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CHAPTER 1
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Historical Aspects
of Mood Disorders
Dean F. MacKinnon, M.D.
J. Raymond DePaulo Jr., M.D.
Depression and mania have been enduring aspects of the human condi-
tion, but the idea that they are pathologies of mood is relatively new. Historical/
mythological figures in the Bible (Ben-Noun 2004), Homer’s writings (Angst and
Marneros 2001; Berrios and Schioldann 2019), and other ancient texts are often
depicted experiencing what a modern reader might interpret as symptoms of depression and mania, but these narratives describe spiritual agonies and divine afflictions,
not medical illness. The history of a diagnostic concept begins with the birth of med
icine.
The history of mood disorders illustrates the complex relationship between clinic
and theory, because descriptions of manic and depressive symptoms have crossed
paths with theories about their nature but have yet to converge on a pathogenic
model. In this chapter, we focus on the following: 1) how the phenomena we now associate with mood disorders were described throughout the history of medicine, 2)
what physicians have thought were the causes of those disorders, and 3) how thera
peutic developments have informed diagnosis and theory. By tracking how we came
to our present state of knowledge, we may glimpse its replacement.
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Descriptions of Mood Disorders
The first medical descriptions in which we might now recognize mood disorder
symptoms emerged in ancient Greek Hippocratic texts and as part of a broader set of
problems associated with perturbations of bodily “humors.” While “melancholic”
described fear and despondency associated with “black bile,” it also referred to delu-
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sional ideation, insomnia, poor appetite, paralysis, and epilepsy. “Mania” was used
to refer to a form of melancholic disease, a strong emotional response, a divine state,
or a kind of temperament (Angst and Marneros 2001). In philosophy, meanwhile, the
ancient Greek concept of a melancholic temperament denoted not mental illness but
a propensity to sad emotions, sometimes linked with creativity (Bos 2009; Pies 2007).
These two aspects of melancholy would meld together, much later, to attach the mul
tifaceted disease melancholia more firmly to melancholic emotional disposition.
Physicians in classical Rome also recognized despondency and fear as common
symptoms in melancholic patients. Galen wrote of such patients, “They find fault
with life and hate people; but not all want to die. For some the fear of death is of prin
cipal concern [whereas others] dread death and desire to die at the same time”
(quoted in Jackson 1986, p. 42). But the “mania” and “melancholia” of Hippocrates
and Galen, and for that matter of Philippe Pinel and Benjamin Rush in the eighteenth
and nineteenth centuries, implied not only emotional suffering but also disturbed
thought—that is, insanity. Galen mentions melancholic patients “who think to have
become a sort of snail so that they must escape everyone in order to avoid having
their shell crushed, while others fear that Atlas, who supports the world, may grow
weary and vanish” (Telles-Correia and Marques 2015, p. 1). Centuries later, Paul of
Aegina similarly described patients who “fancy themselves to be, some, brute ani
mals, and imitate their cries; and others, earthen-vessels, and are frightened lest they
be broken. ... some believe themselves impelled by higher powers, and foretell what
is to come, as if under divine influence; and these are, therefore, properly called demoniacs, or possessed persons” (quoted in Jackson 1986, p. 54).
Somatic symptoms also were often emphasized in Roman depictions of melancholia. Soranus of Ephesus, for example, considered flatulence, coldness in the extremities,
diaphoresis, head heaviness, and greenish-black complexion to be signs of melancholia
(Jackson 1986). Rufus, a contemporary of Soranus, suggested that the gastrointestinal
symptoms defined a “hypochondriacal” form of melancholia localized to the abdomen
(hypo meaning “below,” and chondria referring to the diaphragm), whereas the psycho
logical symptoms pointed to melancholic disturbance in the brain. This notion of several different forms of melancholia proved to be a robust idea that could still be found
in textbooks nearly two millennia later.
