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History of Depression
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History of Depression
Allan V. Horwitz, Jerome C. Wakefield, and Lorenzo Lorenzo-Luaces
The Oxford Handbook of Mood Disorders
Edited by Robert J. DeRubeis and Daniel R. Strunk
Abstract and Keywords
The symptoms that define depressive conditions have been recognized for millennia of
medical history. The earliest Hippocratic writings not only define depression in similar
ways as current works but also use context to differentiate ordinary sadness from
depressive disorder. Sadness was understood as a natural reaction to loss; symptoms
indicated a disorder only if they were not attributable to an identifiable trigger or if they
displayed disproportionate intensity or duration to their triggers. The first serious
approaches to subcategorize different types of depressive disorders developed in the
seventeenth century. Despite agreement that a melancholic or psychotic form of
depression existed, researchers debated the categorization of neurotic or nonpsychotic
depressions until 1980 when the DSM- III introduced major depression as a unitary
category. The DSM’s diagnostic system was historically anomalous because its diagnoses
did not consider the context in which symptoms arose. The only exception within the
DSM, for uncomplicated symptoms that follow bereavement, was removed from the
DSM-5 in 2013 so that depressive diagnoses now thoroughly conflate adaptive responses
to loss with pathological depressions.
Keywords: depression, Hippocrates, DSM-III, diagnosis, melancholia, melancholy, Emil Kraepelin, Sigmund Freud,
major depressive disorder, symptoms
Depression, unlike many conditions in the current psychiatric canon, has a lengthy and
readily identifiable history. Indeed, it is perhaps the most easily recognizable
psychological disorder throughout history; similar symptomatic descriptions occur over a
2,500-year span, representing what historian Stanley Jackson (1986, p. ix) calls a
“remarkable consistency.” From the earliest medical texts in ancient Greece to the
present Diagnostic and Statistical Manual of Mental Disorders (DSM), deep sadness and
Subject: Psychology, Neuropsychology, History and Systems in
Psychology
Online Publication Date: Apr
2016
DOI: 10.1093/oxfordhb/9780199973965.013.2
Oxford Handbooks Online
History of Depression
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its variants—hopelessness, sorrow, dejection, despondency, emptiness, despair,
discouragement—have been mentioned as core features of depression. Related symptoms
have included aversion to food, sleeplessness, fatigue, irritability, restlessness, fear of
death, repetitive focus on a few negative ideas, lack of pleasure or interest in usual
activities, and social detachment.
Yet from the advent of psychiatry until the introduction of the DSM-III in 1980, traditional
psychiatry recognized that even intense sadness with its associated “symptoms” can be a
normal emotional reaction to life circumstances, and took a contextual approach to the
diagnosis of depressive disorder. Its various definitions did not focus on symptoms alone
but emphasized that, to be considered as disorders, depressive reactions must be of
disproportionate duration or severity to the situation in which they emerged. Whether a
condition was diagnosed as disordered depended not just on the symptoms, which might
be similar in normal sadness and in pathological depression. It was also not entirely
defined by the condition’s severity, for normal sadness can be severe and disordered
sadness can be moderate. Instead, the distinction between sadness and depressive
disorder depended on the degree to which the symptoms were an understandable
response to circumstances.
This chapter elaborates the history of this contextual approach to depression providing
the background for how the definition of depression in the DSM-III (1980) overturned
thousands of years of thinking, replacing the more nuanced contextual approach with
relatively precise and communicable symptomatic criteria that largely ignored the
complexities of context, with detrimental side effects for psychiatric diagnosis. Worse, the
DSM-5 (American Psychiatric Association, 2013) for the most part eliminated the slim
remainder of the contextual tradition—the bereavement exclusion—so that the current
psychiatric diagnosis of major depression is entirely symptom based. Indeed, the most
recent DSMs represent a significant regression from the earliest efforts to define
depressive disorder and separate it from normal sadness. Although a symptom-based
definition of depression might prove to be relatively reliable, this reliability comes at the
expense of discriminant validity in distinguishing depressive disorders from normal
sadness reactions.
The Classical Tradition
Writing in the fifth century BC, Hippocrates (460–377 BC) and the school of Hippocratic
physicians that formed around him provided the first known description of melancholia
(the Greek name for pathological states of depression), stated succinctly in Hippocrates’s
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Aphorisms: “Fear or sadness that last a long time mean melancholia” (Hippocrates, 1923–
1931, Vol. IV, p. 185). In addition to fear and sadness, the Hippocratic writings
mentioned as symptoms of melancholia “aversion to food, despondency, sleeplessness,
irritability, restlessness” (Hippocrates, 1923–1931, Vol. I, p. 263). This description is
remarkably similar to the current definition found in the DSM-5 (American Psychiatric
Association, 2013). Unlike DSM-5, however, the Hippocratics did not view depression as a
free-standing condition but linked it with other conditions, especially anxiety (“fear”) and
delusions. On the basis of the latter feature, melancholia was often characterized as
“delirium without a fever.” A combination of anxious concerns and nameless fears,
depressive symptoms such as blackness of mood and suicidal impulses, and paranoid
tendencies such as sullen suspiciousness characterized melancholic conditions. Similarly,
Galen (131–201 AD) indicated that although “each (melancholic) patient acts quite
differently than the others, all of them exhibit fear or despondency” (Radden, 2000, p.
10). He went on to note: “Therefore, it seems correct that Hippocrates classified all their
symptoms into two groups: fear and despondency” (Jackson, 1986, p. 42).
