How Everyone Became Depressed (28 page)

The highpoint of the depressive equivalents doctrine was probably the declaration of Dietrich Blumer, a psychiatrist at the Henry Ford Hospital in Detroit, in 1982 that chronic pain could be an equivalent form of depression. He termed the syndrome “pain-prone disorder” and viewed it “as a variant of depressive disease.”
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The point is not that chronic pain patients might not also be depressed in their heart of hearts. It is that if these patients are also anxious, and fatigued, and have other somatic symptoms, and obsess about the whole business, then perhaps depression is too narrow a diagnosis. These are nervous patients who are also in pain.

The bottom line is that nerves still hover outside the profession, like windy drafts at night in a rickety house. The term has been so useful in the past that medicine’s collective unconscious will not let it vanish. In recent decades, various templates, such as the housewife syndrome, have been adumbrated for understanding nervous illness as an illness of the entire body, not just the mind and brain. That depression continues to clasp the discipline of psychiatry in its clammy embrace is evidence of the failure of the scientific imagination.

C onsider the current landscape of depression. In an ABC poll in 2002, 15% of Americans said they felt “really depressed” once a week or more. Another 17% said once a month. That means that one-third of the American population believes itself to be depressed in a given month.
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If you are riding on a subway train with a hundred other people, one-third of them will be currently depressed, or have just been, or are about to be. That is a lot.

In fact, it is way too many. We know that only 3% of the population is chronically sad. We know that the serious disease, melancholia, is only a fraction of the ranks of the depressed. Far too many people have received the diagnosis of depression.

