where
the problem lies, depression reduced to symptoms is associated to the fact that
symptoms define depression and causes an infinite extension of the term depression,
this is particularly inappropriate”.
146 X. Briffault
Regarding the question “During the last two weeks have you felt (e) sad,
depressed (e), hopeless (almost) all day, (almost) every day?”: “the game is over, the
presupposition is here, a symbolic equation between a list of symptoms and depres-
sion, between the word depression used by lay people and depression”.
A Structural Conflict
The rudeness of the style used is absolutely not unusual in the French world of psy-
chiatry and mental health. The style is even rather polite when compared to the
comments made on the occasion of the release of the campaign in the editorial of
No. 7 “Nouvel Ane”, a journal of the Ecole de la Cause Freudienne (ECF),25 written
by a psychiatrist-psychoanalyst:
[untranslatable play of words based on the acronym of the Agency] “Pestilence”? See the
dictionary: “stench, putrid miasma, infection”. The Agency has launched a massive nation-
wide campaign of disinformation on depression in adults, with TV spots, radio spots, a
guide distributed to one million copies, brochures; media add: interviews, testimonies, pho-
tos. Surveys? There are few or not at all. This unprecedented hype is intended to impose
seven theses: (1) that depression exists and (2) that it is a disease, and (3) that it is gaining
ground in society to the point of becoming a public health problem, and that (4) develop-
ment of medical care is therefore urgently needed, (5) it can be treated with medication and
conditioning; (6) that depression has no existential dimension; (7) that psychoanalysis is of
no use. Huge financial means from the State budget, not without the contribution, at least
indirectly, of pharmaceutical industries, have been serving the unilateral promotion of these
seven theses, all highly questionable.
Beyond the excesses of words that seem to suggest that something fundamental
is being attacked, the text sheds light on seven critical points that correspond to the
rhetorical structure initiated by the NIHM (see above). These seven points render
the campaign of the Agency unacceptable for the ECF as well as for the FFP. These
points are subsumed by the FFP under the question “structure or symptoms”. Thus,
about the “excessive consequences” of depressive symptoms that would justify the
use of medical care in mourning, FFP wrote “excessive? What is it? You suffer too
much from the loss of your child? This is again the problem of using a catalog of
symptoms to define a disease (and not the underlying structure)”. In other places,
“They are all lining up to get into services and have a consultation yet, in contrast if
you take the diagnosis by structure and not by symptoms it is clear that psychotic
depressions and melancholies do not ask help”; “psychiatrists appear only in the
second line, for sure if it is for the kind of depression detected by the test it is prefer-
able (because everybody is concerned, including those who are hysterical, hypo-
chondriacal, obsessive, psychasthenic, and others), but for depressive persons as we
diagnose them, psychiatrists should be first for evaluation and it is not a question of
severity, but of structure”.
25
https://www.causefreudienne.net/
“Structure” has long played a key role in the French intellectual debates in soci-
ology and psychology, and even more so in psychopathology due in particular to the
fact that the theories of Jacques Lacan, one of the most influent psychoanalysts in
France, who relied heavily on this conceptualization of human beings (Corvez
1968; Kurzweil 1980). Together with the structure, it is the question of the meaning
of symptoms that is raised by the FFP, depression being seen in this approach as a
symptom integrated and having a meaning inside a psychic structure and not as a
disease that has symptoms. Thus, a sentence in the booklet stating that “depression
can manifest itself through excessive behaviors: alcohol, scarifications (cuts on pur-
pose), states of agitation, verbal violence…” is deprecated by the French Federation
of Psychiatry in their comments of the draft booklet in the following terms: “Society
of soft-drinks, coca-cola, hamburger and in no case Camembert.26 Alcohol use etc…
are not excessive behaviors and their pathological character is not determined by
whether they are excessive or not but by the meaning they have”. In addition to the
criticism addressed incidentally to the American culture from which the DSM
comes, it is the very possibility of isolating the symptoms from the meaning they
have for the patient that is questioned here. As a logical consequence, all the neuro-
biological explanations of depression (explanations by causes rather than by rea-
sons) are violently disqualified by FFP on behalf of French psychiatry: “very bad,
Reader’s Digest of unassimilated false science at all levels [] it is everything and
nothing, meaningless. Explanation without interest, the alibi for the scientist to say
that this is a real illness, ‘to exonerate’ as it is fashionable to say”. Logically, psy-
chopharmacological recommendations, based on the neurobiological theories of
depression, are also disqualified by this criticism. About the phrase “the duration of
treatment of a depressive episode is therefore usually between 6 months and 1 year”:
“Wow, the pharmaceutical industry managed to convince everyone and now the
machine will operate”.
This conception of depression means that the position defended by the booklet,
which is to send “people with major depressive disorder” – and not “depressed per-
sons” – first to the general practitioner is unacceptable for the FFP, as well as the
idea that psychiatric consultation might not be at once and always psychotherapeu-
tic: “We do not agree on the implicit message of the booklet that psychiatrists are
only second line”. About the phrase: “the psychiatrist may also recommend to
undergo psychotherapy”: “Seeing a psychiatrist is having a psychotherapeutic rela-
tionship, it is not separated from his act even if he gives drugs”. The idea that psy-
chiatrists are “inherently” psychotherapists, and even the only possible
psychotherapists amongst all medical or mental health professions, is a position that
has been defended for decades by French psychiatrists (see for example [Hanon
2001] for more details).
26
“Camenbert” is a French cheese made from unpasteurized cow milk that is quite strong in taste
and smell. It is taken here as representative of a (supposed) French culture that would like and
accept strong real things (psychoanalytical psychopathology) as opposed to a (supposed) American
culture that would produce only pasteurized safe, fake, and tasteless things (DSM
psychopathology).
148 X. Briffault
From Casus Belli…
For FFP holding this position is indeed a casus belli. They write in their comments
“psychotherapy is an act that is inseparable from the act of the psychiatrist, it is not
after, and this formulation is a condition of our agreement to the text, otherwise we
will not sign [the agreement for publishing the booklet]” – thus relaying the domi-
nant position defended for decades by French psychiatry that any psychiatrist is “in
essence” a psychotherapist, a position that indeed does not really correspond to the
quite incomplete training in psychotherapy that French psychiatrists have today
(Effenterre et al. 2012, 2013). They write: “we ask that the term psychodynamic
psychotherapy appears and be referenced as THE psychotherapy that occurs con-
comitantly with the psychiatric consultation”. As a matter of fact, the way FFP
conceptualizes psychotherapy is psychodynamic. About a paragraph in the booklet
that reads as follows:
Specific psychological mechanisms are also involved in depression: chronic feelings of
loss, psychic conflicts, negative beliefs, low self-esteem (e.g. I can not do anything right,
I’m no good …). Some may find their origin in childhood, others may be linked to actual
situations. The quality of early attachment relationships, significant experiences during
childhood that may have been accompanied by a feeling of loss, loneliness, helplessness,
guilt or shame, the consequences of traumatic situations or mourning (not only a person, but
an ideal, or self-image), cognitive, emotional, and relational styles, specific modes of psy-
chological defenses can play a role. */ The negative beliefs, or an excessive focus on the
most pessimistic outlook, may also apply to the world around the person and his future.
Certain events of everyday life, analyzed in their most negative angle automatically trigger
in a depressed person a style of depressive thoughts without it being possible to use its other
positive experiences. It is by acting on these psychic functioning problems that psycho-
therapy has an effect on depression. */
the associated comment is:

If you insist on this very poorly written chapter, I propose the following paragraph: There
are actually numerous mechanisms involved in the genesis of depression to be identified by
a professional, specifically for each person. However, whatever the mechanisms involved,
the depression is always a crisis characterized by a temporary or permanent inability to
develop an acceptable compromise between the dynamic tension existing between the
psyche and the reality on the one hand, the different forces at work in the psyche of the
other.27
These elements – singularity of the mechanisms involved, reference to a profes-

sional having the skills to detect and understand these singular mechanisms, conflict
between reality and psyche on the one hand and between the internal psychological
dynamics on the other – are ones in which we recognize the fundamental Freudian
approach of the psyche and its problems. They are completely antithetical to the
logic driven by the DSM-IV and Evidence-Based Mental Medicine (EBMM), that
results in: standardized nosographies, strictly symptomatic approaches without ref-
erence to the “unobservable” psychopathological underlying dynamics, standard-
27
About the section between /* and */ that is from cognitive-behavioral inspiration, the added com-
ment is « non sense ».
ized diagnostic procedures that require ideally almost no other expertise than the
application of decision trees based on algorithms (First et al. 2002), and statistical
evaluation of the effectiveness of standardized treatments as measured by standard-
ized quantitative indicators using “uniform” groups, at least from the point of view
of the nosography used (Briffault and Martin 2011).
We can see two approaches in this ideological conflict that involve radically dif-
ferent anthropological and epistemological positions (Briffault 2008; Castel 2006,
2010; Ehrenberg 2004c; Descombes 1995, 1996). Yet, far from generating a reflex-
ive collective feedback on the content of the booklet and the categories used, the
conflict between the two approaches is engaged and continues in a balance of power.
FFP is the first to engage this positioning by accompanying the consignment of its
comments by the following requirements, all of them trying to reinforce the leader-
ship of the psychiatrist and of psychodynamic psychotherapy in the French mental
health field:
Four of my remarks are essential for FFP:
1. The removal of some chapters.
2. The place of the psychiatrist.
3. The place of psychotherapy as inseparable from the psychiatric consultation.
4. The place of psychodynamic psychotherapy.
Without these elements I do not see how the FFP could sign the document but I’m sure
these comments will be taken into consideration.
…to statu quo ante bellum
Receipt of the Agency is unfriendly, as illustrated by the message of the head of the
communication service: “The comments of the FFP are saddening and they reveal
an undisguised evil spirit. I wonder if we should not send a written response signed
by the Director of the Agency”. In fact, it is an appeal to authority that will be cho-
sen to solve the problem. During the meeting of the experts group on February, 9
2007, not only the director of the Agency, but also the assistant director of DGS
(Direction Générale de la Santé28), solicited for his support, will come at the begin-
ning of the meeting to say again that:
Summary and priority messages of this book were presented and validated by the expert
group (now reunited) in April 2006.
and that
The purpose of today’s meeting is to validate the booklet. Its presentation will then be
reworked by an editor to homogenize the writing style.
28
An equivalent of the Surgeon General in the USA.
150 X. Briffault
No place is given for major changes in the booklet, and even less for its main
orientations. It is also clear in the notes written for the oral presentation in presence
of the experts that:
We received a number of very constructive comments that can for most of them be very
easily integrated. On the other hand, some remarks (see if we mention FFP) cannot be inte-
grated because they question the very logic of the document (explain why in 3 lines).
The so-called “three lines” consist in a reaffirmation of “the evidence-based ori-

entation of the booklet, which requires going further than single expert opinions, to
be based on data published in the international scientific literature”. This orientation
implies, in fact, the use of DSM, since so-called “evidence-based” studies all use
this nosological standard to characterize depression. The Director of the Agency
and assistant Director of the DGS then join together during the opening of the meet-
ing to reaffirm that the use of DSM is not negotiable, and that the general direction
of the booklet is not negotiable either, without directly addressing any of the com-
ments made by the FFP, avoiding thus an overt conflict.
In truth, none of the “imperative” requirements of FFP will be satisfied. The term
“psychodynamic” will not appear in the book, nor the term “psychoanalysis” or any
other “brand name” of psychotherapy. No section will be removed, and the size of
the booklet will not be diminished. The term “disease” to describe depression will
be used 68 times in the 88-pages booklet. CIDI questionnaire will not be deleted
even if the count of symptoms will not be mentioned – it will be replaced by the
phrase “if you have observed several of these symptoms, this is a warning signal
that should encourage you to talk with a doctor”. Neither the place and role of the
psychiatrists will be changed: they remain in second line after GPs for diagnosing
and treating depression, have a specific role in prescribing psychotherapy, but are on
par with clinical psychologists for their implementation.
Vae Victis
The brief analysis that we have proposed illustrates the central, inescapable, and
uncontestable place occupied by the DSM in the first French campaign about
depression aimed at the general public, similar in this respect to other previous cam-
paigns in other countries. This central role does not emerge from the interactions
between experts to address the problem of what information is relevant to the gen-
eral public about depression; it is raised at the outset and is a direct result of the way
in which problems are initially formulated in institutional demand, including legis-
lation that is binding on state agencies that implement this type of campaign.
However, regardless of the mandatory nature of this axiomatic initially external to
the Agency, it is integrated without difficulty, the ethos of public health being per-
fectly isomorphic to the logic carried by the DSM and the Evidence-Based Mental
Medicine approach. The epidemiological and public health approach is presented as
an obligation within the Agency: “we are constrained in such a document to have a
public health and epidemiology of mental health approach and cannot enter into a
diagnostic approach such as experienced by clinical specialists” (cited above). But
if such an “obligation” exists, it is by no means seen as a constraint, but rather as an
obligation of scientific rigor, and therefore, in the scheme of reasoning employed, as
a moral obligation, to bring to the public the “best available scientific data”. The
science mentioned is necessarily based on epidemiology and quantitative psycho-
metrics: “there is and there can be only one science. By definition there is only one
scientific approach, you apply the same rules everywhere regardless of the object of
study, be it parenting, tobacco, alcohol or mental health, the scientific rules are pre-
determined… There is only one approach, one method, one protocol, the rest is
meaningless verbiage by people who want to reconstruct reality … What counts is
an effective scientific approach and we now know where to find it [] I am always
referring to data from the scientific literature to define [the concepts we use]… I
always put myself behind an official definition” (remarks made by a member of the
Agency coordinating the expert group).
Yet, to think that way is to go against the evidence, mentioned by sociologist
Alain Ehrenberg, that “methods must be adapted to the object being observed and
on which we try to have an effect” (Ehrenberg 2006b). To assume only one scientific
approach is to pretend that the analytical methods of experimental science are the
only one relevant in the analysis of psychological problems, including depression.
This is a highly questionable postulate (Gorostiza and Manes 2011) which is, how-
ever, never criticized if the fields of public health institutions, not only for the socio-
logical reasons of necessary integration of agencies in the chain of public policy
decision already mentioned, but also and especially because “they miss the [episte-
mological and sociological] conceptual tools [needed]” (Ehrenberg 2007) to under-
stand the complex interwoven nature of individual minds, meaning, social
institutions, and mental disorders (Bolton and Hill 2004). The public health system
that imposes its medical approach on mental health has neither the categories of
thought, nor the reasoning methods or methodological tools to think of depression
other than, according to DSM, as a meaningless disease that is ultimately com-
pletely natural and without reasons or context. Indeed, the evidence-based medical
paradigm in which “public health depression” is framed is seriously defended by an
“immune system” that tolerates within that system only elements with an acceptable
axiomatic. As said by an official of the Agency to a newcomer trainee in sociology
as a welcome speech: “It’s simple, Alex, it will be necessary that you choose your
side, either you are engaged in the constructive logic of public health, as is done
here, or you are engaged in a destructive logic, that of sociology that attempts to
derail all actions. Anyway, these people have no actual solutions to offer to prob-
lems related to poor mental health”.
However, the conceptualization of depression generated by this paradigm “is not
the result of an empirical scientific discovery (like the germs that cause infectious
diseases). It is the effect of an heavily theory-laden rewriting of the ordinary moral
content [that constitutes depression] in new neurobiology-compatible terms” (Castel
2010). And the new psychopathological knowledge that is deduced from this rewrit-
ing “gives a much sharper hardness to the medically assisted strategies of normaliza-
152 X. Briffault
tion of intimate life, that is afterwards denounced by sociologists and psychoanalysts”