Although the Hippocratics agreed with contemporary accounts on the symptoms of
melancholia, the Hippocratic definition in Aphorisms also specified the contextual
constraint that the symptoms had to last an unusually long time to constitute
melancholia. This indicates that it is not depressive symptoms alone but symptoms of
unexpected duration that indicate disorder. This insistence that the sadness or fear must
be prolonged is a first attempt to capture the notion that disproportion to circumstances
is an essential aspect of depressive disorder.
Hippocratic writings rarely focused on distinct external causes of melancholic disorders.
Rather, their foundational principle was that health is a state of equilibrium within the
body and that disease is due to a disturbance of this balance (Porter, 1997, pp. 55–62).
The Greeks viewed mental diseases, like disease in general, in terms of four basic
humors: blood, phlegm, yellow bile, and black bile. Each humor possessed two of four
properties: hot, cold, moist, or dry. When the humors were in balance with each other, a
healthy state resulted. Diseases, both mental and physical, stemmed from too much or
too little of one of these humors, a notion that would recur when theories of
neurochemical imbalance were developed at the end of the twentieth century. For the
Greeks, melancholia was connected to an excess of black bile. Yet mental disturbances
that resulted from an excess of black bile were not localized but disrupted a holistic
relationship between individuals and their surroundings. A variety of factors, including
diet, lifestyles, living conditions, and atmospheric elements, could lead to humoral
imbalances.
Traditional diagnostic treatises followed Hippocrates in distinguishing depression as a
disorder from a nondisordered type of deep sadness or fear that could have many of the
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same symptoms but was instead a normal, proportionate reaction to serious losses. For
example, Aristotle (384–322 BCE), or perhaps one of his followers, distinguished normal
states of sadness from pathological disease states, stating that in depression black bile is
“cold beyond due measure” so “it produces groundless despondency” (Jackson, 1986, p.
32). Here, “beyond due measure” refers to responses that are disproportionate to their
circumstances, so the resulting sadness is “groundless.” In contrast, sadness stemming
from losses such as the death of intimates, reversals in fortune, disappointments in
attaining valued life goals, and romantic disappointments could be proportionate to their
contexts and, therefore, not disordered.
Given that the symptoms of normal sadness and depressive illness could be the same,
ancient physicians understood that differential diagnosis required careful exploration
that went beyond the symptoms to the context of the symptoms. For example, Greek
physician Aretaeus of Cappadocia (ca. 150–200 AD) explicitly separated melancholic
patients who “are dull or stern, dejected or unreasonably torpid, without any manifest
cause” from those who experience “mere anger and grief, and sad dejection of
mind” (Jackson, 1986, pp. 39, 40). To illustrate the distinction, Aretaeus recounted his
own version of the diagnostic triumph famous in ancient times of Erasistratus (304–250
BC), 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 unexpressible) 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, p. 40)
Similarly, during the same period, Galen draws this distinction in his case histories. For
example, Galen describes a case in which he is unsure whether the problem 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
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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, p. 213)
In addition, early diagnosticians acknowledged that variations in temperament
predispose some people to more readily or intensely experience sadness or fear.
However, these variations were thought to be within a normal range of reasonably
proportionate responses that did not represent a disorder. Depressive disorders thus
differed from normal reactions, according to tradition, because they either arose in the
absence of situations that would normally produce sadness or were of disproportionate
magnitude or duration relative to their provoking causes. Such conditions indicated that
something was wrong in the individual, not in the environment.
The Anatomy of Melancholy
Subsequent to early Greek and Roman medicine almost no new developments in medical
thinking about melancholy occurred until the end of the eighteenth century. RobeR.
Burton’s The anatomy of melancholy. published in 1621, illustrates the persistence of the
classical tradition. It is the most renowned of all classical discussions of melancholy and
perhaps of any volume ever written about depression. Burton described three major
components of depression—mood, cognition, and physical symptoms—that are still
viewed as the distinguishing features of the condition. However, he insisted that
melancholic symptoms are not in themselves sufficient evidence of disorder. According to
Burton, only symptoms that are without cause provide evidence of disorder. As he
explained in this codicil to his definition: “without a cause is lastly inserted, to specify it
from all other ordinary passions of Fear and Sorrow.” And, he noted, “signs in the mind”
of melancholia included “Sorrow … without any evident cause; grieving still, but why they
cannot tell.”
Burton emphasized that a propensity to melancholy was present in all men, and was a
normal and ubiquitous aspect of the human condition:
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Melancholy … is either in disposition or habit. In disposition, it is that transitory
melancholy which goes and comes upon every small occasion of sorrow, need,
sickness, trouble, fear, grief, passion, or perturbation of the mind, any manner of
care, discontent, or thought, which causeth anguish, dullness, heaviness, and
vexation of spirit…. And from these melancholy dispositions, no man living is free,
no Stoic, none so wise, none so happy, none so patient, so generous, so godly, so
divine, that can vindicate himself; so well composed, but more or less, some time
or other, he feels the smart of it. Melancholy, in this sense is the character of
mortality.
(Burton, 1621/2001, pp. 143–144)
In contrast to normal melancholy that arises naturally after people have suffered losses
and disappointments and that is part of the “character of mortality,” Burton held that
melancholic afflictions are “contrary to nature.” This latter condition, the disorder of
melancholy, he defined as “a kind of dotage without a fever, having for his ordinary
companions fear and sadness, without any apparent occasion” (Burton, 1621/2001, pp.
169–170).