Medieval physicians preserved some ancient elements of melancholic illness for
another 1,500 years. In the seventeenth century, in the full bloom of the Renaissance,
Felix Platter (sometimes spelled “Plater”) in Basel, Switzerland, continued to empha
size abnormal thought over abnormal mood when he described melancholia as “a
kind of mental alienation [mentis alienatio] in which imagination and judgment are so
perverted that without any cause the victims become very sad and fearful” (quoted in
Jackson 1986, p. 91). In contrast to Galen’s examples concerning snails and Atlas, Platter’s examples of false ideation include themes more familiar to modern psychiatrists:
patients with melancholia “have felt themselves driven toward blaspheming God and
committing many horrible things...out of an involuntary compulsion.... Others...
falsely imagine that they are in bad grace with princes and magistrates and that they
have done something wrong and are being summoned to punishment” (quoted in
Jackson 1986, p. 92).
Themes of guilt were seldom described in ancient texts on melancholia, and their
emergence seems to point to an expanding dimension of conscientiousness in the cul-
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ture. From the earliest Christian era, when Paul differentiated the “godly sorrow”
that motivated repentance from “the sorrow of the world” that led one away from sal
vation (Altschule 1967), introspection to gauge the quality of one’s sorrows became a
spiritual habit for many, and ultimately, perhaps, the precursor to seeing mood as a
phenomenon of clinical significance on its own.
Problems we might now associate with nonpsychotic depression, such as sluggish
work and sour attitude, were particularly hard to conceal in a medieval monastery,
where such problems called for diagnosis and correction. A fifth-century scholar, John
Cassian, attributed these phenomena to the sin of acedia (Altschule 1965); a later observer, David of Augsburg, a German mystic and Franciscan friar, noted a spectrum of
ac edia from v ice to mental illness. Whereas acedia could result from mere slothfulness,
or from a selective loss of zeal in religious duties, the most severe forms shaded into
melancholia: “a certain bitterness of the mind which cannot be pleased by anything
cheerful or wholesome. It feeds upon disgust and loathes human intercourse.... It in
clines to despair, diffidence, and suspicions, and sometimes drives its victim to suicide
when he is oppressed by unreasonable grief. Such sorrow arises sometimes...from the
abundance of melancholic humors, in which case it behooves the physician rather
than the priest to prescribe a remedy” (quoted in Jackson 1986, p. 72).
Published in England during the Renaissance, Robert Burton’s The Anatomy of Mel-
ancholy invoked the ancient Greek philosophical view of melancholic temperament as
a prelude to his exhaustive treatise on melancholic illness. The melancholic tempera
ment, or disposition, is familiar and common, perhaps even normal, until it becomes
habitual: “We call him melancholy that is dull, sad, sour, lumpish, ill-disposed, soli
tary, any way moved, or displeased. And from these melancholy dispositions, no man
living is free” (Burton 1652, p. 127). He goes on, “This melancholy of which, we are to
treat, is a habit,...a chronic or continuate disease, a settled humour,...not errant, but
fixed” (Burton 1652, p. 128).
Turning to the symptoms of melancholic disease, Burton emphasizes delusions,
some bizarre, recorded in ancient medical literature: “Some are afraid that heaven
will fall on their heads: some they are damned, or shall be.... Fear of devils, death,
that they shall be so sick of some such...disease, ready to tremble at every object, they
shall die themselves forthwith, or that some of their dear friends or near allies are cer
tainly dead; imminent danger, loss, disgrace, still torment others...that they are all
glass, and therefore will suffer no man to come near them: that they are all cork, as
light as feathers; others as heavy as lead; some are afraid their heads will fall off their
shoulders, that they have frogs in their bellies” (Burton 1652, p. 317).
Only after listing these delusions does Burton turn to descriptions of the mood in
melancholic patients: “Sorrow...is an inseparable companion.... [T]he remembrance
of some disgrace, loss, injury, abuse, etc. troubles them.... [T]hey are weary of their
own lives, and feral thoughts to offer violence to their own persons come into their
minds...they are soon tired with all things” (Burton 1652, pp. 319–320).