(ibid.) – denunciations whose failure we have seen when examining the poor destiny
of the FFP criticisms, and their complete failure to challenge the axiomatic DSM
foundations of the whole making of the depression booklet and campaign.
If there is no denying that the condescending arrogance expressed by the tone of
the criticism helps to reduce their chances of success, this is not the real problem.
This contemptuous attitude only comes to diminish what is already almost zero. In
fact, when we make “psychiatry a branch of natural science, this knowledge gives
stakeholders (patients and caregivers) the insurance they lacked: that of acting in the
name of the truth of the laws of nature, far from any “cosmetic” moral issue – when
this moral reference is not simply held as an harmful filter preventing any objective
understanding of depression” (ibid.).
The analysis presented above illustrates the difficulties encountered by the posi-
tion of the “socialized and speaking” human being (Ehrenberg 2004a, c) – at least
as it is defended by those French psychiatric institutions who endorse it – to retain
an efficient position in the overwhelming public health approach extended to mental
health: “ the existence of a nosographic standard entails a high level of coherence at
all levels of the stakeholders involved in depression and its treatment, which deter-
mines an extremely coherent and highly interdependent system. The normative
power thus generated leads to a strong inertia to change. From the definition of the
scales measuring the way people think, live and act their ‘depression’, through the
definition of treatments, clinical trials, recommendations for good practice, training
of practitioners, national information campaigns, the media, the categories of the
common social grammar … is a complete ‘social construct’ that is ‘held together’
by the DSM and the ‘depression’ to which it gives an existence” (Briffault and
Martin 2011; Briffault 2013): “the object, initially the product of a convention
becomes real after having been transmitted off the shelf and reused by others”
(Desrosieres 2002). The Major Depressive Disorder of the DSM, initially the
product of a convention, becomes real in its use by the public (mental) health sys-
tem. And it has to, if stakeholders are to avoid unmanageable epistemological, soci-
ological, and moral choices, and conflicts that would prevent any attempt to produce
a common, coherent, single voice public health campaign. We need a common
frame and a common language to be able to co-operate. This is the reason why DSM
is used as a kind of “Planck’s wall”, the ultimate possible point of view on the real-
ity of mental disorders, and thus on mental health.
Finally, the major difficulties encountered by the French psychiatrists to have an
accepted voice during the making of this campaign might suggest that the “French
exception” in psychiatry, made of psychoanalytically informed systematic opposi-
tion to the extension of the field of public health and standardized medical nosology
to the field of the psyche, begins to seriously fizzle. Indeed, from the point of view
of public health actors, there is no doubt that this is already the case, as seen in the
opinion of a high level member of the Agency: “These people are paranoid. But as
in any paranoia, there’s a little truth. The problem is that times are changing, and
they feel it as an attack against them, while it is much worse: we almost do not listen
to them anymore”.
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Extrapolation from Animal Model
of Depressive Disorders: What’s Lost
in Translation?
Maël Lemoine
Abstract Animal models of depression are problematic and results drawn from them
is moderately convincing. The main problem, it is often argued, is that it is impossible
to model a mental disorder, i.e. specifically human, in animals like rodents: it is a mat-
ter of resemblance of symptoms. Yet in this field it is generally assumed that animal
models of depression are more or less ‘valid’ according to three criteria: predictive,
construct, and face validity, with only the latter concerned with the resemblance of
symptoms. It is argued here that the problem is actually not with resemblance to the
clinical features or to the factors of depression: it is not their being mental parameters.
It lies, rather, in the fuzziness of the definition of a human entity and in the difficulty
of linking together supposedly involved biological mechanisms into a consistent pic-
ture of the underlying process of the disease. It is therefore not that we cannot model
what we know to be depression, it is rather that we do not know what to model.
Introduction: Translational Research and Extrapolation

in Psychiatry
Philosophers tend to import their own problems into foreign domains, not always for
the sake of the greater good. An alternative strategy in the philosophy of science con-
sists in trying to illuminate problems as scientists encounter them. Modeling mecha-
nisms of diseases in organisms belongs to what is called ‘translational research’. As a
matter of fact, in contemporary medicine, ‘translational research’ is summarized
through the rhetorical motto ‘from the bench to the bedside’. As defined more specifi-
cally by the Translational Research Working Group regarding cancer research,
Translational research transforms scientific discoveries arising from laboratory, clinical, or
population studies into clinical applications to reduce cancer incidence, morbidity, and
mortality. (Translational Research Working Group 2007, 99)1
1
Other definitions have been proposed (see McArthur and Borsini 2008, xix).
M. Lemoine (*)
University of Tours, INSERM U930, IHPST, Paris, France

DOI 10.1007/978-94-017-7423-9_11
158 M. Lemoine
Yet this simple definition contains multiple meanings. In an editorial for the first
issue of Science Translational Medicine, Elias A. Zerhouni, a former director of the
National Institutes of Health and formerly a strong advocate of this approach, states
that the term ‘translational’ can be understood in at least three senses: the rendering
in clinical terms of what is understood at the basic level; the therapeutic application
of basic biological knowledge; and the extrapolation made possible by the “pro-
found unity of biology” resulting from “shared evolutionary pathways” (Zerhouni
2009). Indeed, application does not automatically follow understanding. This seems
to be all the more true in psychiatry, where translational research has recently
become a motto (the first issue of Translational Psychiatry, a publication by Nature
Publishing Group was released in April 2011). Many potential treatments have
resulted in disappointment and many exciting in vivo and in vitro models have failed
to tackle the issue of human mental disorders.
As regards in vivo or animal models, experimental as well as more theoretical
issues have been raised. As a matter of fact, concerns about the rationale of extrapo-
lation from animal models have been both objected to and dismissed by philoso-
phers (LaFollette and Shanks 1995; Schaffner 1998a, b, 2000; Ankeny 2001; Weber
2005), so the question may need further consideration in the specific case of animal
models of mental disorders. More specifically still, scientists spontaneously distin-
guish disorders that seem to hit potentially anyone, such as anxiety and depressive
disorders, and those disorders that seem to threaten only a clinical subpopulation,
such as autistic disorders and schizophrenia; the latter seem to be even harder to
model in animals than the former. The main reason seems to be the impossibility of
modeling mental features that we find hard to understand ‘intimately’ in humans, a
problem scientists apparently consider to be less stringent in the case of mood and
anxiety disorders, where cognitive traits look less mysterious and behavioral traits
far more recognizable.
Is modeling depression along with its mental processes, factors, and symptoms
in animals truly unproblematic? My contention in this chapter is that the main prob-
lem scientists encounter in the field of mental health is not the fact that depression
is difficult to model because its symptoms are ‘mental’, that is, personal, experi-
enced, and contextual (1); rather, it is the fact that human depression is a fuzzy tar-
get of modeling, and that “piecemeal theorizing” (Murphy 2006) is required, which
is a challenge to causal reasoning in medicine in general (2).
Translation and Extrapolation about Depression:

The Mind-Body Problem?
If rodents cannot conceive of guilt, worthlessness, despondency and dejection, or if

they cannot worry about what the future may bring and ‘consider’ suicide, is there
any causal pathway left for them to develop genuine depression? Broadly speaking,
there are two series of objections here:
Extrapolation from Animal Model of Depressive Disorders: What’s Lost in Translation? 159
1. the target condition, i.e. mental disorders, cannot exist in animals (dissimilarity
of animal models to their human target);
2. the causal network relevant to this condition, including mental factors, is not
relevant for animals (impossibility of bypassing mental causality).
In this section, I consider the way translational psychiatry deals with both problems
and conclude that problems raised by modeling mental disorders in animals are not
relevant to the mind-body problem.
How Translational Psychiatry Deals with the Problem

of Similarity to Depressive Symptoms in Animal Models
Feature-to-Feature Resemblance
In this section, I attempt to give a brief presentation of a field largely unknown to

philosophers of psychiatry. When submitted to environmental factors similar to
some of those precipitating depression in humans, like moderate chronic stress,
animal models are expected to produce some behavioral symptoms and biological
changes similar to those found in humans. In an experimental test of a pharmaco-
logical treatment, the animal should not only resemble the human, but the whole
experimental situation should resemble the whole human situation too. This ‘situa-
tion’ is generally construed in the following way:
1. A disease entity instantiates in a human population marked by a genetic vulner-
ability through the occurrence of a pathogenic sequence of events enticing a
neurobiological dysfunction.
2. This dysfunction can be assessed on the basis of clinical symptoms and biologi-
cal markers thanks to diagnostic tests.
3. Any possible chemical treatment is a molecule with a pharmacological target
called the endpoint.
The relevant features of resemblance in this situation are reduced to abstracted and
idealized parameters (see Table 1).
Each parameter in itself is a matter of concern:
– Disease entities do not necessarily cross the boundaries of species.
– Animal species display specific natural and artificial properties with known and
unknown advantages and drawbacks for modeling a specific disease.
– Animal strands are known for specific genetic vulnerabilities, some being an
exaggeration of what can be encountered “in the wild”, that is in a natural human
population.
– Pathogenic sequences of events in humans have only partial correspondents in
mice.
– Too many neurobiological mechanisms are potentially dysfunctional in
depression.
160 M. Lemoine
Table 1 Animal models of depression: Parameters of feature-to-feature resemblance

Parameters (human condition) Corresponding parameters (animal experiment)
Human depressive disorder Animal equivalent of the depressive disorder
Genetic and environmental vulnerability Animal species and strand
factors
Depressogenic sequence of events Stress protocol
Dysfunctional neurobiological mechanism Dysfunctional neurobiological mechanism
Clinical symptoms Behavioral and cognitive changes
Biomarkers Biomarkers
Diagnostic tests Biological, behavioral and cognitive tests
Endpoint Endpoint
Treatment (molecule, vehicle and posology) Treatment (molecule, vehicle and posology)
– Some clinical symptoms of human depression have reasonably convincing equiv-

alents in mice like psychomotor agitation or retardation, insomnia, weight loss,
and even anhedonia, while others do not, such as feeling of guilt or worthless-
ness, irritability, or suicidal ideation.
– Biomarkers, that is, evaluated indicators of the intrinsic causes of an illness, its
clinical course, and its modification by treatment (Frank and Hargreaves 2003),
not pathognomonic or cutting-off signs, cannot generally be measured in situ,
but only indirectly, and a thorough knowledge of the specifics of human and
animal physiology is required to translate.
– Usual clinical tests differ in humans (questionnaires) and in animals (measure-
ment and observation of activity).
– Endpoint of a candidate treatment, i.e. is the locus of action (receptor, behavior),
is ideally the same in both humans and mice, but species may have different
potential acceptors of the molecule leading to different potential side effects.
– A potential treatment itself has to be adapted in many ways, because of differ-
ences in required dosage (Lin 1998), or transposition of places to be stimulated
in the case of transmagnetic stimulation (TMS).
Two concluding remarks are noteworthy. The first is that there are many more
features to compare between species than it seems at first sight. Some are deeply
problematic, others, not at all. The second remark is that scientists generally do not
focus on the possibility of modeling, but rather on the strategic choices to make in
order to design the best model possible. There are obviously good choices and bad
choices, given what biologists generally assume about the inner working or main
symptoms of depression. Nevertheless, all this indeed does not prove skepticism
wrong about the potential results of animal research on depression. My main claim
in this chapter is the reverse, i.e. that skepticism about resemblance of animal mod-
els to psychiatric conditions, if justified, does not entail that no significant result can
come from this field.
Face Validity, Predictive Validity, and Construct Validity
It is crucial to understand that translational research does not assess an animal

model by similarity to the target, but by the validity of the inference. The similarity
of the animal model to its human counterpart is neither a sufficient nor even a neces-
sary condition of the validity of the extrapolation of a result based on animal experi-
ments to a human population.
Many conditions of validity have been proposed and considered, for instance, in
the field of the study of mood disorders, where this reflection happens to be most
developed in translational psychiatry (Van der Staay 2006; van der Staay et al. 2009;
Belzung and Lemoine 2011). Paul Willner proposed the most often cited conception
of validity in this field (Willner 1984, 1994; Willner and Mitchell 2002); he
distinguishes:
• Face validity: “the extent of similarity between the model and the disorder (…)
on as wide as possible a range of symptoms and signs” (Willner and Mitchell
2002);
• Predictive validity: “similar response to treatment” (Willner 1984);
• Construct validity: specific similarity of the animal experiment to the theoretical
entity referred to as the disease and supposed to explain its symptoms, and to this
theoretical entity only.
These three aspects of validity are not only different, but also independent of one
another, so that when one is fulfilled, the others are not necessarily satisfied.
Face validity is what is commonly understood by the ‘resemblance’ of the ani-
mal model to its human target, especially in critical assessments of translational
psychiatry. Yet face validity is not considered as equally important as construct and
predictive validity. About the relations between construct validity and face validity,
for instance, Willner says:
Face validity only requires the demonstration of similarity between the model and symp-
toms of the disorder being modelled. Construct validity does not require superficial similar-
ity which may, indeed, be absent. It does, however, require the demonstration of
homology – the same theoretical constructs must be applicable in the two cases – and an
empirically supported rationale for believing that the construct in question is fundamental
to the disorder, rather than an epiphenomenon. (Willner 1986, 684, my emphasis)
For instance, when examining two standard protocols, the Tail Suspension Test
(TST) and the Unpredictable Chronic Mild Stress (UCMS), Willner notes that while
the first has poor face validity and construct validity but strong predictive validity,
the second has fair face validity and less convincing construct validity (depending
on one’s hypothesis on the relation between stress and depression). A mouse that
stops moving when suspended by its tail bears little resemblance to either the
observable features or any received explanatory model of depression. Yet it is
strongly predictive of the action of a drug in depression, and this is considered suf-
ficient to assess whether a treatment should be tested on humans. A mouse submit-
ted for a protracted time to mild stressors such as nocturnal light, humidified soil,
predator sounds, etc., shows signs very much alike to some of those depressed
162 M. Lemoine
human subjects display, but it can be, and actually is, discussed on a theoretical level
whether what stress entails is indeed an equivalent of depression.
It might be objected that predictive and construct validity also are specific forms
of resemblance. As a matter of fact, predictive validity is more readily interpreted
as a correlation of results of experiments than as a degree of resemblance between,
say, effects of a treatment on mice and on humans. It says, roughly, that when the
experiment is successful on mice, it will also be on humans. As to construct valid-
ity, it is not exactly the similarity of a model to its target, but rather the conforma-
tion of both the model and its target to a theoretical construct. Both what is
observed in the model and in its target must be explained by the same underlying
theoretical disease entity, all other theoretical disease entities excluded. It therefore
depends on the nature of the theoretical construct, that is, whether animal modeling
of depression is possible or not: as a highly sophisticated mental process, depres-
sion is hardly what rodents undergo. Nevertheless, the problem is that there is no
consensual theoretical model of what depression consists of in translational
research. Experimenting on animal models does not beg the question, but indeed
excludes possible explanations – like highly elaborated psychodynamic models.
This should not be considered a reductive claim, but a biological bet. What scien-
tists really expect is not to make a point, but depends on the results of the experi-
ments: it is a strategy, good or bad, not dogma. Of course, some scientists may try
to make reductionist points. Yet objecting that experimenting on animal models
cannot achieve any knowledge of the allegedly corresponding human condition is
indeed both dogmatic and bad strategy.
Some may ask: what if the success of antidepressant medication was precisely
defined through the very hypothesis that animal models implement? For instance, if
‘depression’ was defined as a ‘low level of serotonin in the brain’, then surely a
certain animal model with a low level of serotonin in the brain could provide a won-
derfully predictive model… at a small price. This objection of circularity is to be
carefully considered. So far, the efficiency of antidepressant medication has not
been assessed through biological markers, but rather as a result of scales, like the
MADRS or the HAMD described above, that are not semantically, but empirically
connected (or not) with drug intake.
For all these reasons, the resemblance of the animal model to its human target is
but one series of problems among the more general question of the validity of the
extrapolation, probably the less important, because what matters most is both the
power of prediction and the theoretical interpretability of the model.
How Psychiatry Deals with the Problem of Heterogeneous