Burton was sensitive to the wide individual variation in the nature of loss responses. He
believed that a quite broad range of temperamental reactions to loss was nondisordered
as long as the reactions did not become chronic or self-perpetuating. He noted: “For that
which is but a flea-biting to one, causeth insufferable torment to another, & which one by
his singular moderation, & well composed carriage can happily overcome, a second is no
whit able to sustaine” (Burton, 1621/2001, p. 132). It is only when such normal reactions
to specific events become established as an ongoing condition independent of events that
Burton sees disorder:
(I)t falleth out oftentimes that these Dispositions become Habits, and … make a
disease. Even as one Distillation, not yet growne to custome, makes a cough; but
continuall and inveterate causeth a consumption of the lungs: so doe these our
Melancholy provocations…. This Melancholy of which we are to treat, … a
Chronicke or continuate disease, setled humor … not errant but fixed, … growne
to an habit, it will hardly be removed.
(Burton, 1621/2001, pp. 145–146)
In addition to noting normal variation in temperament, Burton was an astute observer of
the extremes to which normal reactions to loss could go. He noted that the most intense
painful losses included separation from friends and bereavement following loss of a loved
one (“in this Labyrinth of accidental causes [of melancholy] … loss and death of friends
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may challenge first place” Burton, 1621/2001, pp. 357–358) and compellingly described
the extremes that nondisordered grief can reach:
If parting of friends, absence alone, can work such violent effects, what shall
death do, when they must eternally be separated, never in this world to meet
again? This is so grievous a torment for the time, that it takes away their appetite,
desire of life, extinguisheth all delights, it causeth deep sighs and groans, tears,
exclamations, … howling, roaring, many bitter pangs, and by frequent mediation
extends so far sometimes, they think they see their dead friends continually in
their eyes, … Still, still, still, that good father, that good son, that good wife, that
dear friend runs in their minds; a single thought fills all their mind all year long, …
They that are most staid and patient are so furiously carried headlong by the
passion of sorrow in this case, that brave discreet men otherwise oftentimes
forget themselves, and weep like children many months together.
(Burton, 1621/2001, pp. 358–359)
Burton’s magisterial work remains the most comprehensive description of depression
ever compiled. Yet his rambling and disjointed style, not to mention the inconsistencies
and lack of systemization that plagued his work, meant that his vast compendium was not
a useful foundation for the more scientific studies of depression that would emerge in
later centuries. It remained for future diagnosticians to build on Burton’s work and to
disentangle melancholia from other conditions.
Burton’s work is clearly situated within the Hippocratic tradition. In effect, medical
commentators throughout the eighteenth century relied primarily on Greek physicians,
especially Galen, as authorities on depression and other mental illnesses (Simon, 1980).
Likewise, the association of sadness and fear under the general melancholic umbrella
persisted for centuries. The humoral theory of disease also endured in medical
understandings and treatments of melancholy until the end of the seventeenth century
and, sometimes, beyond then. Humoral thought was foundational not only in the culture
of physicians but also in the medical lore of common people and the lay healers. Diseases
resulted from imbalances between the various humors: treatments aimed to correct such
imbalances and restore the body to appropriate equilibrium. Hippocratic preferences for
altering lifestyles continued to prevail over more intensive medical interventions. Fresh
air, exercise, good sleeping, eating, and elimination habits, and control of the passions
remained prominent treatments for melancholy. Such treatments were typically
intertwined with religious, magical, and folkloric methods (Shorter, 1992).
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From the Seventeenth through the Nineteenth Centuries
A radical change in the Western intellectual tradition occurred in the seventeenth
century as the inductive, empirical, and observational methods of Bacon and Newton
overturned the more deductive, intuitive, and relational nature of Hippocratic methods.
Notions of disease specificity also began to emerge, particularly in the work of English
physician Thomas Sydenham (1624–1689). Sydenham proposed that each disease had
natural forms with uniform presentations in different individuals, an idea distinct from
holistic Hippocratic thought. After thousands of years of dominance by Hippocratic views
of humoral imbalance, a new system arose that was based on disturbances of the brain
and the nervous system (Porter, 1997).
Gradually, the capacious category of melancholia that spanned from the Hippocratics
through Burton began to split into more specific manifestations. Depressive conditions
were divided into two major types (Shorter, 2013). The first conditions were marked by
deep mental anguish, hopelessness, complete joylessness, stupor, and suicidal thoughts
and/or actions. These were likely to be chronic and recurrent and require the attention of
specialized healers (then called “alienists”) who treated insane conditions.
In addition to this serious melancholia, a new category of “nervous disorders” began to
emerge that viewed the nervous system as the source of health and illness, emphasizing
the importance of nerves, fibers, and organs. Accordingly, the causes of nervous
conditions were found in physiology, particularly brain lesions. Depressive symptoms
were viewed as one component of a syndrome of “nervous disease,” “nervous illness,”
“neurosis,” or, later, “neurasthenia” that referred to nonpsychotic conditions related to
problems of the nervous system. The depressive component of such states was not seen
as distinct from the variety of heterogeneous anxious and physiological symptoms that
comprised this diagnosis. Nervous disorders encompassed anxiety, fatigue, somatic
preoccupations, and obsessions (Shorter, 2013). Because these conditions were related to
an organic system, they were not seen as mental problems. Nervous disorders fell under
the domain of general physicians, neurologists, and spa doctors (Micale, 2008).
Melancholic and neurotic depressions were not two different points of the same
continuum of severity. Instead, “There are two different kinds of depression, as different
as tuberculosis and mumps; it makes no sense to lump both of them together under the
general term ‘depression’” (Shorter, 2013, p. 80). By the nineteenth century these
conditions were sharply distinguished by their symptoms, causes, and treatments. While
alienists and psychiatrists treated melancholic patients, often within inpatient settings,
nervous patients remained in the community under the purview of general physicians or
specialized nerve doctors.