Whose fault is this?
At the beginning of our story, psychiatry spoke German. From around 1870 to 1933, German-speaking Europe was the epicenter of world psychiatry. This was so for two reasons.
One, German, Swiss, and Austrian psychiatrists saw large numbers of very sick individuals because they practiced in mental hospitals, leaving outpatients to other practitioners. Of course this was true of alienists elsewhere, but there were more mental hospitals in Germany affiliated with universities because Germany had so many universities. Almost all had university psychiatric hospitals. This was not true elsewhere. So German psychiatry was oriented toward the academic study of large numbers of patients, and a genial figure such as Emil Kraepelin used these resources to make big strides.
Second, German psychiatrists had a thorough familiarity with internal medicine because they were also trained as neurologists. From the viewpoint of subject matter, neurology has always been treated as a subspecialty of internal medicine, even though in Central Europe it was hived off to the nerve specialists. In learning so much neurology, German psychiatrists acquired a feeling for brain illness as involving the entire body: They were indeed attuned to looking at the body as a whole, in contrast to Anglo-Saxon psychiatrists, who usually did not also train as internists. (In Toronto, where I live, neurology still is a subspecialty of internal medicine, and the psychiatrists have only a nodding familiarity with it.) This whole-body perspective is entirely salutary, for a disease such as melancholia has deep roots in the endocrine system, and reaches into the adrenal glands. Anxiety sets the entire body aflutter with palpations, gastrointestinal upset, and the like. Having a comprehensive knowledge of internal medicine can be very useful to a psychiatrist in sorting the wheat from the chaff.
The German psychiatrist-neurologists managed to codify and crystallize an enormous amount of information about basic diseases in psychiatry. They sought their main diagnostic implements in the toolbox of psychopathology: the close study of patients’ signs and symptoms. By 1933 German-speaking psychiatry had individuated the main natural disease entities in psychiatry: Ewald Hecker had described hebephrenia (from which “schizophrenia” evolved) in 1871; his tutor Karl Kahlbaum described catatonia in 1874; and the Danish psychiatrist Carl Georg Lange, Denmark’s “first neurologist” who to all intents and purposes might have been German, differentiated periodic depression from melancholia in 1886, thus putting the study of the two depressions on a scientific basis.
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These remain important illness concepts, and Emil Kraepelin’s separation in 1899 of dementia-praecox from manic-depressive illness is one of the cornerstones of psychiatry today. So the contributions of these skilled German-speaking psychopathologists with their deep backgrounds in internal medicine have been epochal.
Now we fast-forward to Freud’s psychoanalysis in the 1920s. With one fell swoop, psychoanalysis managed to discard all of this carefully accumulated knowledge about psychopathology and disease classification and to divert the discipline of psychiatry to the study of what were essentially figments: unconscious conflict as the motor of symptom formation; early childhood socialization as the seedbed of illness in adults; dream analysis and free association as the basis of treatment. The painstakingly accumulated information about psychiatric genetics—some of which, it is true, leaped the rails of science in Hitler’s Germany; the interest in brain anatomy as the seat of psychiatric illness; the fine differences in the presentations of various disease entities: All these were discarded as outmoded and uninteresting literally within the space of a decade! In the annals of modern science, I am unaware of any comparable wholesale demolition of a field of scientific knowledge and its replacement with a fairy castle of fantasies. It is as though the field of cardiology had suddenly been overtaken by a school of investigators who believed moonbeams the key to understanding cardiovascular illness, and the knowledge about coronary occlusions and electrocardiographic findings that had accumulated by 1930 was discarded in favor of a set of moonbeam doctrines.
The parable, though fanciful, is not far-fetched. By the time psychoanalysis began to collapse from sheer incredulity and lack of therapeutic results in the 1960s, psychiatry found itself with the cupboard bare. Little of the former knowledge base had survived. In any event, it was mostly in German, which nobody read anymore. The new sciences of psychopharmacology and neurophysiology confronted a tabula rasa. Moreover, the practitioners of psychiatry had lost that strong connection to neurology and the other subspecialties of internal medicine that had been such a motor of progress. As well, under the influence of psychoanalysis, the university departments of psychiatry were all chaired by analysts and future scientific developments in psychiatry—well into the 1970s and 1980s—would occur in what the English call the “red-bricks,” secondary provincial academic centers rather than in the academic heartland.
Thus, when confronted with “depression,” the new generation of nonanalyst psychiatrists, who were slowly tapping their way back toward biology, were left quite without critical scholarly tools. In the United States in the 1970s, psychopathology was a dead letter, and if treated at academic meetings it would be during the last session of the last day. The study of the major mental illnesses in seriously ill patients, such as melancholia and catatonia, had given way to analytic speculations in outpatients about the role of the patient’s toilet training. And medical colleagues in other specialties soon regarded psychiatry as an esoteric branch of social work rather than as a sister scientific discipline fast-charging its way forward.
It was from the work of Kraepelin and Freud that depression had become a familiar concept in psychiatry. But when DSM-III launched “major depression” in 1980, psychiatrists found themselves quite without defenses. Many sensed that there was a big problem in conflating endogenous depression and reactive unhappiness: We were told that breaking up with your boyfriend was on a par with lying curled into a fetal, melancholic ball. Both could be major depression as long as the “Chinese menu” of criteria was satisfied.
How do we fight back against something like this if we have lost all the skills of the psychopathologist, if we never absorbed enough internal medicine to say “Yoo hoo, there’s something wrong with the endocrine system here,” and if our main source of pharmaceutical knowledge is promotional material from the drug companies—companies that now see in major depression a lot of runway space. The answer is that individual psychiatrists who were uneasy about the depression epidemic exploding about them lacked the critical skills for arresting it. Their private reservations and personal eyebrow raisings were steamrollered by the wave of enthusiasm for depression in the 1980s and 1990s.
Psychiatry’s inability to stop the depression epidemic is an appalling story of the collective failure of a scientific discipline to ward off a public-health disaster. The loss of the view of two depressions—melancholia and nonmelancholia—means that poorly diagnosed patients are denied the benefit of proper treatment while being exposed to all the side effects of classes of medication, such as the Prozac-style drugs, that are ineffective for serious illness.
It is time for a turn-around.

Is it all doom and gloom? I want to close on a positive note. There are lessons here both for doctors and patients that will improve the understanding of what has been called depression. Depressed mood is only a small corner of a much wider illness condition involving feelings of anxiety, fatigue, bodily aches and pains, and worried obsession about the whole thing. It is important to understand that people’s symptoms are real signs of illness, not part of some process of medicalization in which normal worries and feelings somehow become objects of medical attention.