Factors
An additional problem comes from modeling causal factors of depression. This sec-
tion presents how it is addressed.
Multifactorial Determinants of Psychiatric Disorders vs. Animal Research
By famously urging the use of multifactorial models in psychiatry as well as in somatic

medicine, Engel (1977) clearly opposed two attitudes he labeled reductionism and
exclusionism. Whereas ‘reductionism’ was the view that biomolecular models should
suffice to account for diseases both somatic and mental, ‘exclusionism’ was the view
that conditions not amenable to biomolecular models were simply not diseases, which
to some is the case for mental disorders (Szasz 1960). He proposed instead that the
interaction of all factors, biological, psychological, and social, be studied in a system-
theoretic approach. Since then, epidemiological studies of depression have repeatedly
shown the importance of sociological and economical factors in its pathogenesis.
It requires a body and a nervous system to produce a sadness reaction, but it does
not necessarily require stressful or demoralizing environmental conditions to
deplete serotonin, stop hippocampal neurogenesis, or produce chronically high lev-
els of cortisol. Psychological and social factors obviously supervene on some bio-
logical factors, whereas other biological factors do not make any psychological or
social sense. Systemic approaches should therefore take great care to avoid consid-
ering the same factor twice, that is, as a biological as well as a sociological or a
psychological factor. That is obviously not easily operationalized.
On the other hand, it is not necessary for someone working on animal models of
depression to deny or even neglect the causal power of meaningfulness on an intel-
ligent system (Bolton and Hill 2004). It is natural, on the contrary, to assume that if
they exist at all in animals, mental causal factors, i.e. meanings, are already taken
into account in their biological form and should not be ‘added’ somehow. In any
case, cognitive bias, personality types, early-life events such as maternal care depri-
vation, neuroticism, and so on, all have proposed animal equivalents.
The problem is therefore not that some causal factors are not taken into account,
but rather that in animals, the underlying biological phenomena of meanings might
be absent or might underlie something else, so that in the best of cases, only an
incomplete part of the biological mechanisms of depression can be studied. I assume
that most scientists in the field would acknowledge that. I also assume that here
again, what they are doing is a methodological bet rather than an ontological claim:
it is possible to study some essential aspects of depression in a system that does not
display other essential aspects of this mental disorder.
Knowledge Approach vs. Treatment Approach
This methodological bet is an essential thing to understand. Let us take the example
of drug discovery research. The point in modeling is not to create a homolog on
which testing drugs is acceptable. It is not knowledge-based in the sense that scien-
tists would think:
• If we knew how mental disorders worked, we could devise efficient treatments;
• We must experiment to know how they work;
164 M. Lemoine
• We cannot safely experiment directly on humans, we must therefore experiment

on animals;
• What are the best animals to experiment on in order to know how the human
disease works?
• Once we have good models, test of treatments on them will be trustworthy.
This line of thought can be encountered as a rhetorical justification of the method.
However, as a matter of fact, the actual reasoning is rather treatment-based, and
consists in the following:
• We know that some chemical agents have dramatic effects on mental disorders;
• These agents have effects on animals too;
• Which effects, on which animals, will guide us toward selecting the right chemi-
cal agents, i.e. with efficient and specific action, to test on humans?
• In order to restrain the possibilities of further agent candidates, we want to know
how the right treatments work both on animals and on humans, i.e. what the
targets could be.
The crucial point is that the analogy of causal effects is not assessed as a result of a
previously existing theory, but rather that whatever the theory, any effective treat-
ment on humans will have effects on some animals too; the question remains,
though, which molecules affect which animals. Theories are not a starting point, but
only a heuristic tool to restrain the domain of testable molecules.
Relevant Differences: A Philosophical Account of How the Problem

of Heterogeneous Factors Is Successfully Dealt With
A final concern is the possibility of modeling when significant factors differ – such
as guilt, despair, and feelings of worthlessness. Modeling mental disorders such as
depression is but a case of what philosopher Daniel Steel addresses as “the problem
of extrapolation in heterogeneous populations” (Steel 2008). This refers to the pos-
sibility of inferring from one experiment on a test population to properties of a tar-
get population, when both populations differ in causal aspects relevant to the
inferred properties. What is needed, according to Steel, is knowledge that relevant
dissimilarities at corresponding stages of the mechanism of interest in the model
and target have no significant effect on the point of comparison, ‘significant’ mean-
ing affecting the extrapolation. He calls this approach “comparative process trac-
ing” (Steel 2008, 89).
A facilitating condition is that it is possible to abstract some relevant factors,
namely, upstream factors (resulting in the same starting point of the mechanism of
interest), and downstream factors (intervening after the last stage of the mechanism
of interest). The former can be abstracted away provided that there is no bypassing
mechanism linking the upstream factor to a given stage in the mechanism of interest
(Steel 2008, 90). The latter can also be abstracted away, provided that there is no
feedback loop. Mental factors in depression are considered upstream factors,
whereas mental reactions such as rumination are considered downstream factors.

What is at stake is the mechanism that takes place in-between.2
Moreover, what is sought for is not a deterministic, but rather a probabilistic
claim. The existence of any mechanism from X (cause) to Y (effect) in any indi-
vidual in the animal population increases the probability of Y in the animal popula-
tion when X is the case (Steel 2008, 109). At least, this is true if and only if there is
at least one undisrupted mechanism from the cause to the effect, which in turn has
the experimental consequence that any intervention on the cause makes a difference
to the probability of the effect (sublata causa, tollitur effectus). This makes the case
of mental phenomena a particularly difficult experimental problem. The reason is
that they are very sensitive, or causally central, that is, possibly influenced by many
more causal factors than most physical phenomena. Anything, from deprivation of
a particular kind of food (say, chocolate) to living in a particular place, having
undergone such or such experience in the past or having to in the future, can affect
the mood in the most radical way. But this does not make it specific in nature, and it
does not preclude a carefully designed animal model that can teach us something
about causal mechanisms in depression.
All in all, in the case of the study of depression in animal models, the treatment
approach I described above entails the preliminary assumption that what is directly
at stake are the molecular interactions within the brain, and only indirectly the men-
tal or social factors that supervene on them. This, however, does not completely
abstract away mental factors, for it does not abstract away the molecular causal
effects that underlie these factors in the brain. The problem is therefore, to identify
– the modular neuronal mechanism where some dysfunction is implied in the men-
tal disorder in human subjects as well as in animal models;
– the modular neuronal mechanism realizing this particular kind of cognitive pro-
cess that presumably does not take place in rodents (say, despondency after los-
ing a job, despair at the perspective of the void of a life to come without a loved
one, and so on);
– the causal interactions between both modules.
That done, animal modeling applies to the case of mental disorders without any
specificity, provided that what is looked for is a picture of crucial parts of the mech-
anism, not the entirety of the mechanism, and that the approach is treatment-driven
rather than knowledge-driven.
The conclusion is that modeling depression in animals does not raise specific
problems because it is a mental disorder. The reasons why are: (1) most relevant
features can be reasonably considered similar in both animals and humans; (2) face
validity (i.e. resemblance) is but a minor point in extrapolation; (3) mental factors
2
Steel also refers to another facilitating condition, namely, that the inference is about negative or
positive causal relevance only, not on the effect size. Thereby, a certain degree of dissimilarity in
corresponding stages of the mechanism does not affect the soundness of the extrapolation. This
obviously applies to the problem of metabolism referred to above in the case of modeling
depression.
166 M. Lemoine
can be considered as supervening on neurobiological mechanisms; (4) the approach

is generally treatment-based, that is, does not presuppose a known mechanism to be
similar, but rather, an interesting effect to occur in animals too; and (5) relevant fac-
tors can be abstracted away consistently even in the case of mental disorders.
However, this does not mean that mental disorders in general, and depression in
particular, do not pose specific problems to animal modeling. The problem with
animal models of depression is therefore not an instance of the mind-body problem.
What is it, if any?
Something Is Modeled in Translational Psychiatry: What,

Exactly?
The problem of inferring causal relations from animal models of depression to

human targets is not the similarity of the model, but the indeterminacies of the tar-
get. Depressed human subjects are a fuzzy target. The definition of depression as a
syndrome contributes to this fuzziness, and that must have consequences on the
relevance of likely animal models: should they display all the symptoms animal
models can, or a significant subset of them? So does the fact that the various mecha-
nisms known to be possibly involved in depression do not fall neatly in place. In this
situation, the scope of the extrapolation cannot be precisely determined.
Fuzziness
The target population is fuzzily determined, first, through the uncertainty of the
disease entity due to its polythetic semiology, second, through the width of the spec-
trum of mood disorders, and third, through the dimensionality of the criteria of
depressive disorders. Consequently, the poor results of factor analysis and principal
component analysis have repercussions on the evidential power of animal models of
such conditions.
In the Diagnostic and Statistical Manual of Mental Disorders (DSM), a major
depressive episode (MDE) is defined through alternative combinations of symptoms.
This kind of diagnostic definition, called polythetic, leads to much heterogeneity in
the population of people suffering from a MDE. Ostergaard et al. (2011) calculated
that for 5 items out of 9, the first or the second being necessary, the possibilities
number up to 227. Moreover, considering that three criteria contain alternate but
incompatible subcases (either weight gain or weight loss, etc.), the number of pos-
sible forms of MDE could amount to 1497. The result is that many configurations of
symptoms have not even one symptom in common, and many more share only non-
specific symptoms (such as insomnia and weight loss). The problem is that no com-
mon underlying dysfunctional system has yet been discovered from which such
heterogeneous patterns could be causally derived, and thereby the unity of the syn-
drome, justified. What is, then, the possible configuration, or the core symptom, that
animal models should display? Anhedonia and ‘helplessness’ behaviors are most
often proposed; this is a strong theoretical claim, which clinicians may question.
MDEs occur within the course of many mental disorders, including major
depressive disorder (MDD) but also bipolar disorders or schizophrenia. It is a ques-
tion whether the nature of the MDE is the same under the surface of symptoms in
these different cases. Moreover, major depressive disorder is different from but next
to disruptive mood dysregulation disorder, chronic depressive disorder (formerly
known as dysthymia), premenstrual dysphoric disorder, the controversial and aban-
doned ‘mixed anxiety/depression’, substance-induced depressive disorder, depres-
sive disorder associated with a known general medical condition, and a few other
specified depressive disorder and unspecified depressive disorder. It is not so clear
whether there are biological differences underlying these distinctions and above all
how, if biological, these differences could be modeled in animals. Moreover, one
can wonder whether what is induced or observed in animals is specific to MDE. The
Novelty Suppressed Feeding test (i.e., testing whether a rodent will or will not eat
in an unknown environment), for instance, is sometimes considered as a test of anxi-
ety, and sometimes as a test of depression.3 This uncertainty unintentionally reflects
many hesitations in the clinic about the distinction to be made between these two
disorders. The upshot is that whereas animals are supposed to model one mental
disorder, this specificity is highly questionable and there is a genuine problem in
knowing what, exactly, is modeled in a ‘depressed’ mouse.
Two further problems are worth mentioning. The first is the dimensionality of
criteria. Most features of depression can, and maybe should, be assessed quantita-
tively: disturbed sleep and weight change, for example; but things such as loss of
interest and feelings of worthlessness can be quantified as moderate, mild or severe
(see the Beck Depression Inventory (BDI), the Hamilton Rating Scale for Depression
(HDRS/HAMD) and the Montgomery-Åsberg Depression Rating Scale (MADRS)).
It is often noted that the main outcome of such continuity is fuzzy boundaries
between normal and pathological sadness and pessimism. This, too, is a difficulty
for modeling: should only severe cases be modeled? However, these scales are gen-
erally used as a measure of severity rather than presence of a MDE.
Second, there is the problem of the poor results of factor and cluster analyses.
For instance, the key result of Paykel’s study in the 1970s was that the main distinc-
tion was between old subjects with severe depression and young subjects with mild
depression, the former subdividing between psychotic and anxious types, the latter,
between hostile types and those with personality disorders (Paykel 1971). A classi-
cal factor analysis of depression found three profiles, “anxious-tense depression”,
“hostile depression” and “retarded depression” (Overall et al. 1966); yet another
found that the main factors were the neurotic-psychotic axis and the depressive vs.
paranoid factor (Kay et al. 1969). As philosopher Rachel Cooper rightly empha-
sized, the problem with all studies of this kind is theoretical and comes either with
3
As neurobiologist Catherine Belzung explained to me (personal communication).
168 M. Lemoine
the choice or with the interpretation of variables and results (clusters or profile)
(Cooper 2010). In other terms, the problem is the elaboration of the relevant con-
struct. Animal models should conform to that construct, but a prior decision is to be
made: should psychiatrists include observable variables that have clear equivalents
in mice? The second question is: can the result of a cluster or factor analysis in
humans be back-translated into mice?
Mosaicism and Chimerism of Models
Despite the treatment approach I emphasized in the first section, some knowledge
of the whole biological picture is necessary to model the disease. We have some
indeed, but it is very patchy: areas of known mechanisms upon which used treat-
ments act are surrounded by largely unknown causal chains. This situation leads to
what philosopher Dominic Murphy calls, in Psychiatry in the Scientific Image,
“piecemeal theorizing”, that is, the fact that psychiatry about mental disorders in
general employs “generalizations or causal models of limited scope at different lev-
els” rather than “one big elegant theory” (Murphy 2006, 240–1). In the more spe-
cific case of one given mental disorder in turn, Murphy distinguishes global models,
designed to explain all symptoms by one general dysfunction, and modular models,
designed to explain all symptoms by a series of part-dysfunction, each explaining
one symptom or one part of the symptoms.
The requirements of animal experiments are partly responsible for the preva-
lence of piecemeal theorizing and modular models in biological approaches to
depression. One has to choose one putative mechanism to model it. In translational
psychiatry, scientists therefore consider their animal models to instantiate one com-
ponent mechanism of the disease (hopefully the key mechanism). But they do not
exactly know where, in the global plan of the disease, this mechanism stands – that
is, what are its causal relations with the rest. It may be central or peripheral, it may
precede, follow, or add up to other mechanisms in the course of the mental
disorder.
The main biological hypothesis on depression until recently, the monoamine
hypothesis, is an illustration of piecemeal theorizing. The serendipitous discovery
of seemingly effective treatments of depression, tricyclic antidepressant (imipra-
mine), and monoamine oxidase inhibitors (iproniazid), led to research on their tar-
get, mainly, the serotonergic system (Maxwell and Echhardt 1990; McArthur and
Borsini 2008). Further exploration of this biological mechanism in animal models
led in turn to better animal models on the one hand, and better molecules on the
other hand (mostly, with less side effects): chiefly, fluoxetine. Many have thought
that an imbalance in the serotonergic system, grossly in the form of a depletion of
synaptic serotonin, expressed the main mechanism of depression (Hirschfeld 2000).
Yet this position hides a paradox, that of the delay of action of mood regulators: how
can depression consist mainly in a serotonin deficit if normal levels are restored
almost immediately under medication, but improvement occurs only 3 weeks after
the treatment begins? This question has more recently lead scientists to question the
centrality of serotonergic system in depression, and look for complementary, alter-
native, or competing hypotheses. Among others, a possible disruption in hippocam-
pal neurogenesis, which has in turn been linked to a mechanism known to be crucial
in anxiety disorders, the so-called hippothalamo-pituitary-adrenergic axis of stress,
and so on to a dozen other mechanisms possibly involved in depression (Licino and
Wong 2005).
This situation, i.e. many different animal models of various mechanisms of
mostly unknown importance and causal relations with one another, though referring
to the same mental disorder, I propose to call mosaicism of animal models. I distin-
guish it from chimerism of animal models, i.e. the fact that several different animals
are usually required for the instantiation of one hypothesis, each instantiating one
part of the component mechanism of the disease, none instantiating the whole
mechanism. In other terms, there is not one animal model similar to the mental dis-
order according to hypothesis X on its inner mechanisms, but rather several animal
models implementing parts of the whole mechanism supposed to take place in the
disease in humans. For instance, the hypothesis that the s/s polymorphism of the
serotonin transporter gene is a vulnerability factor to depression, and requires that a
whole chain of events from this polymorphism to symptoms of depression be estab-
lished. As a matter of fact, it has been, but not the whole chain into a single model –
it required at least three different rodent models.
Both mosaicism and chimerism of animal models are consequences of modeling
in the dark about the ins and outs of mental disorders. The main outcome of that
necessity to model piecemeal is on the scope of the extrapolation. First, one does
not know the strategic place of the part of the human disease modeled in the animal
and, second, one does not extrapolate from one type of animal to the human target
population on the basis of a one-to-one resemblance, but from several types of ani-
mals to the human target population on the basis of a many-to-one resemblance.
Conclusion
What is lost in the translation of animal models to human targets? It was not a well-
formed meaning, but rather the conviction that there was one in the first place. The
question is not the impossibility of translating mental properties and mental factors
into ‘animal language’. The real problem with animal models of depression is
depression itself. First, the human population to be modeled is not itself strictly
determined, and second, animal models cannot be thought of as experiments about
mechanisms precisely placed and fitting nicely into the sound template of a biologi-
cal theory of this mental disorder, for there is no such theory. They indicate fixed
directions and sound natural facts about those mechanisms, but we do not know
which directions and which facts.
In the face of this problem, there have been theoretical attempts at gathering all
we know about the biology of depression (Kendler et al. 2002, 2006; Willner et al.
170 M. Lemoine
2012). The problem is always about searching either for consistent, if alternative,
underpinning mechanisms of a same clinical condition, or for a relevant definition
of the clinical presentation of the same biological dysfunction. Should we redefine
depression after what we think we know of its underlying biology or should we
search for a biological rationale of what we think we observe of its clinical presenta-
tion? Translational psychiatry of depression is at the heart of this problem. It tends
to use concepts, such as that of ‘endophenotypes’, to resolve the question. As
opposed to exophenotypes, that is, clinical presentations of depression affected by
many environmental and developmental factors, endophenotypes are hypothetical
underlying presentations of genetic factors of depression. In the present field, they
consist in behavioral patterns affected by genetics only, that is, hereditary, possibly
hidden or disguised by cultural or biographical events (John and Lewis 1966;
McArthur and Borsini 2008). Their function is obviously to deconstruct the clini-
cally defined syndromes into (yet) undetermined alternative phenotypes, of which
traditional clinical entities might have been an approximate picture. As endopheno-
types would not necessarily be species-bound, and could be defined after whatever
genetic determinants of depression can be discovered, they would totally redefine
the human condition that depression is into a biological, trans-species condition. If
the unity and reality of the condition were specifically human and relied on mean-
ings, then this attempt would be doomed to failure.
This ultimate consequence of animal modeling – to rewrite the very notion of what
depression is about – is neither to be fought nor favored by philosophers. As a matter
of fact, scientific progress is about the naturalization of prescientific notions such as
movement, heat, reproduction, species, but also diabetes, epilepsy, and, possibly,
schizophrenia and depression. Some of these attempts at naturalization seem to be
bound to fail, some, to succeed: how could a philosopher know which ones can suc-
cessfully be naturalized before they are? For a successful naturalization, i.e., roughly,
an explication of a profane notion through the terms of natural sciences, is not about
the faithfulness of the scientific concept to the prescientific concept (Murphy 2006;
Lemoine 2014). It is about capturing, in a consistent picture, how nature works.
Acknowledgments Professors C. Belzung, neurobiologist, and V. Camus, psychiatrist, have read