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The two leading diagnosticians of the late nineteenth century took sharply different
approaches to depression. German psychiatrist Emil Kraepelin (1856–1926), who spent
his entire career practicing in mental asylums, focused on the melancholic type of
depression. He linked depression with mania under the general umbrella of manic-
depressive conditions, sharply distinguishing it from his second psychotic state of
dementia praecox (schizophrenia). Manic depression and dementia praecox were
homogeneous and distinct entities that presumably had entirely different causes,
prognoses, and outcomes (Kraepelin, 1921).
Early in his writings on classification and diagnosis, Kraepelin (1903) described
melancholia as a separate disorder unrelated to manic-depressive psychosis.
Subsequently, however, he was impressed by the fact that in some cases that initially
looked like melancholia, eventually—often after long periods of time—there developed a
manic episode. He was also persuaded by a study by Dreyfus (1907) that the nature of
melancholia and of the depressive pole of manic-depressive illness is in fact qualitatively
indistinguishable, and thus likely represent the same underling etiology. Kraepelin thus
eventually combined all depressive and manic-depressive mood disorders into one
category that, although encompassing a variety of clinical presentations, had as its
hypothesized source the same underlying pathophysiology: “Manic depressive insanity as
it is to be described in this section, includes on the one hand the whole domain of so
called periodic and circular insanity, on the other hand … the greater part of the morbid
states termed melancholia …. In the course of the years I have become more and more
convinced that all the above-mentioned states only represent manifestations of a single
morbid process” (Kraepelin, 1921/1976, pp. 1–2). However, with the subsequent
development of treatments specific to bipolar versus unipolar illness, all the unipolar
forms were united under the DSM’s major depressive disorder.
Kraepelin’s approach to psychiatric diagnosis is generally credited as the inspiration for
the DSM system, so it is of interest that, unlike the DSM but like most of his predecessors,
Kraepelin believed in the necessity of taking context into account when diagnosing
depressive disorder in order to differentiate it from normal intense sadness: “Morbid
emotions are distinguished from healthy emotions chiefly through the lack of a sufficient
cause, as well as by their intensity and persistence …. Again, morbid emotions sometimes
attach themselves to some certain external occasions, but they do not vanish with the
cause like normal feelings, and they acquire a certain independence” (Kraepelin, 1915, p.
68). Kraepelin, like Aretaeus, offered case illustrations of the danger of false positives
and emphasized the need to consider context—including history—to discriminate disorder
from nondisorder:
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Several times patients have been brought to me, whose deep dejection, poverty of
expression, and anxious tension tempt to the assumption of a circular
[pathological] depression, while it came out afterwards, that they were cases of
moodiness, which had for their cause serious delinquencies and threatened legal
proceedings. As the slighter depressions of manic depressive insanity, as far as we
are able to make a survey, may wholly resemble the well founded moodiness of
health, with the essential difference that they arise without occasion, it will
sometimes not be possible straightway to arrive at a correct interpretation
without knowledge of the previous history in cases of the kind mentioned.
(Kraepelin, 1917, pp. 199–200)
In contrast to Kraepelin, who was generally concerned with the conditions of severe,
hospitalized patients, the second towering figure of the time, Sigmund Freud (1856–
1939), had little concern with psychotic conditions. Instead, Freud was centrally involved
with nervous conditions found in community practices. Yet Freud gave short shrift to
depression, giving anxiety pride of place in his pantheon of neurotic symptoms. Freud’s
sole major essay on depression, “Mourning and Melancholia,” focused on the distinction
between the normality of grief and the disorder of melancholia:
Although grief involves grave departures from the normal attitude to life, it never
occurs to us to regard it as a morbid condition and hand the mourner over to
medical treatment. We rest assured that after a lapse of time it will be overcome,
and we look upon any interference with it as inadvisable or even harmful.
(Freud, 1917/1957)
Freud emphasized that symptoms associated with mourning are intense and are “grave
departures from the normal,” in the sense that grief is greatly different from usual
functioning. Nevertheless, grief is not a “morbid” condition; that is, it is not a medical
disorder that represents the breakdown of a biologically normal response and in fact does
not require medical treatment. Medical intervention, he suggested, could actually harm
the grieving person by interfering with this natural process.
By the early decades of the twentieth century, then, depression was sharply split into
melancholic conditions marked by serious symptoms that were linked to psychoses and
neurotic depression that was one of the psychoneuroses. Whereas melancholic
depression was thought to be due to some as yet unknown brain dysfunction,
nonmelancholic conditions were seen as products of various psychosocial adversities,
especially the loss of a love object. The former usually required some form of inpatient
treatment while the latter could be handled within outpatient settings.
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Between Kraepelin and Freud and the DSM-III
Freud, along with American psychiatrist Adolf Meyer, was the major influence on the
DSM-I (1952) and DSM-II (1968), the two manuals that preceded the DSM-III. Depression,
however, bore a more Kraepelinian stamp. Much in Kraepelinian style, the DSM-I
grouped affective disorders that were characterized by severe mood disturbances
consistent with melancholia as one of the three major categories of psychotic disorders
(the two others were schizophrenic and paranoid reactions) (American Psychiatric
Association, 1952, p. 12). Persons receiving this diagnosis showed “evidence of gross
misinterpretation of reality, including, at times, delusions and hallucinations” (American
Psychiatric Association, 1952, p. 25). In contrast, these earlier manuals conceived of
neurotic depression as an epiphenomenon of an underlying anxiety condition. The very
first sentence of the DSM-I classification of psychoneurotic disorders stated: “The chief
characteristic of these disorders is ‘anxiety’ which may be directly felt and expressed or
which may be unconsciously and automatically controlled by the utilization of various
psychological defense mechanisms (depression, conversion, displacement,
etc.)” (American Psychiatric Association, 1952, p. 31). Psychoneurotic depression was
thus understood as a psychological defense against anxiety.