The traditional emphasis on insanity in descriptions of melancholia did not reflect
the experience of physicians in practice, who rarely saw frank insanity but often saw
sad patients. Analysis of the copious records kept by one seventeenth-century English physician, Charles Napier, demonstrates his practical linkage of melancholy
mood to fear, sadness, troubled mind, and “mopishness” more than to false ideas and
sensory disturbances (McDonald 1983).
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The interplay of temperament, habit, and insanity in the Renaissance idea of melancholy informed medicine until the nineteenth century. The physician William Cullen, of Edinburgh, Scotland, in his influential medical writings and lectures from the
late eighteenth century, describes the melancholic temperament as “slow, disposed to
gravity, caution, and timidity, with little sensibility or irritability, but...liable to mel
ancholia, hypochondriasis” (Cullen 1789/1827, vol. I, pp. 217–218). Cullen considered
melancholia a “partial insanity” (as opposed to the general insanity of mania) and con
trasted it with the health preoccupations in hypochondriasis: “When an anxious fear
and despondency arises from a mistaken judgment with respect to other circumstances
than those of health...it is what I would strictly name Melancholia” (Cullen 1779/1827,
vol. II, p. 533). Cullen also vividly describes mania, again emphasizing the primacy
of abnormal thought over abnormal emotion: “What for the most part more especially distinguishes the disease, is a hurry of mind, in pursuing any thing like a train
of thought, and in running from one train of thought to another. Maniacal persons are
in general very irascible; but what more particularly produces their angry emotions
is, that their false judgments lead to some action which is always pushed with impetuosity and violence; when this is interrupted or restrained, they break out into violent
anger and furious violence against every person near them, and upon every thing
that stands in the way of their impetuous will” (Cullen 1779/1827, vol. II, p. 522).
By the mid-nineteenth century, the idea of melancholia as a disorder primarily of
mood, rather than a distressing disorder of ideation and judgment, had begun to take
hold among psychiatric thinkers (Kendler 2020). In his textbook, German psychiatrist
and neurologist Wilhelm Griesinger lucidly illustrates the change of emphasis. In
melancholia, the mental pain precedes both false ideation and altered function: “A
state of mental pain becomes always more dominant and persistent, but is increased
by every external mental impression. This is the essential mental disorder in melan
cholia, and, so far as the patient himself is concerned, the mental pain consists in a
profound feeling of ill-being, of inability to do anything, of suppression of the physi
cal powers, of depression and sadness, and of total abasement of self-consciousness”
(Griesinger 1861, p. 223).
As ideas about the affective nature of melancholia took shape, medicine as a whole
was undergoing a radical renovation. One can get a quick sense regarding how thor
oughly changed the understanding of medicine was across the nineteenth century
simply by contrasting the section headings in one of Cullen’s texts (Cullen 1779/1827,
vol. II, pp. v–viii) with, say, an early edition of William Osler’s The Principles and Prac
tice of Medicine (Osler 1896). Cullen had three main sections on diseases: “Pyrexiae,”
“Nervous Diseases,” and “Cachexie.” A century later, Osler organized his text into
“Specific Infectious Diseases,” “Constitutional Diseases,” and then a series of sections
for pathologies in each organ system (Osler 1896, pp. vii–xvi). In contrast to Cullen’s
broad categorization of diseases by their major presenting symptom, Osler’s reflected
the modern idea that diseases arise from organic pathology.
By the end of the nineteenth century, major psychiatric textbooks had largely coalesced around a definition of melancholia as a disorder of depressed mood accompanied by a number of other symptoms, on average about twice as many as would later
make up the DSM criteria for a major depressive episode (Kendler 2017). Mania, however, was generally thought of not as an episodic disorder of elevated mood but more as
a chronic, variable insanity ultimately leading to intellectual deterioration (Hare 1981).