and discussed the paper. Thanks to them for having always been an invaluable help since the begin-
ning of my philosophical work in their team.
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Psychiatry’s Continuing Expansion
of Depressive Disorder
Jerome C. Wakefield and Allan V. Horwitz
Abstract In our book, The Loss of Sadness (LoS), published in 2007, we argued
that DSM symptom-based diagnostic criteria for depressive disorder confuse intense
normal sadness with depressive disorder, thus potentially misdiagnosing large
numbers of individuals with a psychiatric disorder when in fact they are responding
to loss or stress with normal human emotions. We detailed the many negative effects
of such misdiagnosis, from unnecessary treatment to meaningless research results
to distorted mental health policy. In this chapter, we review the main developments
since LoS’s publication that bear on its thesis. For example, recent epidemiological
surveys have confirmed that the majority of individuals experience DSM-defined
depression at some point in life, antidepressant medication use continues to rise
sharply, and depression is increasingly treated by general physicians rather than
mental health professionals. Most importantly, the recently published fifth edition
of the DSM (DSM-5) further expanded major depression by eliminating the
“bereavement exclusion,” a clause that acknowledged that mild depressive symptoms
could be normal when they occurred shortly after the death of a loved one. The
DSM-5’s elimination of the bereavement exclusion, we find, was based on largely
spurious arguments, while ample research evidence has confirmed the exclusion’s
validity. In addition, DSM-5 greatly expanded the overall domain of depressive
disorders by adding several new diagnostic categories that are each open to
overdiagnosing the intensely sad individual as being psychiatrically disordered. The
trends we observed in LoS, we conclude, are confirmed by subsequent developments
and are if anything accelerating.
In 1980, the American Psychiatric Association published the third edition of its
official diagnostic manual, The Diagnostic and Statistical Manual of Mental
J.C. Wakefield (*)

Silver School of Social Work and Department of Psychiatry,
New York University, New York, NY, USA
A.V. Horwitz
Department of Sociology, Rutgers University, New Brunswick, NJ, USA

DOI 10.1007/978-94-017-7423-9_12
174 J.C. Wakefield and A.V. Horwitz
Disorders (DSM-III; American Psychiatric Association 1980) at a time when psy-

chiatry was being severely criticized for the unreliability of its diagnoses. To address
these complaints, rather than providing the traditional diagnostic labels with a sen-
tence or two of vague description, DSM-III for the first time provided lists of symp-
toms by which to diagnose each psychiatric disorder, increasing the reliability and
precision of diagnosis and allowing for more productive research. This turned out to
be a watershed moment, providing American psychiatry with a scientific legitimacy
that had previously eluded it. Subsequent editions of the DSM through to the current
fifth edition, DSM-5 (American Psychiatric Association 2013), refined the criteria
but did not alter DSM-III’s basic approach. Moreover, through the widespread
adoption of the DSM system by other countries, and through the DSM’s powerful
influence on the subsequent development of the World Health Organization’s
(WHO) International Classification of Disease (ICD-10; World Health Organization
1992), DSM-III reshaped psychiatric diagnosis worldwide. The ICD followed
DSM-III’s lead with symptom-based guidelines for psychiatric diagnosis – although
it never attempted the precise necessary-and-sufficient algorithms included in DSM.
Among the disorders that DSM-III newly defined in this precise manner was
major depressive disorder (MDD). MDD was defined in terms of symptoms such as
sadness, loss of interest or pleasure in usual activities, insomnia, lessened appetite
or weight loss, difficulty concentrating, a sense of worthlessness or guilt, suicidal
thinking, and other such symptoms. To be diagnosed with MDD, one had to have
symptoms from at least 5 out of 9 symptom groups for at least 2 weeks.
Once this symptom-based definition was in place and widely applied, MDD
became the most important of the several hundred diagnostic categories in the man-
ual. It was by far the most common condition diagnosed in outpatient practices
(Olfson et al. 2002). Community surveys indicated that MDD was the single most
prevalent mental illness in the population (Kessler et al. 2003). The World Health
Organization, calculating the actual and prospective burden of disease imparted by
MDD, found that MDD was the fourth leading cause of disability due to disease
worldwide in 2002 (Ustun et al. 2004), and warned that MDD would become the
second most disabling of any medical condition worldwide by 2030, save only for
HIV/AIDS (Mathers and Loncar 2006). It appeared that we had entered an “Age of
Depression” that replaced or perhaps supplemented the “Age of Anxiety” that dom-
inated the Western world in the post-World War II era.
However, we do not view this new age of depression as the result of a genuine
epidemic of depressive mental illnesses. In our book, The Loss of Sadness: How
Psychiatry Transformed Normal Sorrow into Depressive Disorder (LoS; Horwitz
and Wakefield 2007), we observed that intense normal sadness and depressive disor-
der are distinct conditions that can be manifested by very similar symptoms and thus
can easily be confused, a point already recognized in antiquity. We thus argued that
the seeming epidemic of major depression mainly stemmed from the DSM’s symp-
tom-based diagnostic criteria that conflated normal sadness and depressive disorder
and mistakenly categorized both of these conditions as psychiatric disorders.
Contrary to antipsychiatric critics who see psychiatry primarily as social control
masquerading as a medical field, we do acknowledge in LoS the obvious existence
of genuine and serious mental disorders that should be the target of medical treat-
Psychiatry’s Continuing Expansion of Depressive Disorder 175
ment efforts, including depressive disorders. Just as any biologically designed

bodily process can fail to function properly and can yield a physical disorder, so any
biologically shaped psychological process, such as sadness or grief, can fail to func-
tion properly and can yield a mental disorder (First and Wakefield 2013; Horwitz
and Wakefield 2007; Wakefield 1992, 2006). The problem was not that depressive
disorder does not exist, but that its domain was inflated by DSM’s symptom-based
criteria to encompass much normal human emotion.
LoS received wide publicity and positive reviews, and was named the best psy-
chology book of the year by the Association of American Publishers. The question
remained of what impact it would have on psychiatric diagnosis.
The time was right to reconsider psychiatry’s approach to depression. LoS was
published just as American psychiatrists, after almost a decade of quiet preparation,
began more actively and publicly to prepare the new fifth edition of the DSM (DSM-
5; American Psychiatric Association 2013). LoS provides what we believe is a com-
pelling critique of the DSM-IV criteria for major depressive disorder (MDD) and a
critical analysis of how psychiatry came to mistakenly categorize so many people
who experience intense normal sadness as psychiatrically ill with MDD. Our hope
was that LoS would stimulate changes in the way the forthcoming DSM-5 would
define this diagnosis, hopefully causing the criteria to be amended to narrow the
range of conditions classified as depressive disorders. Our critique, as we will
explain below, did indeed influence the DSM-5 classification of MDD, although not
in the way that we intended.
Proposals for changes to be made to the diagnostic criteria used to identify men-
tal disorders in DSM-5 were made public by the DSM-5 Task Force and by the
many DSM-5 work groups concerned with specific groups of disorders in 2010. The
French edition of LoS (Horwitz and Wakefield 2010), translated by Francoise Parot,
was published just at the time when the proposed revisions were starting to be hotly
debated. That debate intensified over time and absorbed American psychiatry right
up to the publication of DSM-5 in May 2013. This volume of reflections on depres-
sion is appearing a couple of years after DSM-5’s publication. This chapter endeav-
ors to bring the story of depression’s fate in the DSM and society more generally up
to date, filling in the main developments from the time of the publication of LoS to
the publication of DSM-5. Many of the changes in the DSM-5 that we describe are
likely to be reflected as well in the upcoming eleventh revision of the ICD, currently
in preparation.
Terminology
Terminology poses a challenge when discussing whether certain conditions classi-

fied by DSM-5 as depressive disorders are in fact normal sadness. The two domains
of psychiatric disorder and normal suffering usually involve quite different termi-
nology. The medical conditions are described by medical terms such as “diagnosis,”
“symptoms,” and “depression,” whereas normal sadness is generally described by
terms such as “feelings,” “grief,” “suffering,” and so on. However, when considering
whether certain conditions are disorders or normal sadness, the discussion can
become quite tortured if one flips back and forth between vocabularies. More impor-
tantly, one’s choice of vocabulary in disputed cases can beg the very question under
consideration by presupposing or at least suggesting the nature of the condition
being described.
Consequently, as in LoS, for convenience we adopt here the standard termino-
logical convention one finds in most writing on this topic, which is to use the medi-
cal vocabulary of “symptom,” “diagnosis,” and “depression” throughout as a
uniform way to describe both disorders and non-disorders, including conditions
whose status is under dispute. These medical terms are to be understood as purely
descriptive and as neutral with regard to disorder versus normality, so that they do
not imply the presence of a medical disorder. Thus, as used here, normal sadness has
“symptoms” such as insomnia and lessened interest in one’s usual activities,
“depression” is sometimes a normal emotion (a usage that has become quite com-
mon), and a clinician can “diagnose” a condition as normal sadness. We also use the
DSM’s phrase “depressive episode” as well as the phrase “DSM depression” to
denote any condition that satisfies the DSM’s symptom and duration criteria for
MDD (i.e., at least 5 symptoms for at least two weeks), but again neutrally with
respect to whether such episodes are disorders or, contrary to DSM, are sometimes
periods of intense normal sadness. We do not intend for this terminological conve-
nience to in any way demean, implicitly medicalize, or simplify the all-too-human
experience of grieving the loss of that which we love.
The Ubiquity of Depression
One of the most revealing recent scientific developments for an understanding of the
nature of DSM-defined MDD is the improved measurement of the prevalence of
DSM-defined depressive episodes in the general population. In LoS, we docu-
mented a dramatic rise in the estimated lifetime prevalence (i.e., how many people
have the condition at some point in their lives) of major depressive disorder in the
United States. Just a few decades ago, psychiatrists were trained to believe that
perhaps 2–3 % of the population would suffer from depressive disorder, which was
considered a relatively rare but severe disorder (Klein and Thase 1997). Others con-
sidered the true prevalence to be in the vicinity of 1–2 %, if they believed that
“endogenous” depression, a more severe form, was the only form legitimately diag-
nosed as a medical disorder (Parker 2007). These views corresponded to the more
demanding approach to depression diagnosis taken throughout much of medical
history (Horwitz & Wakefield 2007).
The most methodologically advanced studies of the national prevalence of DSM-
defined MDD in the community that were available at the time of LoS’s publication
were cross-sectional studies that interviewed a sample of subjects during one period
of time and asked them to recall whether they had ever experienced each of the
depressive symptoms in the past, and if so, whether they had experienced them
together during a common episode. These recollections were then transformed into
diagnoses and used to calculate how many people have depressive disorders at any
point over a lifetime.
Major DSM-based cross-sectional studies of nationally representative samples,
some of which were reported in LoS, revealed increasingly large numbers of indi-
viduals who at some point satisfied the DSM diagnostic criteria for MDD. The ini-
tial DSM-based study, the Epidemiological Catchment Area Study (ECA), found a
national lifetime MDD prevalence rate of 5.2 % (Robins and Regier 1991). Further
studies with improved methodology trended much higher, including the National
Comorbidity Survey (NCS) rate of 17 % for depressive episodes of all kinds (Kessler
et al. 1994) and 15 % for MDD strictly defined (Kessler et al. 1996), the National
Comorbidity Survey Replication (NCS-R) rate of 16 % (Kessler et al. 2003), and the
National Epidemiologic Survey of Alcoholism and Related Conditions (NESARC)
rate of 13 % (Hasin et al. 2005). Although the NCS’s 17 % rate tends to get cited,
perhaps the most authoritative estimate was Kessler et al.’s (2005) projection of
lifetime risk from the NCS-R data, yielding an overall lifetime MDD risk up to age
75 years old of 23 %, about a quarter of the entire population. Similar lifetime rates
were arrived at in many other countries at about the same time using similar cross-
sectional methodology, including rates in Germany, the Netherlands, Norway, Italy
and Hungary ranging from 15 to 18 % (Hasin et al. 2005).
The magnitude of these prevalence rates puzzled even some prominent epidemi-
ologists, who acknowledged that normal reactions to stress might have been mis-
classified as depressive disorder (Narrow et al. 2002; Regier et al. 1998). Attempts
to resolve the problem by limiting diagnosis to conditions in which there was dis-
tress or role impairment were not very successful in reducing prevalence (Wakefield
and Spitzer 2002), perhaps because normal negative emotions such as sadness can
be intense and are inherently distressing and often impairing of one’s usual role
performance. Consequently, these “clinical significance” criteria did not really dis-
tinguish disorder from normality (Spitzer and Wakefield 1999; Wakefield 2009;
Wakefield and First 2013; Wakefield et al. 2010). Moreover, a troubling question
went unexpressed at the time: if the DSM criteria do in fact confuse normal sadness
with psychiatric disorder, then is it possible that even these high rates are too low
and that with full information we would find even more people in the community
that satisfy the DSM-defined MDD criteria?
In terms of full information, the question about all of these cross-sectional stud-
ies was the accuracy and completeness of memory; were respondents recalling all
of the symptoms they had experienced years before the interview? In fact, memory
is known to be notoriously unreliable about such feelings when recalled many years
later (Kruijshaar et al. 2005). The only way to establish the true prevalence of DSM-
defined MDD in the community would be to follow individuals longitudinally and
periodically assess them while symptoms were still fresh in their minds.
At the time that LoS’s manuscript was in preparation, two initial longitudinal
studies that were methodologically limited but still quite informative had been
recently published, but did not come to our attention in time to be reported in the
book. First, Wells and Horwood (2004) reported on a representative sample of a