The DSM-II also grouped psychotic depression with states of mania, much in Kraepelinian
fashion. It defined the category of major affective disorders as follows: “This group of
psychoses is characterized by a single disorder of mood, either extreme depression or
elation …” (American Psychiatric Association, 1968, p. 35). It continued to submerge
depressive neurosis within the broader category of anxiety conditions, stating that
“Anxiety is the chief characteristic of the neuroses” (American Psychiatric Association,
1968, p. 39). In contrast to the prominence these manuals accorded psychotic forms of
depression, they viewed psychoneurotic depression as one type of defense mechanism
against anxiety. During the 1950s and much of the 1960s, nonpsychotic forms of
depression were largely submerged into the broader conception of psychoneuroses.
Although psychotic forms of depression were central to psychiatric theory, research, and
practice before 1980, in the study of neurotic depression, numerous and often competing
diagnostic systems existed and none had preeminence over the others (Grob & Horwitz,
2010). Most researchers agreed with the DSM-I and DSM-II that melancholic (or
psychotic) depression—a particularly serious state marked by vegetative symptoms,
delusions, and hallucinations—was a distinct type of disorder (e.g., Kiloh & Garside,
1963; Klein, 1974; Mendels & Cochrane, 1968; Paykel, 1971). Although researchers
History of Depression
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concurred that a separable, psychotic form of depression existed, they could not reach a
consensus about the nature of nonpsychotic types of depression.
Researchers argued over whether these depressions were continuous or discontinuous
with psychotic forms, on the one hand, or with normality, on the other. They disputed
how many forms neurotic conditions took and even whether they had any distinct forms
at all. Diagnosticians who argued for discrete types could not agree on how many types
existed. Some concluded that in addition to a melancholic, psychotic type, depression had
only a single neurotic type (Kiloh & Garside, 1963). Others suggested that three or more
distinct, neurotic states of depression existed (Hamilton & White, 1959; Paykel, 1971;
Raskin & Crook, 1976). Various classifications of depression embraced from a single to as
many as nine or more separate categories (Kendell, 1976). Still others conceived of
neurotic depression as more closely resembling a personality or temperament type than a
disease condition (Eysenck, 1970). Nor was it known whether some milder forms of
depression were early indicators of eventual psychotic forms. In addition, little consensus
existed about the particular symptoms that were essential to definitions of nonpsychotic
forms of depression and more disputes abounded over whether depression should be
classified according to its symptoms, etiology, or response to treatments.
In 1976 the prominent psychiatric diagnostician R. E. Kendell published an article whose
title accurately conveyed the situation at the time: “The Classification of Depressions: A
Review of Contemporary Confusion.” Kendell outlined 12 major systems of classification,
most of which had little to do with the others. He concluded (1976, p. 25) that “there is
no consensus of opinion about how depressions should be classified, or any body of
agreed findings capable of providing the framework of a consensus.” In 1979, just a year
before the publication of the DSM-III, psychiatrists Nancy Andreasen and George
Winokur (1979) likewise noted the presence of “a hodgepodge of competing and
overlapping systems” in research about depression. Similar to the other major diagnoses
in psychiatry at the time, opinions regarding the classification of depression at the end of
the 1970s featured an extraordinarily broad range of unresolved conflicts on how best to
measure this condition. Yet in 1980, responding to this period of confused debate
characterized by the highly unsettled state of empirical findings and lack of definitive
theory about the nature of nonpsychotic depression, psychiatry would nonetheless adopt
a definitive set of symptomatic criteria for depression that has remained stable until the
present.
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Sources of the DSM-III
One of the 12 classifications of depression that Kendell reviewed in his 1976 article was
“The St. Louis Classification” developed by a group of psychiatrists at Washington
University (Horwitz, 2011). During the era in which psychodynamic perspectives
dominated the psychiatric profession, the Washington University Department of
Psychiatry was an outpost of traditional medically minded thinking. Led by Samuel Guze
and Eli Robins, this group’s primary concern was to develop a reliable system of
diagnosis that could differentiate the etiology, prognosis, and drug responses of various
conditions. They developed operational criteria for 14 disorders, known as the “Feighner
criteria” after the psychiatric resident who was the first author of the article that
described them (Feighner, Robins, Guze, Woodruff, Winokur, & Munoz, 1972).
The Feighner criteria for depression required fulfillment of three conditions. First,
patients must have a dysphoric mood marked by symptoms such as being depressed, sad,
or hopeless. Second, the criteria required five additional symptoms from a list including
loss of appetite, sleep difficulty, loss of energy, agitation, loss of interest in usual
activities, guilt feelings, slow thinking, and recurrent suicidal thoughts. Finally, the
condition must have lasted at least 1 month and not be due to another psychiatric or
medical illness (which were classified as “secondary affective disorders”). Patients whose
symptoms arose from preexisting mental or physical illnesses would receive a diagnosis
of a secondary affective disorder.
What was the basis for the Feighner criteria of depression? In contrast to the widespread
belief that a strong empirical research base underlay the diagnostic criteria leading to
the DSM-III (e.g., Kendler, 1990; Sabshin, 1990), in fact, the evidence supporting its
classification of depression was very limited. Only one of the five publications cited in the
footnotes to the article provided empirical substantiation for the depression criteria
(another citation refers to unpublished research by Robins and Guze). This was a study by
psychiatrist Walter Cassidy and several colleagues that reported findings from a
quantitative study of 100 patients called “manic-depressive” and 50 medically sick
controls (Cassidy, Flanagan, Spellman, & Cohen, 1957).