The first lesson is that we have got to get the emphasis off low mood, which is the essence of the concept of depression. People with the nerve syndrome are not necessarily sad, weepy, or down in the dumps any more than the population as a whole. They feel ill at ease in their bodies, preoccupied with their state of mind, and are unable to get their thoughts off their internal psychic condition. This book proposes nerves as a good label for what they have, given that I, as a historian, have a fondness for concepts that have stood the test of time. But this is not mandatory. We do not have to call what they are experiencing nerves. We can invent some other term. The main point is to move the discussion’s center of gravity off the term depression.

Indeed, there is some evidence that this is happening already. In recent years scholars such as David Barlow, at the Center for Anxiety and Related Disorders at Boston University, have begun to signal the intrinsic connection between depression and anxiety.
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Increasingly, depression is being conceived as a total body experience—an unwitting reversion to the nerves concept— rather than as a disorder of mood. There is evidence that pain, depression, and anxiety are all mediated via the γ -aminobutyric acid B (GABA-B) receptor; neuroscientist Salvatore Enna, for many years head of pharmacology at the University of Kansas, says, “In the long term I would hope that our work would reveal the role of the GABA-B receptor in mediating pain and the emotional response to it with the aim of developing drugs that could be used to ameliorate these conditions.”
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The immune system is also pulled in. One team of researchers at Harvard University proposes “surrogate markers” for depression that include measures of immune function such as tumor necrosis factor-alpha levels.
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Neurobiologist Paul Patterson at the California Institute of Technology wrote in 2011 that “There is now little doubt that the immune system and immune-related molecules are an integral part of the story of major depressive disorder.”
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At the National Institute for Mental Health, a group led by Thomas Insel and Bruce Cuthbert known as the Research Domain Criteria (RDoC) project sets out to identify the neural circuits responsible for behavioral domains. The range of the investigators is the entire body. They write, “In this manner, depression might be viewed akin to the way that a fever is viewed today, suggesting specific tests for a panel of potentially active diagnostic markers that will steer the clinician to the appropriate treatment among any number of possible disordered processes that might underlie the depression.”
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We are a long way from Prozac here.

The second lesson is for doctors. But I want to make it clear that I am speaking as a historian capable of identifying agents that in the past have a record of failure or success. We know that in recent history the current crop of drugs referred to as antidepressants are ineffective in real depressive illness, which is to say melancholia,
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and somehow land wide of the mark in treating nervous illness. Innovation in psychopharmacology is desperately needed, given that no truly new drugs for patients who are agitated, upset, and preoccupied with their bodies have been developed in the past 30 years. My job is not to pioneer new trails in psychopharmacology. But I cannot help observing that in the past, effective agents for nervous illness did exist that today have been largely forgotten. Patients who are worn out and weary require stimulation; those who are agitated and preoccupied require sedation. And you know: Half a century ago the pharmaceutical industry marketed a highly successful combination of barbiturates and amphetamines—Smith Kline’s version, called Dexamyl, hit the market in 1950—that treated both domains of illness at once. Until the Food and Drug Administration and the Drug Enforcement Agency swept this combination from the market in the 1970s, along with almost all other barbiturates and amphetamines (except for a few tightly controlled indications), Dexamyl was widely effective in treating nervous illness.
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Today, of course, this has been forgotten, and one English psychiatrist told me that he simply would not be able to make his fingers move to write a prescription for either barbiturates or amphetamines. That is a cultural, not a scientific, reflex, born of decades of overwrought hype about the exceptional dangers of barbiturates and amphetamines.

All drugs are dangerous in that all have side effects, but the risks have to be weighed against the expected benefits, which in the case of the barbiturates and amphetamines in the treatment of mood disorders are considerable. This is not an argument for the revival of Dexamyl or of the amphetamines and barbiturates as drug classes, but a flare in the night to alert physicians that the treatment of nervous illness requires some combination of sedation and stimulation. It does not require “antidepressants.”

The last lesson is for patients. Millions of people have been led to believe that they are depressed when in fact their illness involves much more than their mood––it involves their entire brain and body. It is the whole that has to be treated, not the mood as such—because their feelings might well reflect demoralization, discouragement, discomfort, or disarray, but not depression. These are separate concepts. A skilled psychopathologist can tease them out. (In a recent interview Richard Shader at Tufts University, one of the kingpins of U.S. psychopharmacology, deplored the ignorance of many younger clinicians, “who don’t know the difference between being demoralized and being depressed.”
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