cohort of youths born in the New Zealand city of Christchurch in 1977, who were
given mental health assessments starting at age 15 (in 1992) that included questions
about the depressive symptoms they had experienced the previous year. The youths
were re-interviewed at ages 16, 18, and 21 years. In just the 7-year study period
between the ages of 14 and 21 years old, 37 % of Wells and Horwood’s (2004)
sample satisfied DSM MDD criteria at one or more points, supporting the notion of
radically higher prevalence rates than were reported in cross-sectional studies.
Moreover, 54 % reported key depressive symptoms of depressed mood or loss of
interest, so even those who did not qualify for MDD often would have qualified for
minor or subthreshold depression or adjustment disorder with depressive features.
The second study not reported in LoS was a longitudinal study starting in 1978
but continuing through to 2007 (Parker 1979, 2007), in which Wilhelm and Parker
followed a cohort of students who took a one-year post-graduate course in teacher
education at a Sydney college, measuring a variety of depression-related variables
every 5 years. When the study began, they asked participants whether they had
experienced depression in the broad sense that includes normal mood variation,
defining depression as any “significant lowering of mood, with or without feelings
of guilt, hopelessness and helplessness, or a drop in one’s self-esteem or self-regard”
(Parker 1979, p. 128). Fully 95 % of the sample reported having such experiences,
with 91 % reporting having had them in the past year, and with a mean number of
episodes occurring in the past year of 6.3 episodes (Parker 1979, 2007). This nicely
illustrates the ubiquity of normal depressive mood shifts. Regarding lifetime preva-
lence of MDD, based on the initial interview and three subsequent interviews,
Wilhelm and Parker’s sample had a lifetime MDD prevalence rate over a period of
15 years of 35 % (Wilhelm et al. 1996). If one includes in depressive disorder both
major depression and DSM minor depression (the latter requiring 3–4 symptoms for
2 weeks), then 57 % of the sample had experienced a depressive disorder. When the
sample was examined after 25 years, with the sample’s average age having increased
from 23 to 48 years old, the lifetime cumulative MDD prevalence rate was 42 %
(Wilhelm et al. 2006).
Two more incisive studies with improved methodology that appeared subsequent
to LoS’s publication have come close to satisfactorily resolving the question of
lifetime prevalence of DSM-defined MDD for a substantial age range, though not
yet for the entire lifespan. Moffitt et al. (2007, 2010) longitudinally followed a rep-
resentative cohort of individuals in Dunedin, New Zealand over the years from
childhood to adulthood. The respondents were periodically interviewed only about
symptoms they had experienced during the past year before the interview, maximiz-
ing accuracy of recall. The result was that, in contrast to the standard estimate of
17 % lifetime prevalence of MDD derived from cross-sectional studies, the Dunedin
study yielded roughly a 17 % prevalence rate of MDD in any one given year. The
cumulative Dunedin lifetime rate of MDD over the four one-year measurements at
ages 18, 21, 26, and 32 (i.e., the percentage who satisfied DSM criteria for MDD at
any one or more of the four one-year evaluation points) was 41.4 %. This lifetime
rate does not include individuals who had depressive episodes only before age 18 or
after age 32, or had them only during the other 10 years between the ages of 18 and
32 that were not sampled in the four one-year evaluations, so full lifetime preva-
lence would be considerably higher.
A second longitudinal study by Rohde et al. (2013) essentially replicated the
main results of the Moffitt et al. study. Rohde et al. found a 51 % cumulative inci-
dence of MDD in a U.S. cohort of Oregon children followed longitudinally from
childhood to age 30, with interviews at roughly 6-year intervals covering the time
since the previous interview rather than just the previous year. MDD prevalences
just during the “emerging adult” (ages 18–23 years) and “adult” (ages 24–30 years)
periods were 28 % and 26 %, respectively. Recalculating from Rohde et al.’s tables
and counting only MDD in emerging adulthood and newly emerging cases in adult-
hood, Rohde et al.’s findings indicate a minimum incidence of DSM MDD between
ages 18 and 30 of 44 % (an underestimate because cases in adulthood recurrent with
episodes experienced before emerging adulthood are missed in this count). This
result is comparable to Moffitt et al.’s (2010) finding for the same ages of 41 %.
However, neither the Moffitt et al. nor the Rohde et al. studies considered MDD
first-onsets that occurred after the early thirties. We don’t yet have longitudinal stud-
ies for the lifetime of community samples, so we don’t know what the prevalence of
DSM-defined MDD would be across the entire lifespan. The best that can be done
at present is speculatively to extrapolate total prevalence, using cross-sectional stud-
ies to indicate roughly how many first onsets occur in older individuals.
For example, in the cross-sectional National Comorbidity Survey Replication
(NCS-R), using careful life-history-review methodology, Kessler et al. (2005) found
that 50 % of the cases reported first onset after the age of 32. Eaton et al. (1995)
similarly found in the ECA that of those satisfying the DSM MDD criteria, “50 %
meet the criteria before they are 35” (p. 969). Because the NCS-R and ECA are
cross-sectional studies, the first onsets in later years are overestimated because
some failed to recall earlier episodes. But even if we assume that the actual first-
onset rate is half of what was reported, that would mean that about 25 % (instead of
50 %) of all DSM-defined MDD cases have first onset after the early 30s. That
would mean that the prevalence from the Rohde et al. study represents 75 % of the
overall rate, and the overall rate would then be 4/3 of the Rohde rate (because the
additional 25 % is one-third of 75 %). Extrapolating from the Rohde et al. report,
the projected (speculative) lifetime DSM-defined MDD prevalence would then rise
to about the two-thirds of the entire population (i.e., 4/3 × 51 % = 68 %).
In sum, recent studies confirm that even the implausibly high prevalence esti-
mates available at the time LoS was published were much too low. Depressive dis-
order, a condition considered relatively rare just a few decades ago, if defined via
DSM symptom-based criteria, occurs in the majority of individuals. This is just
what one might expect if disorder and normal sadness are being confused by the use
of symptom-based criteria. These astonishingly high rates have led to fresh calls by
leading scholars to rethink the diagnostic threshold between normal sadness and
depressive disorder (Goldberg 2011; Maj 2011a, b; Parker 2011; Tyrer 2009), the
very task we began in LoS.
The Tidal Wave of Antidepressant Use
Since LoS’s completion, the rates of antidepressant use have continued to skyrocket
in the United States, with multiple studies showing a rise of about 400 % in just a
decade from the early or mid 1990s to the early or mid 2000s (Mojtabai 2008; Pratt
et al. 2011). Moreover, the rise is taking place fastest among the less severe depres-
sions for which the evidence of benefit is weakest (Mojtabai 2008). Recent reports
indicate that in the United States about one in every nine adults and, shockingly,
about of a quarter of all adult women in their forties and fifties, are taking these
drugs at any given time (Pratt et al. 2011).
The international data indicate a worldwide trend towards expanding use of anti-
depressant medication beyond any plausible application to genuine depressive dis-
orders or related disorders. According to the Organization for Economic Cooperation
and Development (OECD), countries such as Iceland, Australia, Canada, Denmark
and Sweden are reaching rates of antidepressant use approaching that of the Unites
States – that is, 8–10 % or more of adults taking antidepressant medications at any
one time – with rates generally doubling over the past few years (OECD 2013). For
example, during the period from 2000 to 2011, rates of antidepressant use grew by
150 % in Germany and by over 100 % in many other OECD countries, including
Italy, Australia, Spain, Portugal, Denmark, and the United Kingdom (OECD 2013).
France, already one the highest users of antidepressants in the OECD in 2000, none-
theless saw its rate of use grow by about another 20 % between 2000 and 2011
(OECD 2013), with approximately 10 % of the country’s population reimbursed for
at least one antidepressant at any one time, mostly prescribed by general medical
practitioners (Mercier et al. 2011).
Of particular concern is an expansion internationally and in the United States of
antidepressant use for milder forms of sadness that may not even carry a psychiatric
diagnosis (Hollingworth et al. 2010; Mercier et al. 2011; Mitchell et al. 2009;
Mojtabai 2013). Other factors hypothesized to account for increased use include
guidelines that recommend increased duration of treatment to prevent relapse
(Moore et al. 2009), extension of antidepressants to related anxiety conditions such
as social phobia and generalized anxiety disorder (Hollingworth et al. 2010; Mercier
et al. 2011), and even depressive reactions to the economic downturn (Gili et al.
2013), although data suggest that rates of antidepressant use were already rising
rapidly before the downturn (OECD 2013). A recent study revealed that in Europe
as a whole, 8 % of all individuals and 10 % of middle-aged adults took antidepres-
sants in 2010, with about three-quarters of those taking them for over a month
(Blanchflower and Oswald 2011). Moreover, under the influence of culturally
sophisticated marketing campaigns, the upswing in depression diagnoses and anti-
depressant prescriptions in the United States and Europe over the past few decades
is now being replicated in other countries that formerly had relatively few depres-
sion cases, such as Japan (see Kitanaka 2016, this volume; Watters 2010).
These increases in antidepressant use have occurred despite growing skepticism
about the effectiveness of these medications. Evidence increasingly suggests that
the improvement that occurs with antidepressant treatment is largely attributable to

placebo effects (Kirsch et al. 2002, 2008; Moncrieff et al. 2004; Pigott et al. 2010).
Other evidence suggests that most patients do not benefit, but that possibly there is
a beneficial effect for a small subgroup, perhaps consisting of more severe depres-
sions (Gueorguieva et al. 2011; Kirsch et al. 2008; Thase et al. 2011).
This upward trend in antidepressant use has also occurred despite increasing
evidence that the negative side effects of antidepressants are considerably greater
than generally thought (Read et al. 2014). Indeed, some researchers are finally
attempting to explore the question of why human beings are biologically designed
to experience sadness at all, and what the costs might be of interfering with this
response (Andrews and Thomson 2009). There is also growing concern about the
challenges of going off these drugs after prolonged treatment due to serious nega-
tive reactions, often labeled a “discontinuation syndrome” to avoid any connota-
tions of dependence or addiction. Such difficulties are reported by a substantial
percentage of patients, ranging between 20 and 75 % in various studies (Lane 2011).
Disturbingly, difficulties going off of antidepressants, while related to length of time
taking them, seems to affect some patients who are on antidepressants for as little as
six weeks (Haddad 2001; Haddad and Anderson 2007; Schatzberg et al. 2006;
Warner et al. 2006; Zajecka et al. 1997). Nonetheless, perhaps influenced by phar-
maceutical advertising and by a perception of beneficial effects on patients, general
medical practitioners tend to see antidepressants as a safe and effective treatment for
depressed mood (Mercier et al. 2011). The entire area remains actively controver-
sial in both scholarly and popular publications (Angell 2011a, b; Horgan 2011;
Kirsch 2010; Kramer 2011; Melander et al. 2008; Oldham et al. 2011; Stewart et al.
2012; Sunday Dialogue 2011).
Medicalization of Treatment
Trends in treatment, and specifically shifts in who treats depression and how it is
treated, reflect a growing view of sadness as a medical disorder that is a “brain dis-
ease” best treated by physicians and with medication. A combination of factors,
including the rise of novel antidepressant medications, the perception that there is
an epidemic of untreated depressive disorder based on epidemiologic surveys apply-
ing DSM diagnostic criteria to community samples, and the current popularity of a
brain-disease model of depression, have been influential in changing treatment pat-
ters. In the United States, there has been a documented shift towards treatment of
depression by general physicians and towards medication rather than
psychotherapy.
The most authoritative treatment and provider data concerning recent outpatient
depression treatment in the U.S. comes from Marcus and Olfson’s (2010) analysis
that compares the 1998 and 2007 Medical Expenditure Panel Surveys, which are
surveys sponsored by the Agency for Healthcare Research and Quality to provide
estimates of the use of health care services in a nationally representative sample of
the US civilian non-institutionalized population (in 2007, N = 29,370). Each survey

consists of three rounds of in-person interviews during the study year, as well as a
medical events diary kept by the respondent. By comparing two successive surveys,
Marcus and Olfson are able to identify trends across a decade of growth and change
in depression treatment.
One of Marcus and Olfson’s (2010) major findings was that the use of psycho-
therapy in outpatient treatment of depression is decreasing, with the percentage
receiving psychotherapy going from 54 % in 1998 to 43 % in 2007 (Marcus and
Olfson 2010). This continues a trend documented in an earlier study of a drop from
71 to 60 % getting psychotherapy between 1987 and 1997, the period during which
SSRI antidepressants became available (Olfson et al. 2002). Marcus and Olfson also
report that about 35 % of outpatient depression patients received both psychother-
apy and medication in 2007, implying that the percentage receiving psychotherapy
alone was very small, perhaps about 8 % of depression outpatients.
As to providers, as one might expect, the vast majority of 2007 depression out-
patients saw physicians, of which about half were psychiatrists. The figure for how
many outpatients saw physicians closely tracks the figure for medication use, with
85 % seeing a physician (including psychiatrists and other physicians) and 82 %
receiving medication in 2007. Of the prescriptions written for antidepressants in
recent years, 80 % were written by general physicians, and of those, about three-
quarters were written with no accompanying formal psychiatric diagnosis (Mojtabai
and Olfson 2011). Seeing a physician is obviously a necessary condition for receiv-
ing a prescription for medication, but these data also tell us that seeing a physician
with any hint of depression is virtually a sufficient condition for receiving medica-
tion. A striking finding is the limited involvement of non-physician mental health
professionals in the overall provision of outpatient depression treatment. The previ-
ous decade had seen a major increase in the physician portion of outpatient treat-
ment from 69 to 87 % of all depression outpatients, and a drop in the psychologist
share from 30 to 19 % (Olfson et al. 2002). In 2007, both psychologists (21 %) and
social workers (7 %) served rather small percentages of the outpatient depression
group. The very low figure for social workers, which has stayed about the same
since 1998, is particularly striking since they constitute by far the largest segment of
the mental health profession in the United States. It would appear that the medical-
ization of depression has generally worked to direct these cases to physicians.
LoS and the DSM-5’s Bereavement Exclusion
LoS used a wide range of evidence to show that the fundamental flaw of the MDD
diagnosis was its use of symptoms without consideration of the contexts in which
they developed. It surveyed thousands of years of medical history, which routinely
separated normal sadness that arises and persists in the context of some loss from
depressive disorders that are unrelated to their contexts. Reviewing the evolutionary,
social, and psychological literatures on sadness, we described normal sadness as
having three basic qualities. First, it was inherently context specific in the sense that
it is biologically designed to emerge in response to a specific range of the “right”
stimuli consisting of losses and stresses and not to occur in response to events out-
side that range. The second component was that the emotional and symptomatic
severity of the response was of roughly proportionate intensity to the magnitude of
the loss that generated it, with the understanding that there is great individual vari-
ability as well as cultural shaping of the intensity of response. The third and final
component of nondisordered sadness was that symptoms not only emerge but also
persist in accordance with external contexts, but then naturally remit when the con-
text changes for the better or as people reconstruct their lives and their meaning
systems to adapt to their losses. Depressive disorders, according to us, always lack
at least one of these qualities of nondisordered reactions.
One particular aspect of the MDD diagnosis was of special interest. MDD’s
symptom-based definition contained one exception – diagnoses were not given to
bereaved people unless their symptoms were still present after two months or were
especially severe. This exception was known as the “bereavement exclusion” (BE),
and was stated, somewhat confusingly, as follows:
The symptoms are not better accounted for by Bereavement, i.e., after the loss of a loved
one, the symptoms persist for longer than 2 months or are characterized by marked func-
tional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic
symptoms, or psychomotor retardation. (American Psychiatric Association 2000, 356)
In other words, patients are exempt from a diagnosis of depression if their symp-
toms are better explainable as part of normal grief following the loss of a loved one.
It is well known that grief can occasionally trigger a genuine mental disorder (Parkes
1964), so the BE could not simply exclude all depressive feelings after loss from
diagnosis. Instead, based on classic studies of normal grief (Clayton et al. 1968), the
BE distinguished the kinds of depressive feelings that are common in normal
general-stress reactions (e.g., sadness, crying, difficulty sleeping, lessened appetite,
loss of interest in or lack of pleasure from usual activities, difficulty concentrating,
fatigue) and thus would indicate a likely normal response to loss from those more
severe symptoms (e.g., psychotic ideation, suicidal ideation, psychomotor retarda-
tion, sense of worthlessness, marked impairment in functioning, prolonged dura-
tion) that possibly indicated that the reaction had become pathological. Thus, to be
excluded from MDD diagnosis, depressive feelings after a loss had to pass six tests;
they had to be of normal-range duration (the DSM-IV defined a normal period of
depressive feelings during bereavement after the death of a loved one as lasting no
more than 2 months) and they had to include none of the five other especially seri-
ous symptoms. An episode that would otherwise have enough symptoms to qualify
as MDD but occurred after loss and had only general distress symptoms and none
of the six marks suggestive of pathology was called an “uncomplicated” bereave-
ment-related depression and was excluded from MDD diagnosis.
Wakefield et al.’s (2007) Study Showing that the BE Should