The criteria of Cassidy et al. (1957) for depression required that patients “(a) had made at
least one statement of mood change, including any of the following: blue, worried,
discouraged, and 16 equivalent expressions and (b) had any 6 of the 10 of the following
special symptoms: slow thinking, poor appetite, constipation, insomnia, feels tired, loss of
concentration, suicidal ideas, weight loss, decreased sex interest, and wringing hands,
pacing, over-talkativeness, or press of complaints” (Cassidy et al., 1957, p. 1535).
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Feighner himself noted that he “relied a lot on an article by Cassidy” (Kendler, Muñoz, &
Murphy, 2010, p. 136) and his eponymous criteria made only four relatively small
changes to these conditions, dropping constipation, adding feelings of self-reproach or
guilt, expanding insomnia to encompass sleep difficulties, and combining weight loss with
anorexia into one item (Kendler et al., 2010). In addition, the Cassidy diagnostic criteria
did not mention any necessary duration of symptoms, perhaps because all patients in
their study were hospitalized and most had symptoms that endured for more than 6
months. The Feighner criteria added the stipulation that the symptoms must last for at
least 1 month, a far shorter duration than that typifying the Cassidy hospitalized sample.
Several aspects of the Cassidy criteria are noteworthy. First, all of the patients in the
sample were “considered sick enough to require hospital observations, and in most cases
the patients were admitted for electroconvulsive treatment” (Cassidy et al., 1957, p.
1535). The diagnosis was thus grounded in melancholic symptoms that characterized
state hospital patients, which could differ substantially from psychoneurotic depression
found in outpatient settings or acute psychiatric wards, not to mention untreated
community populations. In addition, Cassidy et al. (1957, p. 1542) recognized the inexact
nature of their criteria, stating that “The question immediately arises as to whether all
these patients did, in fact, have manic-depressive disease. At present, one cannot go
beyond saying that the patients had a psychiatric illness….” In particular, the Cassidy
group noted the unresolved relationship of manic-depressive disease to patients with
melancholia, manic-depressive psychoses, anxiety, alcoholism, and manic-depressive
personality types. They clearly believed that their diagnostic criteria were highly
exploratory and far from the last word on depressive diagnoses and their relationship to
criteria for other diagnoses.
Likewise, the Feighner group presented their criteria as a tentative first step that
awaited future validation and noted that they were “not intended as final for any
illness” (Feighner et al., 1972, p. 57). Similarly, Kendell (1976, p. 25) did not place any
special priority on the Feighner measurement of depression, noting that “no evidence has
been offered to suggest that it is anything more than a convenient strategy.” Yet just 4
years after Kendell made this assessment, the Feighner classification of depression
became almost the sole basis for the DSM-III diagnosis. Indeed, by 1989, the article in
which the Feighner criteria first appeared was the single most cited article in the history
of psychiatry (Feighner, 1989). In a remarkably short period of time the process of
diagnosing depressive disorder was transformed from a contentious battle among many
competing systems to the unchallenged dominance of a single classification, the DSM-III
diagnosis of Major Depression. How did this hegemony come about?
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The DSM-III
DSM-III formulated depression in a radically new way relative to the previous 2500 years
of medical diagnosis. Its definition of major depressive disorder (MDD) required either a
dysphoric mood or loss of interest or pleasure in usual activities. In addition, at least four
of the following symptoms must be present nearly every day for a period of at least 2
weeks: (1) poor appetite or significant change in weight; (2) insomnia or hypersomnia; (3)
psychomotor agitation or retardation; (4) decreased sexual drive; (5) fatigue or loss of
energy; (6) feelings of worthlessness, self-reproach, or excessive or inappropriate guilt;
(7) diminished ability to think or concentrate or indecisiveness; and (8) recurrent
thoughts of death or suicidal ideation or suicide attempt (American Psychiatric
Association, 1980, p. 213).
These criteria almost completely mirrored the Feighner criteria, which themselves closely
resembled the original Cassidy diagnosis. The only major changes the DSM-III made to
the Feighner criteria were to, first, exempt from diagnosis anyone who meets these
symptom criteria if their symptoms are due to bereavement after the death of a loved one
that lasts no more than 2 months and are not of extreme severity (American Psychiatric
Association, 1980, p. 214). The earlier criteria, in contrast, contained no exceptions other
than for symptoms that arose from a preexisting mental or physical condition. Second,
the DSM-III lowered the necessary duration of symptoms from 1 month to 2 weeks and
the necessary number of symptoms from six to five. Finally, the DSM-III abandoned the
differentiation that Kendell had considered at the core of the Feighner criteria: “The most
important feature of this classification is the distinction it draws between primary and
secondary affective disorders” (Kendell, 1976, p. 23).
Departing from diagnostic conceptions about depression over the previous 250 years, the
DSM-III unified depressive conditions into a single category. In contrast to the sharp split
of depression into psychotic and psychoneurotic forms in the DSM-I and DSM-II, MDD
embraced both unipolar psychotic and psychoneurotic forms of depression. Melancholic
depression—the central depressive condition before the DSM-III—became a subtype of
MDD (American Psychiatric Association, 1980, p. 215). Meeting criteria for the subtype
required lack of pleasure or emotionally reactivity, as well as three symptoms from a list
including either distinct quality of mood, symptoms of greater severity in the morning,
early-morning awakening, marked psychomotor retardation, weight loss, or excessive
guilt. There is an understanding that the melancholic subtype had some correspondence
to the classical conceptualization of depression (Parker, 2000). However, people could
qualify for a diagnosis of melancholy only if they already meet the criteria for MDD.