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At about the same time that Osler was linking pathology and nosology, German psychiatrist Emil Kraepelin had begun to take note of patterns in the symptoms and
course of illness in the severely ill patients under his care, and to conceive of manicdepressive insanity as an episodic disorder of affect regulation.
In the chapter “Manic-Depressive Insanity” in his seminal general textbook of psychiatry, Kraepelin (1920) posits a predisposition to episodic pathological mood states:
“Manic-depressive insanity runs its course in attacks, whose appearance is in general
independent of external influences. This fact shows us that the real, the deeper cause
of the malady is to be sought in a permanent morbid state which must also continue to
exist in the intervals between the attacks” (p. 117). These fundamental “permanent
morbid states” consist of depressive, manic, irritable, and cyclothymic temperaments.
For Kraepelin, the depressive temperament, reminiscent of the melancholic disposition of old, “is characterized by a permanent gloomy emotional stress in all the experi-
ences of life” (Kraepelin 1920, p. 118, emphasis his). Such patients, from youth onward,
are tormented by guilt; are sexually unsatisfied, anxious and avoidant, indecisive, and
lacking in self-confidence; are prone to suicidal thoughts and sometimes actions; and
tend to have “nervous” or psychosomatic complaints. Manic temperament, in contrast,
is one of “constitutional excitement” with a permanently “exalted, careless, confident”
mood, a sense of superiority to one’s surroundings, and unsteadiness or restlessness in
actions, but a lack of perseverance that hinders progress in life. Such patients “live in
constant feud. They interfere in everything, overstep their rights, make arrangements
which they are not entitled to make” (Kraepelin 1920, p. 128). The irritable tempera
ment is a mixture of the manic and depressive temperaments, whereas the cyclothymic temperament is characterized by frequent flux between the two.
Kraepelin’s work suggested that in psychiatry, as in the rest of medicine, classifying
diseases by shared clinical features beyond common symptoms could help clinicians
to prognosticate, to test therapeutic approaches, and to investigate causes. However,
this approach has left open an important question: Who decides where to draw the
boundaries, and for what purpose? “The clinician wants classes into which he can put
his patient’s illness after a reasonably brief period of investigation, and which will
assist him to make a prognosis and decide on treatment.... [The researcher] wants his
classes, and his words, to have some fixity, so that he can generalize and summarize
and communicate his observations: he cannot work in circumstances where the case
that he calls an endogenous melancholia another man may call a reactive depression,
and a third man call a paranoid schizophrenic” (Lewis 1938).
Government agencies also had use for reliable diagnostic classification of mental
impairment. The U.S. Census had counted “idiocy” and “insanity” in households between 1840 and 1880. After that, the Census initiated an enumeration specifically of
institutionalized people, and in analyzing these data aimed for a more nuanced typology than “idiocy” and “insanity,” arriving at five diagnoses that would be somewhat
familiar to modern psychiatry: melancholia, mania, monomania, dementia, and dipsomania, along with two that the modern reader might not consider primarily mental
disorders: paresis and epilepsy. A more detailed Census classification scheme to track
institutionalized patients emerged in 1918, with input from the psychiatric profession, adding “involutional melancholia” and “manic-depressive psychosis” along
with other serious disorders, and was in use into the 1940s (Grob 1991). By the midtwentieth century, the psychiatric profession had begun to grasp that advancement of
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the field would entail developing its own, more clinically relevant classification
scheme; the American Psychiatric Association (1952) updated the Census nomencla
ture, and thus developed a system that included not only the diagnoses of institutionalized patients, but also the problems of outpatients, and thus added descriptions of
a “psychoneurotic” depressive reaction and a “cyclothymic” personality along with
many other non-mood-disorder diagnoses.
In spite of the effort to promote diagnostic reliability, in clinical practice diagnostic
inconsistency remained endemic (Spitzer and Fleiss 1974) and strongly influenced by
local custom. For example, many patients who would have been diagnosed with an
affective psychosis by a British psychiatrist in 1970 would have received a diagnosis
of schizophrenia by an American psychiatrist (Kendell et al. 1971). Clinical investiga
tors were thus moved to develop their own sets of operationalized diagnostic criteria.