Be Extended to Other Stressors
The BE was especially important because it was the sole exception to the symptom-
based nature of the MDD diagnosis. In contrast to the DSM, we believe that bereave-
ment was not a unique exemption to the depression criteria but was a model for all
kinds of loss situations. Remarkably, the distinction between uncomplicated versus
complicated depressive episodes that the DSM applied to bereavement-related
depression to distinguish normal from abnormal depressive responses to loss had
never been applied to depressive reactions to other stressors to see whether it worked
there as well, despite the fact that accumulating evidence suggested that transient
normal depressive responses to other stressors are common.
With colleagues Michael First and Mark Schmitz, we conducted a study to
examine whether depressive reactions to other stressors, such as loss of a valued
job, marital dissolution, financial ruin, loss of possessions in a natural disaster, and
negative medical diagnosis in oneself or a loved one, also fell into the same pattern
of milder uncomplicated responses and more severe complicated and possibly dis-
ordered responses (Wakefield et al. 2007). The study, published soon after LoS,
examined whether depressive-like feelings after other stress-related losses that did
not feature especially severe symptoms or extended duration – and thus were also
“uncomplicated” according to the DSM’s definition in the BE – were similar to
uncomplicated bereavement-related depressions in other respects, and thus presum-
ably also normal-range responses that should be excluded from diagnosis. Follow-up
studies addressed some weaknesses in the initial study and confirmed the results
(Wakefield and Schmitz 2013a, b).
We found that all kinds of loss-triggered episodes of depression that were not
especially severe or prolonged and met the requirements for being “uncomplicated”
(i.e., included only general-distress-type depressive feelings and not any of the six
features suggesting pathology) had similar symptoms, durations, treatment histo-
ries, and degree of impairment as uncomplicated bereavement (Wakefield et al.
2007; Wakefield and Schmitz 2013a, b). Moreover, all loss-related uncomplicated
MDD conditions differed greatly from other MDD conditions in a variety of ways
indicating lower levels of pathology indicators, suggesting normal emotional condi-
tions (Wakefield and Schmitz 2012a).
Our empirical research thus convincingly showed that the depression criteria
mistakenly singled out bereavement as the single exclusion to the MDD diagnosis.
The mental health consequences of uncomplicated bereavement were similar to
depressions that stemmed from any kind of loss whether the death of a loved one,
divorce, unemployment, and the like and were distinct from complicated depressive
conditions. The critical distinction was not between bereavement and other losses
but between uncomplicated conditions following loss and conditions with espe-
cially severe patho-suggestive symptoms such as suicidal thoughts, marked func-
tional impairment, morbid preoccupation with worthlessness, or psychotic
symptoms, or prolonged duration. These findings seemed to indicate that the
bereavement exclusion should be extended to cover all kinds of losses that weren’t
particularly intense or lengthy. We proposed this narrowing of the domain of MDD
as a target for DSM-5 revision, and a first step towards reigning in the excessive
diagnosis of MDD in cases of intense normal sadness. We estimated that correcting
this one problem alone, by excluding from MDD diagnosis uncomplicated depres-
sive reactions to recent losses, would reduce the prevalence of community cases of
DSM-diagnosable depressive illness by about 25 %.
DSM-5’s Reaction: Elimination of the Bereavement Exclusion
Researchers connected to the development of the DSM-5 reacted with alarm to

these findings. One prominent member of the DSM-5 depression task force, psy-
chiatrist Kenneth Kendler, used his own data set to test our contention. His findings,
however, replicated our own: depression that developed after bereavement was
identical to that following other stressful life events, and fell into the same two
classes of uncomplicated and complicated reactions with overall similar features
(Kendler et al. 2008). All parties were in agreement on this point. However, there
was a vast difference in how they interpreted its implications. For Wakefield et al.,
given that the BE’s excluded cases are not disorders, the similarity to analogous
reactions to other stressors meant that those reactions to other stressors are not dis-
orders either. We therefore argued that the DSM criteria should be revised to expand
the BE to apply to uncomplicated reactions to all major stressors. However, to
Kendler and others working on DSM-5, the similarity just showed that it was wrong
to single out bereavement for exclusion, so something had to change. “The DSM-IV
position is not logically defensible,” Kendler wrote in a subsequent piece (2010). A
later analysis suggested that it was Kendler’s many claims in support of eliminating
the BE that were indefensible (Wakefield 2011).
Rather than agreeing that the BE should be extended, Kendler and others rea-
soned in the opposite direction. They agreed that given the similarity bereavement
could not be singled out, but argued that this likeness only implied that “either the
grief exclusion criterion needs to be eliminated or extended” (Kendler 2010). Either
option would resolve the inconsistency. Those who supported eliminating the exclu-
sion altogether argued that since the uncomplicated other-stressor responses are
now considered disorders by the DSM, the similarity result simply meant that we
had been wrong all along about the bereavement cases. However, the fact is that the
pathological versus normal status of depressive reactions to stressors other than
grief had not been empirically studied at the time of DSM-III in the way that grief
had been studied, and the issue of whether other reactions should be excluded sim-
ply never came up. The question of how such reactions should be understood has
never been considered seriously or empirically evaluated by any DSM work group
in any revision of the manual, and remains an unresolved issue. In any event, propo-
nents of elimination of the BE strongly resisted extending the BE to other stressors,
which would have lowered the number of conditions diagnosable with MDD and
thereby potentially missed some genuine cases.
The president of the American Psychiatric Association in 2011–12, John Oldham,

similarly reacted to this research by emphasizing the lack of justification for a
unique bereavement exclusion, and embracing the implication that therefore the BE
should be eliminated, not extended, because all such reactions should be considered
disorders:
(The bereavement exclusion is) very limited; it only applies to a death of a spouse or a loved
one. Why is that different from a very strong reaction after you have had your entire home
and possessions wiped out by a tsunami, or earthquake, or tornado; or what if you are in
financial trouble, or laid off from work out of the blue? In any of these situations, the exclu-
sion doesn’t apply. What we know is that any major stress can activate significant depres-
sion in people who are at risk for it. It doesn’t make sense to differentiate the loss of a loved
one as understandable grief from equally severe stress and sadness after other kinds of loss.
(Brooks 2012)
Oldham and many others argued, as had Kendler et al. (2008), that because
uncomplicated depressive reactions during grief look similar to uncomplicated
reactions to other stressors, and because the DSM considers the reactions to other
stressors to be disorders, therefore the bereavement exclusion should be eliminated
in DSM-5. However, the DSM-IV equally considered the uncomplicated
bereavement-related depressive reactions to be normal, so once the uncomplicated
depressive reactions to various stressors were discovered to be equivalent, the argu-
ment could be run in either direction with equal appeal to the authority of the
DSM. Thus, citing the DSM became irrelevant. Once the bereavement-related
depressive feelings and depressive feelings related to other stressors and losses were
shown to look the same, this created a real dilemma for the DSM-5 that could not
be resolved by appealing to features of the DSM-IV, because the DSM-IV was
inconsistent on the very point at issue. The question then became whether all of the
uncomplicated depressive reactions to loss or stress – that is, all of the reactions to
bereavement and to other stressors that had none of the six patho-suggestive fea-
tures and thus could potentially be best explained as part of a normal reaction –
should all be excluded from or included in major depression diagnosis. None of
those arguing for the elimination of the BE ever directly addressed this question on
empirical grounds.
Other proponents of abandoning the BE argued that the presence of the DSM’s
depressive symptoms themselves, regardless of context or type, constituted a disor-
der. “When someone has a myocardial infarction (MI), physicians regard it as an
instantiation of cardiac disease, regardless of its ‘context’,” psychiatrist Ronald Pies
claimed. “The MI may have occurred in the context of the patient’s poor diet, smok-
ing, and high levels of psychic stress – but it is still an expression of disease” (Pies
2008). For Pies, depression is depression, just as a heart attack is a heart attack. For
all of these psychiatrists, the clinical symptomatic similarity of uncomplicated
depression during grief to uncomplicated depression after other stressors indicated
that the BE should be abandoned, not extended.
Pies and other proponents of eliminating the BE claimed that physicians don’t
fail to diagnose serious diseases such as heart attacks, cancer, or tuberculosis that
had environmental precipitants. Likewise, they argued, all depressive conditions

should be diagnosed, regardless of their cause. Yet, unlike a heart attack, grief is a
naturally designed and self-limited response, not a failure of natural functioning like
a heart attack. Moreover, physicians do take context into account in deciding
whether, for example, heightened pulse or blood pressure likely signify a disorder
or a reaction to circumstances in the individual’s life. However, there is a difference
between psychiatric and other medical diagnosis in this regard simply because psy-
chological functions are biologically designed to be highly sensitive to environmen-
tal context, and in fact it is this context-dependence that makes them adaptive and
useful. Fear, for example, would not be very useful if it was happening all the time
or randomly; it is useful because it is selectively triggered by perceived danger.
Sadness similarly is highly sensitive to context, so that context must be taken into
account when evaluating whether a disorder exists. In any event, the BE in DSM-IV
already classified most depression during grief as MDD based on the presence of
even one of the six features that were prohibited from exclusion. The notion that
depression was depression just as a heart attack was a heart attack was both false
and could not justify changing the previous criteria that considered especially severe
grief as a disorder.
An important form of evidence in a consideration of diagnostic validity is predic-
tive validity, whether over time the sequelae of a condition suggest it was a disorder
or not. The BE debate was transformed when studies of the predictive validity of the
BE began emerging. Several studies showed that at either one- or three-year follow-
up periods after an episode of uncomplicated bereavement-related depression, peo-
ple were no more likely than the non-depressed to have subsequent depressive
episodes or various forms of anxiety (Gilman et al. 2012; Mojtabai 2011; Wakefield
and Schmitz 2012a).
These results were soon generalized to all stressors; uncomplicated depressive
reactions to stressors in general turned out to be much lower on pathology indicators
than other forms of depression (Wakefield and Schmitz 2013b). To address the cri-
tique that grief was not unique and so there was no justification for the BE, Wakefield
and his collaborators went on to conduct studies that showed an even more striking
finding: people who developed uncomplicated depressions after all kinds of losses
were more similar to those who were never depressed than to those who had com-
plicated depressive conditions. Using data gathered at two points of time, they
found that individuals with uncomplicated cases have similar recurrence rates
(3.4 %) to people with no history of depression (1.7 %) during a one-year follow-up
period; both groups had far lower rates than those with complicated cases (14.6 %)
(Wakefield and Schmitz 2013c). The analysis was replicated in another data set and
also applied to other possible sequelae of depression, such as anxiety disorders and
suicide attempts (Wakefield and Schmitz 2014a, b). Not only were those with
uncomplicated stress-related depressive conditions similar to one another, but they
were far more comparable to people who had never been depressed than ones with
serious or enduring symptoms.
These findings posed a stark choice for the DSM-5 mood disorders work group.
On the one hand, they could expand the bereavement exclusion to cover all uncom-
plicated responses to loss-related stressors. On the other hand, they could abolish
the BE so that all symptoms meeting the two-week MDD criteria were mental
disorders. This was an especially consequential decision because MDD had been
psychiatry’s central diagnosis for the past 30 years. Extending the bereavement
exclusion threatened both the symptom-based principles that were foundational for
psychiatric diagnosis since 1980 and a substantial portion of the potential clientele
of mental health professionals.
Given the international influence of the DSM, it was not only in the United States
that concern was expressed about the proposed elimination of the BE. Given the
limited ability of most nations’ mental health systems to meet the treatment needs
of the enormous numbers of genuinely psychiatrically disordered individuals, some
European clinicians reacted to the proposed elimination of the BE by questioning
whether it made sense to encompass a large number of false positive diagnoses to
avoid the small chance that a case might be missed. For example, an article in the
German national newspaper Suddeutche Zeitung described a report issued by the
German Society for Psychiatry and Psychotherapy, Psychosomatics and Neurology
(DGPPN) on the DSM-5 changes, and reported on an interview with Wolfgang
Maier, President of the Society and Director of the Psychiatric Clinic of the
University of Bonn (Weber 2013). Here is a translation of part of the article:
The specialist organisation DGPPN advises against overdiagnosis in the DSM-5. There is
the ‘danger of pathologising ordinary states of suffering as well as natural adaptation and
aging processes’, says the president of the DGPPN and director of the psychiatric clinic of
the University of Bonn, Wolfgang Maier, in a statement on Monday.
The statement names a number of examples, where the new catalogue shifts the bound-
aries between health and sickness in an inadmissible way according to the DGPPN. Thus,
in the DSM-5 a sadness of over two weeks after a death shall be diagnosed as depression if
it shows its usual symptoms: cheerlessness, lack of drive/energy, indifference, sleeping
problems, lack of appetite.
“Such an overdiagnosis constitutes a threat, which is put up with by the APA authors
with open eyes,” says DGPPN president Maier: “Their premise is, we prefer false positive
diagnoses rather than we fail to see a real sick person.” But this is, according to Maier, a
calculation that doesn’t work, alone for economical reasons, at least not in Germany. One
should always take into consideration that a diagnosis entitles the person affected to a provi-
sion of medical care through the system, whose resources are limited. The consequence
could be that for the psychically truly sick there will be less possibilities for treatment.
(Frances 2013a)
An additional generally unstated issue in the European response to DSM-5 is that

in many European countries with generous disability benefits there are large num-
bers of individuals classified as disabled based on depression diagnoses that may
not in all cases represent a genuine disorder. Further broadening the scope of depres-
sion to include what seem to be normal reactions seemed to open the floodgates to
increased public expenditures for psychiatric claims that may not be warranted.
However, this issue played a small role in the debate, which was focused on whether
the change was indeed a diagnostically valid one.
The Death of the Bereavement Exclusion
The symptoms and two-week duration criteria for Major Depressive Disorder
(MDD) that appeared in the DSM-5 replicated the criteria of the earlier DSM-IV-TR
(2000). The one major change to MDD criteria in the new edition of the manual was
that it eliminated the bereavement exclusion from the category’s diagnostic criteria.
The DSM-5 mood disorders work group insisted that all conditions that met MDD
symptom and duration criteria should be liable to a diagnosis of depression. William
Coryell, a work group member, explained this decision in a DSM-5 website posting
defending the decision after some negative commentary appeared in the New York
Times, explaining that bereavement-related depression is similar to other depres-
sion. He quoted the work group’s own earlier posting and a review article by Kendler
et al.: “The DSM-5 Mood Disorders Work-group has recommended the elimination
of the bereavement exclusion criteria from major depressive episodes in light of
evidence that ‘the similarities between bereavement related depression and depres-
sion related to other stressful life events substantially outweigh their differences’
(Kendler et al. 2008)” (Coryell 2012).
This rationale begged the crucial question of whether all uncomplicated depres-
sive reactions to stress (whether caused by bereavement or other losses and stress)
were different from other MDD in a way that suggested they are normal emotional
responses. The implicit assumption that the excluded depressions were similar to
other depressions was based on three reviews of the literature by overlapping authors
all of which claimed that the excluded depressions were in fact quite similar to all
other MDD (Lamb et al. 2010; Zisook and Kendler 2007; Zisook et al. 2007). These
reviews were later shown in a “review of the reviews” to be spurious because they
cited no studies that were directly relevant to the question at issue (Wakefield and
First 2012a). Such evidence was just starting to be generated. Two more recent
reviews focus on the empirical evidence generated out of the debate and its interpre-
tation and provide strong support for extending the BE to all major stressors rather
than eliminating it (Wakefield and Schmitz 2012b; Wakefield 2013a).
Despite going ahead with the elimination of the BE, in response to intense criti-
cism the DSM-5 added a note to the MDD diagnostic criteria that states:
Responses to a significant loss (e.g. bereavement, financial ruin, losses from a natural disas-
ter, a serious medical illness or disability) may include the feelings of intense sadness,
rumination about the loss, insomnia, poor appetite, and weight loss noted in [the symptom
criteria], which may resemble a depressive episode. Although such symptoms may be
understandable or considered appropriate to the loss, the presence of a major depressive
episode in addition to the normal response to a significant loss should also be carefully
considered. This decision inevitably requires the exercise of clinical judgment based on the
individual’s history and the cultural norms for the expression of distress in the context of
loss. (American Psychiatric Association 2013, 161)
It is of interest that the note, by referring to several stressors and neglecting to

mention any durational limit, in effect recognizes two of the points we made in LoS
and subsequent publications. First, uncomplicated normal depressive reactions can
occur in response to any stressor, not just bereavement. Second, the two-month
durational limit for uncomplicated bereavement-relate depression in DSM-IV is

unrealistically brief and without any scientific foundation – a conclusion supported
by recent research that suggests that 6 months or 1 year would be a more valid cut-
point (Wakefield and Schmitz 2012a, b, 2013a, b; Wakefield et al. 2011a, b).
This note, however, is not part of the formal diagnosis and does not contain any
diagnostic criteria. The MDD criteria themselves encompass all uncomplicated nor-
mal sadness reactions as well as depressive disorder, and then the note suggests that
it is up to the clinician to make a further judgment about the suitability of the diag-
nosis. The interpretation of the note is itself a matter of contention. Most DSM-5
work group members believe this note to be largely superfluous, perhaps applying
to the rare case or to subthreshold conditions, but not actually changing the fact that
virtually all conditions satisfying MDD symptom and duration criteria are now con-
sidered MDD whether or not they follow loss of a loved one or any other stressor;
most members of the work group believe that the work group completely eliminated
the BE, and this is how it is being represented in the revisions of major instruments
used for diagnosis and research (Michael First, personal communication). On the
other hand, one prominent member of the work group, Mario Maj (2013), argues
that the note leaves MDD diagnosis after a stressor entirely open to clinical judg-
ment that can override the formal criteria, and thus in effect opens the door to the
kind of subjective clinical judgment about MDD diagnosis that was problematic
prior to DSM-III and was the reason for creating descriptive criteria in the first
place. In any event, experience suggests that a note like this one will not be used by
researchers and thus will have little or no impact on thinking in psychiatry. Such
notes without criteria are inevitably ignored by researchers as well as by most clini-
cians, thus do not change the fact that DSM-5 eliminated the BE and, in so doing,
created the likelihood of millions of additional incorrect diagnoses among a vulner-
able population.
The DSM-5 criteria without the BE in effect modify the earlier definition in two
major ways. First, any grieving person with depressive feelings is liable to a depres-
sive diagnosis after a two-week period, rather than a two-month period, which many
experts believed was already far too short (Kleinman 2012). Second, the criteria no
longer require the presence of especially severe depressive symptoms during
bereavement to be included as having MDD. Anyone who has suffered the loss of
an intimate and has normal symptoms of grief such as sadness, a loss of pleasure,
sleeping and eating problems, and fatigue that last for a two-week period following
the death would meet the new criteria. Not only did the DSM-5 newly pathologize
millions of people who are not currently diagnosed, but it missed the opportunity to
correct the criteria and depathologize even larger numbers of people with normal
depressive feelings who are currently liable to diagnosis.
Each of the committee’s arguments for eliminating the BE was seriously defi-
cient. Consider the DSM-5’s own definition of mental disorder:
A mental disorder is a syndrome characterized by clinically significant disturbance in an
individual’s cognition, emotion regulation, or behavior that reflects a dysfunction in the
psychological, biological, or developmental processes underlying mental functioning.
Mental disorders are usually associated with significant distress or disability in social,
occupational, or other important activities. An expectable or culturally approved response

