How Everyone Became Depressed

The rise and fall of the nervous breakdown

Poop or Go Blind?

Why psychiatry fears the past

Sometimes you don’t know whether to poop or go blind. We keep getting hammered with “new findings” about depression, as though the investigators were planting first flags on unknown soil. “Scientists closer to finding tests for depression biomarkers,” we learn in a headline in this week’s (June 7) Psychiatric News, a piffle sheet that the American Psychiatric Association publishes for the profession.

You know, there supposedly aren’t any biomarkers for depression, but, hey, we’re going to fix that! This whole concept illustrates how fundamentally failed psychiatry’s relationship to the past has been, because there are biomarkers that already exist. Merely that they’ve been forgotten.

It drives me crazy to see this reassurance repeated time and again, “no biomarkers for depression.” But in 1968 Dr. Bernard Carroll discovered that the dexamethasone suppression test (DST), already in use for Cushing’s Disease, was able to single out melancholically depressed patients: You give them a dose of the artificial steroid dexamethasone the night before, and 24 hours later their serum cortisol, produced by the adrenal gland, is still high — as opposed to the non-depressed controls whose cortisol post-dexamethasone normalizes quickly.

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This is a perfectly valid biomarker for serious depression. Melancholic depression. It was widely bruited in the 1970s and 80s, then in a series of conferences with big domes (who hadn’t a clue), it was dropped! (Shorter & Fink, 2010).

What Carroll had discovered was a dysfunction of the hormonal axis that runs from the hypothalamus in the brain, through the anterior pituitary gland, to the adrenal gland, the so-called HPA axis. There is a thyroid axis that is similarly dysfunctional in serious depression.

There are other existing biomarkers as well aside from the DST. Seriously depressed patients have all kinds of sleep abnormalities, discoverable in sleep studies. They tend to have elevated serum cortisol. Treatment with tricyclic antidepressants and electroconvusive therapy normalizes these various axes and metrics. This is old news. But it is forgotten news.

In the same article in the Psychiatric Times we learn that depressed patients respond to scopolamine, derived from various solanaceous plants, including “deadly nightshade.” It was first isolated in 1881 and by the First World War was in wide use as an analgesic and anti-agitation agent, often used in agitated depression. In 1922 German psychiatrist Hans Gruhle said they employed scopolamine in the Heidelberg University Psychiatric Hospital to control agitation (Psychiatrie für Aerzte, 2nd ed 1922, 261)

Hello NIMH investigators! Where were you in 1922? Not born yet, eh? Too bad. Those folks who taught you your history of psychopharmacology sure did a bang-up job.

The history of drug treatments in psychiatry is just filled with agents like scopolamine that had been forgotten for decades and then somehow come back to life as though Columbus had just discovered America. Charlie Shagass’s “barbiturate sedation threshold,” 1954, is a good example. The vanishment of the electroencephalograph in drug studies is another example. But what happens then? Are these old tests and treatments somehow disproven? No! Simply cast aside. (Shorter, 2005: 39)

Psychiatry is unlike any other medical specialty in its contempt for the past. Why is that? Partly it’s because, in the twentieth century psychiatry underwent two major erasures of knowledge, while other medical specialties did not experience even one. The first great wiping clean of the blackboard occurred in the 1920s, when psychoanalysis triumphant threw the entire first generation of biological psychiatry into the ashcan. This was valid information that had been painstakingly accumulated for decades. The analysts simply had no use for anything that situated psychiatric illness in the brain. For them, intrapsychic conflict (“the mind”) was all that counted. Out went all those early findings about histological (tissue-level) abnormalities in chronic psychotic illness. You couldn’t see unconscious conflict in the mind with a microscope and the analysts weren’t interested.

Then in the 1970s it was payback time, as the newly triumphant biological psychiatrists threw all the psychoanalytic learning about toilet-training-gone-bad into the ashcan and advanced under the banner of psychopharmacology. So yet another wrenching change occurred! All the previous psychotherapeutic knowledge of decades was discarded and it was, once again, tabula rasa, but this time writing with the new chalk of neurotransmitters and “major depression.”

So you can see why psychiatry fears the past: It’s continually being wiped out and best not to get too curious about it. But midst the past dross about “hysteria” and other failed ideas, there are gems. And people who know about these gems find all this crowing from NIMH absolutely hilarious.

Edward Shorter, Ph.D., is the Jason A. Hannah Professor in the History of Medicine at the University of Toronto.

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