The Feigner criteria (Feighner et al. 1972; Kendler et al. 2010) and the Research Diag
nostic Criteria (Spitzer et al. 1978) provided what were essentially early drafts of the
criteria for affective disorders that appeared in DSM-III (American Psychiatric Asso
ciation 1980). Notably, during the process of cleanly delineating affective disorders for
DSM-III, the old concept of manic-depressive illness (which sometimes had been ap
plied to patients who had only depressive episodes) evolved into “bipolar” and “unipolar” disorders contingent on the presence of mania or hypomania (Pichot 1995).
Systems such as the Feigner criteria and the Research Diagnostic Criteria, as well
as DSM-III, dropped many symptoms that were commonly described but hard to
assess reliably, such as depersonalization and vague somatic complaints. While these
omissions might have improved diagnostic reliability, they arguably impoverished
the clinical concept of what constitutes a mood disorder (Kendler 2016). DSM diagnostic rules for mania and major depressive disorder have remained largely unchanged since 1980, but there have been two notable updates to the larger classification
scheme. One update from DSM-III-R to DSM-IV in 1994 was the adoption of criteria for
bipolar II disorder (American Psychiatric Association 1987, 1994). The most significant change for the purposes of a textbook on mood disorders was the removal, between DSM-IV and DSM-5 in 2013, of “mood disorders” as a general category of
illness in favor of two separate diagnostic classes for depressive disorders and bipolar
and related disorders (American Psychiatric Association 2013).
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Theories of Mood Disorders
The current concept of “mood disorders,” therefore, applies to a subset of the patients
with psychosis whom the ancients would have called “melancholic” or “manic”; to a
group of anguished patients without psychosis who present with various physical
complaints considered as the “hypochondriacal” subtype of melancholia or perhaps
as “neurasthenia” by nineteenth-century medicine (Ware and Weiss 1994); and to
some sad and unproductive souls who committed the “sin” of acedia, but whom nontheologians might have thought of as expressing the melancholic disposition described by ancient philosophers.
Developments in nosology and in theory have crossed paths at times but have
rarely if ever moved along together (Ghaemi and Goodwin 2009). Whereas diagnostic
concepts evolved glacially from Hippocrates to Kraepelin, theories to explain mood
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disorders have advanced in a more discontinuous fashion, starting with the ancient
and resilient humoral theory and abruptly changing course in the Renaissance as sci
entific approaches to knowledge took hold and expanded. We know much more now
about the biological correlates of mood disorders, and how to alter their course, but
this knowledge has not yet informed stable nosological concepts.
The humoral theory applied ancient concepts of four essential qualities—hot versus cold, wet versus dry—and substances—earth, fire, air, water—to explain abnormal internal bodily processes. Disease was thought to represent a perturbation or
imbalance of four bodily fluids, or humors (each with its own qualities)—blood,
phlegm, and two different kinds of bile, or “choler”: yellow and black (i.e., melan
cholic). Philosophers also employed this rubric in an early psychology of temperament (Bos 2009). Aside from the view common both to ancient Greeks and modern
physicians that medical disorders, including melancholia, are essentially problems in
bodily functioning, little of humoralism remains today in medicine.
Nothing much challenged the humoral theory of melancholia until Renaissance
physicians began to apply each new scientific theory from chemistry (Paracelsus),
anatomy (Andreas Vesalius), and physiology (William Harvey) to understand the nature of melancholic illness, without altering the clinical definition of melancholia.
Seventeenth-century English physician Thomas Willis saw the body as composed of
a limited number of essential chemicals, including salt, water, earth, sulfur, and spirit.
In combination and under various circumstances, the chemicals could mix and fer
ment, in health giving rise to a “transparent, subtle, and lucid” quality, and in melancholy becoming “obscure, thick, and dark,...as it were in a shadow, or covered with
darkness” (both Willis quotes from Jackson 1986, p. 111).