to a common stressor or loss, such as the death of a loved one, is not a mental disorder.
(American Psychiatric Association 2013, 20)
This definition of mental disorder uses “the death of a loved one” to illustrate the
difference between a painful but normal emotion and a mental disorder. Surely after
the loss of a loved one it is not only within expectable range but a “culturally
approved response” to experience general distress symptoms such as sadness, lack
of sleep, lessened appetite, loss of interest in usual activities, and difficulty concen-
trating on usual tasks. The MDD definition as explicitly stated thus appears to be in
tension with the DSM’5 own sensible requirement that “An expectable … response
to a common stressor or loss, such as the death of a loved one, is not a mental
disorder.”
The removal of the BE also undermines the central logic behind psychiatric diag-
nosis itself. The point of distinguishing one diagnosis from another is that distinc-
tions help specify the causes, courses, outcomes, and treatments of the condition.
Yet, combining uncomplicated depressive symptoms that stem from grief, unem-
ployment, divorce, and the like with those that are disproportionate to their contexts
does the opposite: it blurs conditions with environmental causes with those stem-
ming from some dysfunction within the individual, those that are transient and
unlikely to recur with ones that are more enduring; and those that are likely to
improve enduringly on their own from those that may require professional interven-
tions. The decision to remove the BE from the MDD criteria also challenges the
as-yet-unrealized assumption that mental disorders will ultimately be found to stem
from abnormal brain functioning (Greenberg 2013, 240). As diagnosticians have
long recognized, normal brains (or minds) naturally respond to losses with periods
of sadness. Neuroscientific research that relies on the DSM-5 criteria will hope-
lessly confound brains that are operating normally with those that are
dysfunctional.
The DSM-5 work group also argued that the bereavement exclusion could pre-
vent grieving people from getting treatment that can help them. The Chair of the
work group, Jan Fawcett, cited the effectiveness of medication in helping the
BE-excluded cases as the primary reason for eliminating the exclusion (Fawcett
2010). Reviews supporting elimination of the BE (Zisook and Kendler 2007; Zisook
et al. 2007) cited as the only or primary evidence of medication benefit psychiatrist
Sidney Zisook et al.’s one study of 22 recently bereaved people, in which they
reported that over half of those were treated with the anti-depressant buproprion
improved after two months (Zisook et al. 2001). Yet, this study had no placebo
group and its claimed success rate of a little more than half (13 of 22) did not exceed
placebo recovery rates in other studies. Early bereavement is, after all, a period in
which it is well documented that symptoms plummet without medication (Clayton
et al. 1968). The claims of drug benefit made on the basis of this uncontrolled study
would not be taken seriously in any scientific branch of medicine.
Proponents of removing the BE exclusion also cited the possibility of untreated
grief leading to suicide in the absence of treatment. They urged diagnosis of the
bereaved on the grounds that the benefits of treating people who have “suicidal
ideation, major role impairment or a substantial clinical worsening” far outweigh
the costs of eliminating the exclusion (Kendler 2010). “I’d rather make the mistake
of calling someone depressed who may not be depressed,” Zisook stated, “than
missing the diagnosis of depression, not treating it, and having that person kill
themselves” (Zisook 2010). This was a disingenuous argument: the preexisting
DSM-IV bereavement criteria already considered grieving persons with especially
severe or impairing symptoms such as suicidal risk as not meeting the exclusion
criteria. Recent studies have confirmed that the reference to possible suicide attempts
was sheer scaremongering and that the evidence shows uncomplicated depressive
reactions to stressors, which exclude suicidal ideation, do not involve elevated sui-
cide attempt rates, as one would expect given the screening for suicidal ideation
(Wakefield and Schmitz 2014a, b).
Finally, the abandonment of the bereavement exclusion in the DSM-5 risks an
enormous pathologization that can occur when the MDD criteria consider bereaved
people as disordered. Given that about 40 % of grieving people meet these criteria a
month after their loss, it is likely that a majority of the bereaved could be diagnosed
with MDD after the two-week period the diagnosis specifies (Clayton et al. 1972;
Clayton 1982). In the U.S. alone, some 8 to 10 million people suffer the loss of an
intimate every year and about half of these would meet the new criteria for bereave-
ment. Because nearly everyone will suffer the loss of an intimate, abandoning the
bereavement exclusion renders a majority of the population liable to a diagnosis of
depressive disorder at some point in their lives.
The elimination of the bereavement exclusion in the DSM-5 thus has no good
conceptual, empirical, or treatment-related grounds. “There is no scientific basis,”
Wakefield and First concluded after reviewing the evidence, “for removing the
bereavement exclusion from the DSM-5” (2012a, 9). Moreover, as one critic noted,
the BE “was necessary: without it the DSM loses its credibility” (Greenberg 2013,
114). Another leading critic, Allen Frances, asserted: “This was a stubbornly mis-
guided decision in the face of universal opposition from clinicians, professional
associations and journals, the press, and hundreds of thousands of grievers from all
around the world” (Frances 2013b, 186). Remarkably, even psychiatrists’ col-
leagues in general medicine questioned the DSM-5’s elimination of the BE, with
editorials appearing in leading medical journals largely siding with the critics
(Editorial 2012; Friedman 2012).
In the course of the debate, two legitimate empirically supported points were
made by those arguing for elimination of the BE. The first point was that the BE was
stated in DSM-IV in a confusing way, so that without proper training a clinician
could easily get confused as to how to apply the exclusion (Corruble et al. 2009).
The appropriate way to address this problem is by rephrasing the exclusion, not by
eliminating it. If we eliminated every frequently misapplied but scientifically valid
diagnostic criteria set in the DSM, then MDD itself would have to be eliminated
because it is known that general practitioners, who do the majority of treatment of
MDD, misdiagnose more cases than they correctly diagnose.
The second legitimate empirically supported point is that the exclusion’s validity
is dramatically reduced when individuals already have a history of depressive disor-
der before the loss occurs (Wakefield and First 2012a). In such cases, there is a high
likelihood not only of a depressive reaction to the loss, but of later recurrences or a
chronic episode that in the long run reverses the exclusion (which requires limited
duration). When one looks at those who have clinically problematic depressive
reactions to loss, a large percentage consist of those who have experienced depres-
sive disorder before the loss. In fact, this caveat was already implicitly taken into
account in the DSM-IV BE’s initial instruction that an episode should be diagnosed
as MDD only if it is not better explained by normal bereavement. A depressive reac-
tion to loss in an individual who has experienced recurrent depression in the past
that was not itself explainable as a normal reaction to loss cannot be best explained
as normal, but rather is most likely a recurrence (or at very high risk of becoming a
recurrence) of the long-term depressive vulnerability. In such cases, the power of
the “normal response to loss” explanation is weakened considerably, and a diagno-
sis of MDD becomes appropriate. However, this reasoning is not made explicit and
so there is the real danger of the BE being applied automatically to recurrent cases.
Although such recurrent cases are only a very small fraction of BE candidate cases,
they account for a large percentage of later recurrences and should be more clearly
and explicitly excluded from the exclusion.
To address both the clarity of the exclusion and the need to avoid applying the
exclusion to recurrent cases, Wakefield and First (2012a) drafted a revised statement
of the exclusion. However, their draft applied only to the bereavement case and not
to other stressors, and it did not take into account the increasingly strong empirical
evidence that a longer durational threshold than the DSM’s 2 months is more valid.
With these two additional corrections, an alternative statement of a “major stressor
exclusion” might look as follows:
If the episode occurs in the context of a major loss or stressor, it is not diagnosed as major
depression if it is better explained as a normal distress reaction. If the episode includes any
one or more of the following features that are suggestive of major depression, then it is
disqualified form being considered normal distress and should be diagnosed as major
depression: duration greater than 6 months; suicidal ideation; morbid preoccupation with
worthlessness; marked psychomotor retardation; prolonged and marked global functional
impairment; psychotic symptoms; or a history of major depressive disorder in the past.
Stressor-related depressive episodes that have none of these features should be given a
diagnosis of “normal bereavement-related depression, provisional.”
What led the DSM-5 to alter the MDD diagnosis in the face of such powerful
opposition? The charitable way of viewing the arguments of the proponents of the
new DSM-5 criteria is that they are genuinely interested in alleviating the suffering
that accompanies grief. Yet, drugs and psychotherapy are not known to be more
effective for uncomplicated grief than simply letting the condition run its natural
course. A more cynical explanation it that the removal of the BE can expand the
clientele of mental health professionals. Because drugs are by far the most common
response to grieving people who seek treatment, the DSM-5 changes could also
produce a bonanza of new clients for pharmaceutical companies. Eight of the eleven
members of the APA committee that recommended the new criteria had financial
connections to the drug industry (Whoriskey 2012), and the consultant to the work
group, Sidney Zisook, who provided most of the public defense of eliminating the
BE, had been the lead author on the one study of using medication during early
bereavement-related depression that was cited by the work group to justify the BE’s
elimination. The chairman of the work group, Jan Fawcett, enthusiastically pro-
pounds drug treatments for depression: “I’m still working at 78 because I love to
watch patients who have been depressed for years come to life again. You need
those medicines to do that” (Whoriskey 2012). While drugs can help some people
overcome grief, the new MDD criteria will mostly encompass people whose natural
suffering will heal without interference from powerful medications. In any case, the
criteria they replaced provided ample protection that grieving people with espe-
cially severe or prolonged conditions would receive depressive diagnosis.
Perhaps the best explanation for the DSM-5’s decision stems from the nature of
professional legitimacy. Psychiatry is primarily a legitimate source of treatment for
pathological conditions. The BE recognized that one form of common loss was not
pathological but extending this logic would have also excluded many others from
diagnosis and treatment. Expanding the BE could have had led to a major contrac-
tion in the number of people who meet diagnostic criteria for depression. The evi-
dence forced the DSM-5 committee to accept that bereavement was equivalent to
other losses but it then had no choice but to abandon the exclusion in order to main-
tain psychiatry’s range of authority.
DSM-5’s Expansion of the Categories of Depressive

and Grief Disorders
We have focused thus far on DSM-5’s elimination of the bereavement exclusion

because this is the DSM-5 change that is most relevant to the argument of LoS,
which focused on MDD as the primary locus of psychiatry’s confusion of normal
sadness with mental disorder. However, the overall changes to the category of
depressive disorders went well beyond this change. Indeed, DSM-5 dramatically
altered – and in a variety of ways greatly expanded – the domain of diagnosable
depressive illness, compounding the problem of potential overdiagnosis and the use
of psychiatry to control normal human variation.
Three of the other changes are particularly notable, because they introduce new
categories of disorders. Two of the new categories are depressive disorders intro-
duced into the main list of depressive disorders, and the other is a new disorder of
grief that is listed as a target of further study.
First, DSM-5 depressive disorders include a controversial new child depressive
disorder category, Disruptive Mood Dysregulation Disorder (DMDD). DMDD
diagnostic criteria include temper outbursts on average at least 3 times a week with
generally irritable or dysphoric mood between outbursts, lasting for a year. Diagnosis
of DMDD precludes diagnosis of oppositional defiant disorder (ODD), although

most DMDD cases qualify for ODD diagnosis. This largely unstudied diagnosis
was introduced to address an embarrassing problem for psychiatry – the excessive
diagnosis of child bipolar disorder, and the consequent overtreatment of children
with heavy-duty medications such as mood stabilizers and antipsychotics. DMDD
is aimed at providing an alternative category for the diagnosis of such children.
Difficult children often present with chronic irritability and dysphoria punctu-
ated by frequent tantrums, and this is often interpreted as indicating bipolar disor-
der. However, research suggests that such children are in fact generally neither
experiencing an early form of bipolar disorder nor a stable mood disorder. Many
children with these symptoms are brought to treatment by desperate parents, but the
children seem to outgrow these behaviors and almost all are alternatively classifi-
able as having oppositional defiant disorder (Axelson et al. 2012). Consequently,
the new DMDD diagnosis means that children whose defiance and tantrums are
causing distress to parents may now come to be illegitimately diagnosed as having
a mood disorder and receive antidepressant medication. Many children with various
problems present with these symptoms, so the potential for overdiagnosis is sub-
stantial. Admittedly, if one is going to overdiagnose, depressive disorders have
somewhat more benign medication implications than bipolar disorders, but it
remains uncertain that this category will be used to shift the bipolar diagnoses into
depression rather than simply opening up a new way to diagnose a large number of
normal children as depressively disordered.
A second new category of disorder, Premenstrual Dysphoric Disorder (PMDD),
has been added to DSM-5. This category was extremely controversial when first
suggested for earlier DSM editions, and was listed in the appendix of DSM-IV as a
category requiring further study. It has now been “promoted” to a full, regularly
listed depressive disorder. PMDD has long been controversial due to concerns that
the category would inevitably pathologize a common and natural female response
that varies in intensity but is not a mental disorder except under very rare circum-
stances. The diagnostic criteria require that during the week before onset of menses
and subsiding in the week following menses the patient experience at least five
symptoms with marked severity, including depressive symptoms (e.g., mood
swings, increased sensitivity, tearfulness, irritability or increased conflict, depressed
mood, anxiety, decreased interest in usual activities, difficulty concentrating,
fatigue). It is claimed that only a modest percentage of women, perhaps 8 %
(European Medicines Agency 2011), would qualify for diagnosis, but there is the
potential for extending this vaguely defined diagnosis to many more women given
that as many as 90 % of women report significant premenstrual symptoms (Halbreich
2004; Halbreich et al. 2003). Since the Food and Drug Administration has already
approved antidepressants for the treatment of PMDD, the inclusion of this category
in DSM-5 was a foregone conclusion.
Finally, there is a new grief disorder, Persistent Complex Bereavement-Related
Disorder (PCBD), listed for further study. Although also concerned with grief, this
category is not related to the elimination of the bereavement exclusion. The BE
specifically concerned depressive symptoms during grief, and specified when such
depressive symptoms should be diagnosed as disordered versus considered part of

normal grief. PCBD is concerned with the non-depressive symptoms of grief, which
before DSM-5 have never been subject to disorder diagnosis in the DSM. These
non-depressive grief feelings include, for example, yearning for the lost person,
being pained by or avoiding reminders of the person, feeling disbelief that the per-
son is gone, preoccupation with the deceased or with the circumstances of the death,
bitterness or anger over the loss, blame oneself or feeling guilty that one did not do
enough to save the person, wanting to join the deceased, loneliness or detachment,
and a sense of meaninglessness or emptiness. The proposed diagnostic criteria spec-
ify that if several of such symptoms continue for over a year after the loss at an
intense level, then the grief reaction is to be considered pathological. Grief
researchers themselves continue to argue for a six-month threshold for disorder
rather than one year (Prigerson et al. 2009; Shear et al. 2011), claiming that grief
that lasts that long has become interminable and has gone off track. However, these
proposals have little relation to what research studies actually show, which is that
many people, especially those who have lost a close dependent relationship, con-
tinue to progress in their mourning process and to further adapt to the loss long after
6 months or even a year (Wakefield 2012, 2013b). Thus, there is the potential for
massively pathologizing intense normal grief, even when no depressive symptoms
are involved.
Note that although PCBD is listed as a category requiring further study that has
no official diagnostic code, it is explicitly mentioned as a diagnostic option under
the coded main-list category of “other specified trauma- and stress-related disor-
ders” (the DSM-5 version of DSM-IV’s “not otherwise specified” disorders). Thus,
this disorder can in fact be diagnosed immediately within the DSM-5 system.
In sum, the DSM-5 made dramatic changes to the diagnosis of depressive and
grief conditions quite aside from the elimination of the bereavement exclusion and
the consequent expansion of MDD. DSM-5 also added three new categories of dis-
order addressing the experiences of children, women, and the grief-stricken, respec-
tively. Each of these categories might well encompass some genuine disorders, but
they are all drawn in broad terms and defined in terms of symptoms common among
normal individuals. They each, therefore, make the problem of false positive diag-
nosis potentially worse and provide a foundation for a possible new epidemic of
overdiagnosis. They clearly reveal psychiatry’s ongoing refusal to take seriously the
problem of distinguishing normal intense emotion from psychiatric disorder.
Conclusions
When DSM-5 finally emerged, it went in the direction opposite to that we had sug-
gested in LoS and in subsequent research articles. Rather than more carefully draw-
ing the distinction between intense normal sadness and MDD to make diagnosis and
research more valid, DSM-5 expanded MDD diagnosis as well as diagnosis of
depressive disorder in general into ever more areas, accelerating the trends we
observed in LoS. The pathologization of sadness is thus proceeding more rapidly