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Moreover, the current definition that emphasizes the presence of specific symptoms
departs from the contextual tradition. The submersion of melancholia into the broader
MDD category ensured its fall into obscurity (McPherson & Armstrong, 2006;
Zimmerman & Spitzer, 1989). Likewise, the category of “Dysthymic Disorder (or Neurotic
Depression),” which was inserted into the manual to mollify psychoanalysts, never gained
traction as a well-established disorder (Bayer & Spitzer, 1985; McPherson & Armstrong,
2006). Indeed, because this diagnosis required a 2-year duration, it was inherently
applicable only to persons with the most longstanding types of mood disorder. Major
depression was the sole depressive diagnosis of any importance.
The MDD diagnosis that emerged in the DSM-III was in many ways a major achievement.
It succeeded in establishing a single standard of measurement that has been almost
universally adopted in psychiatric research on depression (McPherson & Armstrong,
2006). It thus facilitated communication and understanding among the research
community and provided diagnostic criteria that clinicians and researchers from a variety
of theoretical persuasions could use. In addition, it realized the major aim of Spitzer and
his colleagues to create a reliable way of measuring depression.
Although the MDD diagnosis was a major accomplishment for research-oriented
psychiatrists, it also entailed serious deficiencies. The emphasis on creating measurable
and reliable diagnoses came at the expense of establishing validity. The DSM-III itself
defined a valid mental disorder as a “behavioral, psychological, or biological” dysfunction
in the individual, which the DSM-IV later specified “must not be merely an expectable and
culturally sanctioned response to a particular event, for example, the death of a loved
one” (American Psychiatric Association, 1994, p. xxi). In line with this definition, the
MDD criteria excluded bereaved people from diagnoses unless they have particularly
longstanding or severe symptoms (e.g., including marked psychomotor retardation or
morbid feelings of worthlessness). They did not, however, exclude people whose
symptoms arose from other life events such as the dissolution of a romantic relationship,
loss of a valued job, or failure to achieve a long-desired goal, thus suggesting that these
responses are not “expectable” or “culturally sanctioned.” This reasoning was contrary to
the centuries-long understanding that such people do not have individual dysfunctions
but are responding naturally to undesirable losses in their lives (Horwitz & Wakefield,
2007).
The failure to allow exclusions other than bereavement enhanced the reliability of the
MDD diagnosis because clinicians and researchers might disagree on whether depressive
symptoms represent appropriate contextual responses. However, as the diagnostic
tradition from the Hippocratics through Freud emphasized, the use of symptoms, without
regard to the context in which they develop and are maintained, combines nondisordered
people whose symptoms result from some loss with those people whose symptoms either
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are inexplicable or are disproportionate to their social context. Likewise, the diagnosis
encompasses conditions that are as brief as 2 weeks as well as those that persist for long
periods of time. They also treat severe symptoms such as suicide attempts or feelings of
worthlessness as comparable to common symptoms such as insomnia and fatigue. The
result is that the MDD diagnosis encompassed an extraordinarily heterogeneous range of
conditions under a single label. In effect, it ignored the pre-DSM-III consensus that
melancholic depressions were distinct from psychoneurotic ones.
The many issues that the varied classifications of depression could not resolve before the
publication of the DSM-III suddenly disappeared. Questions over how many distinct types
of depression existed, the relationship between psychotic and neurotic forms of
depression, and whether depression was best measured by dimensions or categories
were all settled by fiat. Although the Feighner group framed their criteria as a tentative
first step toward the eventual establishment of a reliable and valid classification scheme,
the DSM-III adopted these criteria with few changes. Moreover, save for the removal of
the bereavement exclusion in DSM-5, which moved even further away from the classical
contextual approach, the MDD criteria remained almost intact in subsequent manuals,
the DSM-III-R, DSM-IV, and DSM-IV-TR (American Psychiatric Association, 1987, 1994,
2000). The wholesale, and largely arbitrary, adoption of one among a number of
competing ways of defining depression perhaps accounts for why—more than 30 years
after its promulgation—research on depression has yet to yield any major breakthroughs
in the understanding of the etiology, prognosis, or treatment of this condition (Blazer,
2005; Frances, 2013; Horwitz & Wakefield, 2007; Shorter, 2013).
The Consequences of the DSM-III Diagnosis of Major
Depression
The MDD category in the DSM-III encompassed all of the heterogeneous categories of
endogenous, exogenous, neurotic, and even psychotic forms of depression that existed
before 1980. MDD captured both amorphous and short-lived reactions to psychosocial
problems as well as serious and chronic conditions that in the past had been associated
with melancholic depression. This heterogeneous quality of the MDD diagnosis is
especially consequential when the diagnosis is used outside of hospital settings.
An underlying assumption behind the use of the Feighner criteria as the foundation of the
MDD diagnosis is that measures developed in hospitalized populations of severely
impaired patients could be applied to all depressive conditions. Yet within hospitalized
populations the symptoms that appeared in the diagnostic criteria can be assumed to be
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severe and, usually, long-lasting. Yet MDD is used not just in inpatient institutions but in
all settings that require diagnoses, including general medical practice and private mental
health practices and clinics. It is also the diagnosis used in epidemiological investigations
among untreated community populations, in research studies, and in treatment outcome
assessment. The DSM-III diagnosis of major depression in effect became the arbiter of
what depression was in clinical and clinical research settings, community studies, and the
culture at large.