A few generations later, around the turn of the eighteenth century, Dutchman Herman Boerhaave based his theory of melancholia on Harvey’s model of circulatory
physiology, and saw it as a result of slowing or congestion of blood flow. Albrecht von
Haller, in eighteenth-century Switzerland, in his work on the nature and anatomy of
nerves, opined that the qualities of sensibility and irritability were essential to understanding diseases such as melancholia and that these qualities arose from variations
in the motion of a “nerve fluid” flowing through axons. In contrast, other theorists
saw a Newtonian source of melancholia in the (putative) mechanical oscillatory and
vibratory motions of the nervous system (Jackson 1986).
The nineteenth-century conceptual metamorphosis from melancholia to mood disorders began, perhaps, with the advent of Romanticism and its regard for feeling over
reason, but its widespread incorporation into scientific medicine followed develop
ments in psychological science, such as the counterintuitive idea expounded by the
American philosopher William James (and refined by later experiments [Schachter
and Singer 1962]) that affect emerges not merely from thoughts but also from actions
motivated by provocative circumstances: “Common-sense says, we lose our fortune,
are sorry and weep; we meet a bear, are frightened and run; we are insulted by a rival,
are angry and strike.... [T]he more rational statement is that we feel sorry because we
cry, angry because we strike, afraid because we tremble” (James 1884, p. 190). So if a
mood disorder made one sad, angry, or fearful without external cause, this theory implies that in order to make sense of the experience, the mind could invent such a
cause—and so a primary emotional disturbance can create false or even delusional
ideas.
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The emerging science of psychology in the twentieth century offered alternatives
to the Kraepelinian assumption that the clinical syndromes of mania and depression
arose from a specific disease process in the body. Johns Hopkins psychiatrist Adolf
Meyer proposed in his “psychobiological” approach that what others had considered
to be discrete disease entities could more dynamically be understood as reaction pat
terns (Lidz 1966). For example, as cogently summarized by Aubrey Lewis (1934), “depressive states may appear as reactions (protective at any rate in intention, designed
to withdraw the individual from an ill-adjusted situation), with concomitant phe
nomena on various levels—vegetative, kinetic, and topical mental.... There may be
sadness, with feelings of difficulty and dearth of ideas and activity, or actual retarda
tion” (p. 33).
Sigmund Freud (1917/1957), in contrasting melancholia with mourning, saw melancholia as complicated by ambivalence, which is either “an element of every loverelation formed by this particular ego, or else it proceeds precisely from those experi
ences that involved the threat of losing the object” (p. 256). He noted that mania often
travels with melancholia when with its resolution “a large expenditure of psychical
energy, long maintained or habitually occurring, has at last become unnecessary, so
that it is available for numerous applications and possibilities of discharge.... All such
situations are characterized by high spirits, by the signs of discharge of joyful emotion
and by increased readiness for all kinds of action” (p. 254).
The third wave of modern psychological theories of mood disorder, after Meyerian
reactive withdrawal and Freudian ambivalent mourning, came in the behavioral
model of “learned helplessness” (Seligman 1972), in which animals subjected to
stressful situations entered a depression-like state with symptoms reminiscent of human depression—withdrawal, inertia, diminished appetite, disinterest in mating, and
so forth. Although limited as a model of human depression (Henkel et al. 2002), it has
proved useful as a means to assess the likely therapeutic efficacy of antidepressant
medications (McArthur and Borsini 2006).
