Most people diagnosed with depression today aren’t depressed, according to Edward Shorter, a historian of psychiatry, in his latest book How Everyone Became Depressed: The Rise and Fall of the Nervous Breakdown.
Specifically, about 1 in 5 Americans will receive a diagnosis of major depression in their lifetime. But Shorter believes that the term major depression doesn’t capture the symptoms most of these individuals have. “Nervous illness,” however, does.
“The nervous patients of yesteryear are the depressives of today,” he writes.
And these individuals aren’t particularly sad. Rather, their symptoms fall into these five domains, according to Shorter: nervous exhaustion; mild depression; mild anxiety; somatic symptoms, such as chronic pain or insomnia; and obsessive thinking.
As he writes in this recent blog post:
… The problem is that many people who get the diagnosis of major depression aren’t necessarily sad. They don’t cry all the time. They drag themselves from bed and go to work and plow through family life, but they aren’t sad. They may well have one of the “D-words” — dysphoria, disenchantment, demoralization — but they aren’t necessarily depressed.
Instead, what do they have in addition? They’re anxious. They’re exhausted and often report crushing fatigue. They have all kinds of somatic pains that come and go. And they tend to obsess about the whole package.
What they have is a whole-body disorder, not a disorder of mood. And that is the problem with the term depression: it shines the spotlight on mood, a spotlight that belongs elsewhere.
Severe depression, which has been lumped in with depression, is a completely different disorder. It’s a serious illness akin to melancholia, a term used around the mid 18th century to the early 20th century. Melancholia speaks more accurately to the gravity of this severe depression and its serious symptoms, which include despair, hopelessness, lack of pleasure in one’s life and suicide.
Shorter also describes melancholia as a “dejection that appears to observers as sadness but that patients themselves often interpret as pain.” It’s recurrent. “Melancholia digs deep into the brain and body, putting patients in touch with their most primeval – and often sinister – impulses. Fantasies of murder and suicide are common themes.”
So how did everyone become depressed?
Shorter names three main culprits: psychoanalysis, which shifted the emphasis away from the body and solely to the mind; the pharmaceutical industry, “the marketing to the public of drugs for depression on the grounds that they rested on an unshakable foundation of neuroscience”; and the Diagnostic and Statistical Manual (DSM).
Before 1980 (and the DSM-III), psychiatry had two depressions: melancholia, which was also called “endogenous depression;” and nonmelancholia, which was called a variety of names, such as “reactive depression” and “neurotic depression.”
After 1980, with the publication of the DSM-III, we were introduced to one term. The manual did include melancholia as a subtype of “major depressive episode.” But, according to Shorter, this was “a pale shadow of the historic melancholia, with its crushing burden of intolerable pain.” It was there “in letter, not in spirit.”
In the book Shorter harshly criticizes this diagnostic decision. He writes:
Whereas melancholia designated a small population of people with life-threatening illness, the diagnosis called simply “depression” was applied to millions. Before DSM-III in 1980, psychiatry had always had two depressions, and now it had only one, and that depression, which began life in 1980 as “major depression,” was a scientific travesty, a poor limp thing of a diagnosis that did not necessarily mean that the patient was sad at all – which is what a depressive mood diagnosis is supposed to convey – but was unhappy, aggrieved, tried, anxious, uncomfortable, or had nothing at all really wrong; the doctor had put her on antidepressants because he or she could think of nothing else to do.
Throughout the book Shorter features stories, case histories, diary excerpts and experts’ quotes along with research and survey data that bolster the need for separate diagnoses.
For instance, he cites one study where “depressed” patients most frequently picked words such as dispirited, sluggish, empty and listless — not sad — to describe how they felt. In the National Comorbidity Survey of 1990-1992, lack of energy appeared to be a prominent symptom for people with depression and anxiety.
Shorter also cites Bernard Carroll’s work. In 1968 Carroll, a psychiatrist and endocrinologist, discovered a biochemical marker for depression, a “promising lead” that’s largely been forgotten. According to Shorter:
…Carroll discovered that administering a synthetic steroid drug called dexamethasone to melancholic patients uncovered an unsuspected dysfunction of their endocrine system: It keeps their cortisol levels high. Cortisol is a stress hormone. Unlike normal subjects, if you gave them dexamethasone at midnight, their systems did not experience the normal late-night-early-morning reduction of cortisol; this nonreduction correlated with the severity of the illness, and it disappeared after patients were successfully treated for their depression. Later studies found that the endocrine systems of patients with most other psychiatric diagnoses showed normal suppression in response to dexamethasone. Thus, melancholic patients had a distinctive dysfunction of the hypothalamus-pituitary-adrenal axis called ‘DST nonsuppression.’
Other illnesses share this suppression. But they’re not mistaken for melancholia, Shorter says. In fact, he compares the accuracy of the DST to the diagnostic test for epilepsy.
The marker of cortisol nonsuppression is not biologically unique to melancholia: it occurs in severe physical illness and in some psychiatric disorders that are unlikely to be confused with melancholia, such as anorexia nervosa and dementia. Yet the dexamethasone suppression test, or “DST,” has about the same ability to diagnose melancholia properly, without too many “false negatives” and “false positives,” that the interictal (between seizures) electroencephalogram has in epilepsy: useful but not perfect. The DST provides evidence that most melancholic patients, whether unipolar or bipolar, have an underlying biochemical homogeneity that is entirely lacking in other psychiatric disorders.
Ultimately, Shorter calls for a de-emphasis of sad mood in 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.”
He also calls for a division of depression. He believes that lumping melancholia with depression is dangerous. “…[P]oorly diagnosed patients are denied the benefit of proper treatment while being exposed to all the side effects of classes of medication, such as Prozac-style drugs, that are ineffective for serious illness.”
In sum, having one term to describe melancholia and “nervous illness” simply makes no sense. As Shorter writes, these two illnesses are as different as “tuberculosis and mumps.”