The significance of the MDD criteria changed when they were applied to outpatient
populations and, especially, to community populations in which their application can
result in many false-positive diagnoses (Wakefield, Schmitz, First, & Horwitz, 2007). In
these settings, low mood, poor appetite, insomnia, fatigue, lack of concentration, and the
like are typically common responses to ubiquitous stressful experiences such as the loss
of valued relationships, jobs, or goals that, as noted, even the DSM definition of mental
disorder did not categorize as valid disorders. Indeed, Robert Spitzer, the head of the
DSM-III task force, acknowledges that in regard to MDD: “the DSM is not consistent even
in applying its own definition of mental disorder to the diagnostic criteria sets for specific
disorders” (Horwitz & Wakefield 2007, p. viii). When diagnoses require just 2-week
duration they can include many short-lived responses to stressors. Moreover, the lack of
exclusion criteria other than bereavement virtually ensured that the criteria could not
separate natural symptoms of sadness from dysfunctional depressive disorders.
Because the MDD diagnosis that emerged in the DSM-III encompassed symptoms that
typified very severe and enduring symptoms as well as those that were short-lived and
common signs of distress such as sadness, fatigue, sleep and appetite difficulties, or lack
of concentration, it is no surprise that following the publication of the DSM-III depression
became by far the most common diagnosis in outpatient mental health treatment. Indeed,
by the beginning of the twenty-first century Major Depression constituted a full 38% of all
diagnoses in outpatient settings out of the hundreds of possibilities (Olfson et al., 2002).
Major Depression also became the major target of a new class of drugs, the selective
serotonin reuptake inhibitors, which came on the market in the late 1980s. Because the
DSM-III depression criteria could encompass such a wide variety of everyday
psychosocial problems, it made the most marketing sense to call them “antidepressants.”
In fact, these capacious drugs were, and are still, used to treat an enormous variety of
conditions including not only depression but also anxiety, obsessions, alcohol abuse,
eating disorders, and a host of undifferentiated symptoms. The label “antidepressant”
reinforced the popularity of the depression diagnosis because if some condition was
treated with an antidepressant it must be depression.
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The overwhelming marketing success of the MDD diagnosis came at the cost of hindering
scientific research. It left unresolved whether melancholic depression—the central
depressive condition before the DSM-III—is a distinct condition or simply the most severe
type of major depression (Taylor & Fink, 2006). The melding of serious melancholic
conditions with transient stress-related sadness creates a roadblock in the way of finding
a condition with a distinct etiology, prognosis, and treatment. It also thwarts progress in
finding the possible biological roots of depression by combining distinct states that might
represent brain dysfunctions with natural products of psychosocial stressors.
Pre-DSM-III controversies over whether depression is best viewed as a categorical or
dimensional condition likewise remain unresolved. In addition, the question of how to
distinguish depressive disorders from depressive personality types is unsettled. Whereas
the DSM-III generated consensus about the operational definition of depression,
questions about whether depression is continuous or categorical, how many categories it
has, what its relationship to melancholic conditions is, and how it can be distinguished
from normal sadness seem no closer to resolution now than they were when the DSM-III
arose.
Conclusions
What is striking from this brief overview of conceptualizations of depressive disorder
from Hippocrates to the DSM-III is, first, the remarkable consistency of the symptoms
that are mentioned—by and large the same kinds of symptoms that current diagnostic
manuals emphasize. And, second, there is a remarkably solid and well-elaborated
tradition of distinguishing disorder from normal emotion via various versions of the “with
cause” versus “without cause” criterion that goes back to ancient times. Because
stressful life events can precede serious and long-standing depressions, “disproportionate
to cause” seems to characterize dysfunctional conditions better than the traditional term
“without cause.” The entire 2,500-year record indicates an understanding that
pathological depression is an exaggerated form of a normal human emotional response.
Thus, diagnosticians understood that the first step in understanding a patient’s condition
must be to use the relation of symptoms to their triggering causes to distinguish the
normal from the disordered. The power, consistency, and rationale of the
“disproportionate” medical understanding of depressive disorder form the backdrop for
our own era’s radical departures in diagnostic approach. Finally, the historical tradition
preceding the DSM-III sharply distinguished severe states of melancholic depression from
less disabling psychoneurotic depression, which it often associated with cooccurring
symptoms of anxiety.
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In the urgent quest for reliability, the adoption of the current depression criteria for the
most part inadvertently rejected the previous 2,500 years of clinical diagnostic tradition
that explored the context and meaning of symptoms in deciding whether someone is
suffering from intense normal sadness or a depressive disorder. The DSM-III
criteria, which persist into the present, also blurred the traditional distinction between
melancholic and neurotic depression, calling both forms “Major Depression.” The
unwitting result of this effort, especially as psychiatry turned from the serious conditions
of inpatients to the far more heterogeneous conditions of outpatients and community
members, was to be a massive pathologization of normal sadness. Ironically, this can be
argued to have made depressive diagnosis less, rather than more, scientifically valid. The
sole remnant of the “disproportionate to cause” tradition was the bereavement exclusion
that remained in DSM IV-TR. The removal of this criterion from the diagnostic criteria in
DSM-5 indicates that far from making diagnostic progress, the recent history of the mood
disorders shows significant regression in understanding the most basic of all distinctions
—the difference between normal sadness and depressive disorder.
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Allan V. Horwitz
Allan Horwitz is Board of Governors Professor of Sociology at Rutgers University. His
most recent books are The Loss of Sadness: How Psychiatry Transformed Normal
Sorrow into Depressive Disorder (Oxford University Press, 2007, with Jerome
Wakefield), Diagnosis, Therapy, and Evidence: Conundrums in Modern American
Medicine (Rutgers University Press, 2010, with Gerald Grob), and All We Have to
Fear: Anxiety and the Boundaries of Normality (Oxford University Press, 2012, with
Jerome Wakefield).
Jerome C. Wakefield
Department of Psychiatry, New York University
Lorenzo Lorenzo-Luaces
Department of Psychology, University of Pennsylvania