DSM-III’s unification of mood disorders into a small number of diagnostic categories (albeit with the ability to subtype them) obviated the debate over whether there
was a “melancholic” type of illness that arose de novo (or endogenously) from a bio
logical vulnerability, as well as a “reactive” or “neurotic” type of depression that had
its basis more in psychological maladjustment to stressful circumstances (Nelson and
Charney 1980; Taylor and Fink 2008). The concept had proven intuitively attractive,
and gibed with clinical experience: some patients seem clearly to be suffering from adversity, whereas others are ill (and sometimes very severely ill) for no discernible external reason. However, judging whether a patient has sufficient reason to feel depressed
introduces a degree of interpretation that weakens diagnostic objectivity: “If the physician can enter into the patient’s feelings and understand the illness as the natural outcome of situations in which the patient has been, then he calls it psychogenic or
reactive; if he cannot then he calls it autonomous.... No doubt this too is a personally
valuable way of reviewing the illness, but it has the disadvantages...[associated with]
such subjective judgments” (Lewis 1938, p. 877).
There has remained among many thoughtful psychiatrists the sense that DSM’s
lumping of all mood disorders into a few symptom-defined categories overlooks
something essential about the nature of mental illness (Coryell 2007; Taylor and Fink
2008); however, (for better or worse) this did not lead the developers of DSM-5 to re-
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establish a melancholic/endogenous versus neurotic/reactive distinction. Temperamental vulnerability, life events, losses, and adjustments to adversity play a limited
role in a limited number of DSM-5 diagnoses and none whatsoever in a diagnosis of
major depressive or bipolar disorder.
Therapy and Theory
Prior to the modern era, there were essentially three things a physician could do about
someone with melancholia: 1) wait and hope for the best; 2) provide commonsense,
supportive care in the form of rest, reassurance, and healthy living; or 3) try the sorts
of interventions indicated by the prevailing theory, technology, and practice ethos. The
latter included purging, trepanning, bloodletting, herbal or nutritional additives,
physiological stress (e.g., heat or cold), coitus (or avoidance of coitus, depending on
the authority), and so on. The unpleasantness of some of these interventions could
help explain why someone suffering with depressive or manic symptoms but still in
possession of rational faculties might have chosen not to consult with a physician.
Compounds extracted from nature were the earliest sedatives and stimulants, and
also served as tools to alter a patient’s mood, if only transiently. These include the
medicinal plants belladonna and mandrake, which produce anticholinergic calming
effects; the ephedra plant, which yields a prototypical form of our modern amphetamine stimulants; and the more familiar and self-administered intoxicants ethanol,
coca, and morphia. Any of these, of course, might worsen melancholia over the long
run, but could potentially quell anxiety or arouse action in someone with a not-toosevere case of mania or depression (Shorter 2009).
Treatments demonstrated to alter the course of illness all began with serendipitous
observations. Stories behind the discovery of the therapeutic effects on mood disor
der of lithium, imipramine, chlorpromazine, iproniazid, and valproic acid share a
common theme in that all of the treatments were developed or used for other pur
poses before their antipsychotic, antidepressant, or antimanic properties were discovered: lithium as a treatment for gout, imipramine as a neuroleptic, chlorpromazine as
an antihistamine, iproniazid as an antituberculosis drug, and valproic acid as an antiepileptic (Cade 1949). The dozens of medications currently marketed for mood disor
ders are essentially extrapolations from these discoveries.
Theories of the pathological basis of mood disorder have sometimes been reverseengineered to fit the putative mechanism of action of an agent in the treatment of a
particular kind of mood disorder. Thus, the discovery that the early antidepressants
seemed to work through their influence on monoaminergic receptors led to a resilient
hypothesis of affective disorder pathophysiology (Lambert et al. 2000; van Enkhuizen
et al. 2015) and even to the leakage into popular culture of people speaking of their
depression as being a deficiency of serotonin. Although there is abundant evidence
that serotonin perturbations are associated with depression and that altering sero
tonin activity leads to resolution of the depressive syndrome (in some patients), there
are some weak spots in the hypothesis (Baumeister et al. 2003; Hirschfeld 2000). Nevertheless, the monoamine hypothesis has generated a robust research framework
(Mulinari 2012) and is thus a model for how therapeutic success can inform the search
for an etiology.
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