and more boldly, and with more blatant disregard of the scientific evidence, than we
ever imagined possible. In this chapter, we have provided some perspective on these
developments by offering an overview of how psychiatry, more than ever, is confus-
ing the normal with the disordered and encompassing normal sadness within the
category of major depressive disorder.
As The Loss of Sadness showed, the distinction between normal sadness and
depressive disorder has been part of Western science, philosophy, and literature
since the earliest recorded documents. Only since 1980 has this distinction been
greatly eroded and become in danger of being substantially lost. The change to
decontextualized symptom-based criteria for depressive illness was instrumental in
triggering the Age of Depression that we now inhabit, because psychological func-
tions are by their nature contextually sensitive, so that symptoms that are normal
responses versus disorders cannot be generally discriminated without context
(Wakefield and First 2012b). Our book posed a choice for psychiatric diagnosti-
cians: they should either recognize the distinction between normal, albeit painful,
emotions and mental disorders or risk pathologizing all forms of suffering. The
DSM-5 chose the path towards the latter option. However, in abandoning the
bereavement exclusion and greatly expanding the categories of depressive disorder,
DSM-5 might have overreached. Time will tell if this affront to common sense,
empirical evidence, and intellectual coherence will destroy the profession’s credi-
bility as the official social arbiter of normality and abnormality.
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Index
A B
Abraham, Karl, 12, 111 Barthes, Roland, 7
Adaptation, 50, 58, 72, 73, 80–82, 84, Beck Depression Inventory (BDI), 167
86, 87, 129, 188 Bereavement exclusion, 6, 14, 71, 82, 83,
ADHD, 10, 44, 50 99, 182, 183, 185–197
Adolph, Grünbaum, 88 Bipolar disorder, 21, 22, 31,
Agency, 57–60, 63, 127, 128, 138, 140, 141, 167, 195
143–146, 149–152, 181 Burnout, 44
Alcohol, 25, 122, 138, 147, 151 Burton, Robert, 3, 97
Amygdala, 88, 97–99
Anhedonia, 74, 78, 104, 105, 160, 167
Animal model, 13, 95, 157–162, 165, C
166, 169 Capability, 41–43, 45
Antidepressant, 6, 19, 30, 32, 35, 58, 60, Capgras, Joseph, 102
61, 80, 96, 100, 104, 123, 124, Caspi, Avshalom, 20, 75, 83, 122
162, 168, 180, 181, 195 Cavell, Stanley, 47
Antipsychiatry, 58 Child abuse, 25
Anxiety, 4, 9, 10, 21–23, 39, 45, 73, 76, Classificatory looping. See Looping effect
87–89, 113, 116–118, 123, 143, Clinical
158, 167, 169, 180, significance, 124, 177
187, 195 utility, 11, 30, 33, 36
Approach Cognitive-behavioral therapy (CBT), 45, 118
categorical, 7, 18 Cognitive neuroscience, 11, 40, 47–51, 70
contextual, 11, 32, 33 Coherence, 13, 128–131, 152, 197
dimensional, 8, 128 Comorbidity (comorbid), 87, 88
pragmatic, 11, 32, 33, 35 Cooper, Rachel, 69, 167
Aristotle, 3, 4, 129 Corticotropin-releasing factor (CRF), 88
Attenuated psychosis syndrome, 31 Cortisol, 22, 163
Austin, John L., 111, 139
Autism, 50, 71
Autistic disorders, 17, 158 D
Autonomy, 9, 11, 40–46, 48–50, 52, Delirium, 2
53, 63 Dementia, 24

DOI 10.1007/978-94-017-7423-9
206 Index
Depression, 1–14, 17–25, 30, 32–36, 39–42, Evidence-Based Medicine (EBM), 138
44, 45, 56–64, 70–90, 95–105, 111, Evolutionary psychology, 10, 12
112, 114–116, 118, 121–128, Evolved defense, 70, 71
138–143, 145–148, 150–152, Exophenotypes, 13, 170
158–170
Diagnostic and Statistical Manual of Mental
Disorders (DSM) F
DSM-III, 34, 44, 69, 174, 185, 190 False positive, 6, 8, 31, 74, 75, 99, 122,
DSM-IV, 7, 14, 53, 71, 121, 143–145, 188, 196
148, 175, 183, 185–187, 190, 192, Family history, 34
193, 195, 196 Feinstein, Alvan, 22
DSM-5, 1, 5, 7, 11, 14, 18, 30, 31, 33–36, First, Michael, 83, 99, 175, 177, 184, 189,
69–71, 74, 97, 99, 123, 128, 174, 190, 193, 197
175, 182–183, 185–197 5-HTT gene, 75, 122
Differential diagnosis, 30–36 Food and Drug Administration (FDA), 123,
Disability, 5, 17, 19, 24, 25, 45, 50, 143, 195
144, 174, 188–190 Foucault, Michel, 43, 49, 63
Disruptive mood dysregulation disorder Freud, Sigmund, 12, 19, 47, 110,
(DMDD), 167, 194 113–117
Distress, 6, 19, 25, 31, 33, 35, 36, 122,
123, 126, 127, 130, 132, 143, 144,
177, 184, 189–191, 193, 195 G
Distressing, 23 Galen, 3, 5
Durkheim, Emile, 63 Generalized anxiety disorder (GAD),
Dysfunction, 9, 30, 70, 72, 73, 75, 78, 21, 180
84, 88, 125, 159, 165, 168, 170, Genetic factors/genetics, 17, 70, 90, 170
190, 191 Goffman, Erving, 46, 51, 60
Dysphoria, 195 Goldberg, David, 10, 21–24, 121, 179
Grief, 4, 20, 36, 102, 111–113, 116, 117, 123,
132, 145
E Guilt, 6, 41–43, 47, 52, 74, 114, 117, 148,
Eating disorders, 17 158, 160, 164, 174, 178
EBM. See Evidence-Based Medicine (EBM)
ECA. See Epidemiological Catchment Area
Study (ECA) H
Ehrenberg, Alain, 11, 41–43, 47, 49, 96, 139, Hacking, Ian, 9, 60, 61, 126
143, 149, 151, 152 Hamilton (depression rating scale), 34,
Electroconvulsive therapy, 30 124, 167
Elias, Norbert, 52 Harmful dysfunction, 125
Empathy, 43–45, 48, 82, 131, 132 Hippocrates, 4
Endophenotypes, 170 Horwitz, Allan, 6, 13, 14, 30, 69, 71, 82, 96,
Engagement, 13, 128–131 99, 100, 102, 125, 126, 139, 143,
Enhancement, 39, 63, 129 174, 175
Environmental mismatch, 71
Epidemiological Catchment Area Study
(ECA), 177, 179 I
Epidemiology/epidemiological Imipramine, 34, 168
studies, 10, 11, 18, 21, 34, 144, Individualistic, 40, 41, 51, 52, 117
145, 151, 163 Intentionality, 12, 50, 111, 112,
Erasistratus, 4 114, 118
Esquirol, Jean-Etienne, 2 International Classification of Disease-10
Essentialism, 8 (ICD-10), 1, 11, 34–36, 121, 143,
Evans-Pritchard, Edward, 40 144, 174
Index 207
J N
Jackson, Stanley W, 2, 5, 70, 74 Narcissism/narcissistic pathology, 6, 42, 114
James, Henry, 12, 109, 110, 114–118 National campaigns, 13, 17, 139
Jaspers, Karl, 23 National Comorbidity Survey (NCS), 177
Johnson, Samuel, 2 National Institute for Mental Health (NIMH),
63, 69, 84, 90, 138, 139
Naturalism, 95
K Neoliberalism/neoliberal economy, 6, 11
Kant, Immanuel, 48 Nesse, Randolph, 70–76, 82–85, 87, 88,
Kendler, Kenneth, 18, 20, 33, 34, 81, 83, 90, 125
170, 185, 186, 189, 191, 192 Neural correlates, 95, 98, 100, 104
Kitcher, Philip, 101 Neuroimaging, 97, 100
Klein, Melanie, 5, 12, 115–117 Neuroticism, 22, 84, 88, 163
Klerman, Gerard, 32
Kraepelin, Emil, 3
O
Obsessional compulsive disorder (OCD), 23
L Oppositional defiant disorder (ODD), 195
Lacan, Jacques, 12, 116, 117, 147 Overdiagnosis, 188, 194–196
Lewis, Aubrey Sir, 2, 33, 170
Looping effect, 60
Loss events, 18–20 P
Low mood, 3, 12, 73–76, 84 Panic disorder, 23
Lypemania, 2 Persistent Complex Bereavement-Related
Disorder (PCBD), 195, 196
Personality, 17, 22–25, 41, 43, 51, 58, 59,
M 63, 84, 124, 128, 145, 163, 167
Maj, Mario, 11, 18, 30, 32, 33, 36, Pharmacotherapy, 34, 35
82, 83, 179, 190 Pinel, Philippe, 2
Major depression. See Depression Placebo, 19, 34, 123, 124, 181, 191
Major depressive disorder (MDD). Positive mental health, 39, 64
See Depression Postpartum depression (PPD), 77, 86
Maternal attachment, 21 Poverty, 43, 45
Mauss, Marcel, 40, 48 Precursors, 31
McIntyre, Alasdair, 40 Premenstrual dysphoric disorder (PMDD),
Mechanisms, 12, 48, 57, 58, 70–72, 75, 76, 167, 195
78, 83, 96, 98, 101, 102, 104, 113, Primary care, 12, 13, 19, 21, 121–132
115, 125, 148, 157, 159, 163, 165, Prodromes, 31
166, 168–170 Prozac, 6, 63
Medical model, 70 Pseudo-demented epression, 24
Melancholia, 2, 4, 12, 19, 32, 36, 97, Psychoanalysis/psychoanalytic, 10, 40,
103, 110–112, 114–116, 118, 44, 47–51, 58, 63, 111, 115, 118,
123, 125 146, 150
Mild depression. See Depression Psychotherapy, 30, 33, 35, 45, 46, 58, 59,
Montgomery-Åsberg Depression Rating Scale 89, 147–150
(MADRS), 167 Psychotic depression, 4, 116, 146
Mood disorder, 34, 39, 95, 97, 99, 101, 112, Public health, 12, 13, 39, 138–140, 144–146,
122, 161, 166, 188, 189 150–152
Morbidity, 43–46, 157
Mourning, 6, 7, 12, 19, 109–119,
146, 148 R
Murphy, Dominic, 70, 84, 86, 158, Reductionism, 96, 163
168, 170 Reliability, 33, 74, 174
208 Index
Research Diagnostic Criteria (RDC), 33, 34 Suicide, 4, 21, 31, 56–59, 63, 64, 79, 82,
Research Domain Criteria (RDoC), 70, 84, 90 84, 85, 114, 142, 158
Resilience, 62, 64, 130
Ricoeur, Paul, 129
Risks, 21, 31, 34, 35, 60, 73, 80, 84, 85, T
95, 105, 122 Taylor, Charles, 2, 130
Roberts, Robert C., 98, 99, 103, 105 Threshold (diagnostic threshold), 7, 24, 30, 32,
Rousseau, Emile, 46 34–36, 73, 179, 193, 196
Rumination, 12, 75, 77–81, 85, 86, 88, 89, Tiredness, 6
103, 165, 189 Translational (medicine/research/psychiatry),
10, 13, 157–162, 166–170
S
Schizophrenia, 2, 4, 17, 31, 46, 50, 71, V
122, 158, 167, 170 Validity
Schmitz, Mark, 34, 83, 184, 187, 189, conceptual validity, 11
190, 192 construct validity, 161, 162
Séglas, Jules, 2 face validity, 161, 162, 165
Selective serotonin reuptake inhibitors predictive validity, 161, 162, 187
(SSRIs), 30, 182 Vulnerability, 20, 21, 25, 58, 59, 62, 74, 100,
Self-control, 42, 43, 45, 52 122, 159, 160, 169, 193
Self-governance, 57, 62–64
Self-help, 39, 50, 62
Serotonin, 6, 8, 76, 96, 162, 163, W
168, 169 Wakefield, Jerome, 6, 9, 13, 14, 19, 30,
Simmel, Georg, 51 34, 71, 82, 83, 96, 99, 100, 102,
Social construction, 9, 10 125, 126, 139, 143
Social functioning, 44, 46 Winch, Peter, 40, 49, 51
Social phobia, 10, 180 Wittgenstein, Ludwig, 49, 109, 119
Social stigma, 31 Working memory (WM), 79, 88, 103
Somatic symptoms, 4, 19, 23 Workplace, 11, 40–42, 44, 46, 48, 56–59,
Spectrum, 17, 39, 75, 166 61–63
Spitzer, Robert, 33, 177 World Health Organization (WHO), 5, 138,
Starobinski, Jean, 2, 3 141, 143, 145, 174
Stressor, 18, 36, 77, 82, 83,
161, 184–193
Subjective experience, 36 Y
Suicidal ideation, 160, 183, 192, 193 Young, Allan, 56, 64

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History, Philosophy and Theory of the Life Sciences

ISSN 2211-1948 ISSN 2211-1956 (electronic)

Library of Congress Control Number: 2015959694

Springer Dordrecht Heidelberg New York London

Printed on acid-free paper

Introduction: Depression, One and Many .................................................... 1

An Insider View on the Making of the First French

Index ................................................................................................................. 205

Xavier Briffault is a social scientist and epistemologist working on mental health

Pierre-Henri Castel PhD in Philosophy, PhD in Psychology, 52, is French. He is a

Steeves Demazeux is an associate professor of philosophy at the Université

Christopher Dowrick, M.D., FRCGP is professor of primary medical care in the

Alain Ehrenberg is a sociologist and director of research at the CNRS (Centre

Luc Faucher is full professor in philosophy at the Université du Québec à Montréal

Modularity of Emotions (2008) and the editor of Philosophie et psychopathologies

Allan V. Horwitz is board of governors professor in the Department of Sociology

Junko Kitanaka, Ph.D. is a medical anthropologist and associate professor in the

Maël Lemoine is an associate professor in the philosophy of biomedical science in

Mario Maj is professor of psychiatry and chairman at the University of Naples

Jerome C. Wakefield is university professor, professor of social work and professor

Jerome C. Wakefield and Steeves Demazeux

J.C. Wakefield (*)

© Springer Science+Business Media Dordrecht 2016 1

A Short or a Long History?

The historiography on depression indicates the profound difficulty of finding the

Some Arguments in Favor of the Long History View

Whereas some medical historians have documented the swarming multiplicity of

now classify as “psychotic depression” – overlapping with what we now might

What Is the Meaning of the Depression Epidemic

depression. Others researchers have focused on changes in lifestyle, such as our

have no positive place in society as justifiable, excusable phenomena that relieve

“Diagnosis Creep” and the Philosophical Sociology of Concept

The dramatic changes in estimated prevalence concerning depression raise another

Integrating Biological and Social Views of Depressive Disorder

Third, due to normal variations unfavorable to the social resculpting process,

Overview of the Contributions

Sketch, in Defence of Some Psychoanalytic Views” examine depression from

developments and provide a retrospective account of the controversial influence of

© Springer Science+Business Media Dordrecht 2016 17

circumstances. The current concept is a blunderbuss approach which gathers

The Case for Heterogeneity

Can Homeostatic Responses to Adverse Circumstances

How Can Bereavement Be Distinguished from Depression?

of melancholia behaves like an open wound, drawing to itself energies…from all

Some Determinants of Vulnerability to Depression

The Importance of Anxiety in Depressive States

Epidemiological studies of mental disorders in the community all show substantial

Multiple Co-morbidity, or Depressive Syndromes Influenced

anxiety and depression. It is also extended to the overlapping syndromes of com-

Depression Presenting with Somatic Symptoms

Depression Accompanying Chronic Physical Illnesses

These depressions are often poorly recognised by generalists, whose attention is

Depression Due to Drugs, Both Licit and Illicit

Abstract One of the principles of the “neo-kraepelinian credo”, articulated in the

© Springer Science+Business Media Dordrecht 2016 29

The Evolving Target of Psychiatry

adolescents, or when it is considered to be a consequence of an alliance between

The Differentiation between “Normal” Sadness and Clinical

been found to be redundant by most clinical and epidemiological studies (e.g.,