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Authors: Robert Whitaker

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With this understanding of psychiatric medications now in mind, it is possible to pose the scientific question at the heart of this book: Do these drugs help or harm patients over the long term? What do fifty years of outcomes research show?

*
The NIMH researchers also looked at a number of other possible associations between variable neurotransmitter levels and response to an antidepressant. They measured norepinephrine metabolites and dopamine metabolites; they divided their depressed patients into bipolar and unipolar groups; and they evaluated their response to two antidepressants, imipramine and amitriptyline. They found mild associations between several of these subgroups and their response to one or other of the drugs; I have focused here on their findings regarding whether (a) depression is due to low levels of serotonin, and (b) if the subgroup of patients with low levels of serotonin responds better to a drug that selectively blocks the reuptake of this neurotransmitter.

*
Over the long term, it appears that serotonin release falls to an abnormally low level, at least in certain regions of the brain.

part three

Outcomes

6
A Paradox Revealed

“If we wish to base psychiatry on evidence-based
medicine, we run a genuine risk in taking a closer
look at what has long been considered fact.”


EMMANUEL STIP, EUROPEAN PSYCHIATRY (2002)
1

The basement in Harvard Medical School’s Countway Library is one of my favorite places in Boston. After stepping off the elevator, you enter a huge, somewhat dingy room, filled with the musty smell of old books. I often stop a few feet inside the doorway and take in the grand sight: row after row of bound copies of medical journals from the early 1800s to 1986. The place is almost always empty, and yet there are rich histories to be discovered here, and soon, as you begin to piece together a particular narrative of medicine, you are hopping from one journal to the next, the pile of books on your desk growing ever higher. There is the thrill of the chase, and it seems too that this part of the library never disappoints. All of the journals are organized in alphabetical order, and whenever in one article you find a citation that interests you, all you have to do is walk a few feet and inevitably you find the journal you need. At least up until recently, the Countway Library seems to have purchased nearly every medical journal that was published.

This is where we can begin our quest to find out how psychiatric drugs affect long-term outcomes. The research method we’ll need to follow is straightforward. First, to the best we can, we’ll have to flesh out the natural spectrum of outcomes for each particular disorder. In the absence of antipsychotic medications, how would people
diagnosed with schizophrenia likely fare over time? What chance—if any—would they have of recovering? How well might they fare in society? The same questions can be asked in regard to anxiety, depression, and bipolar illness. What would outcomes look like in the absence of anti-anxiety drugs, antidepressants, and mood stabilizers? Once we have a sense of a baseline for a disorder, we can trace the outcomes literature for that illness, and we can hope that it will tell a consistent, coherent story. Do the drug treatments alter the
long-term
course of a mental disorder—in the patient population as a whole—for the better? Or for the worse?

Since chlorpromazine (Thorazine) was the drug that launched the psychopharmacology revolution, it seems appropriate to investigate schizophrenia outcomes first.

The Natural History of Schizophrenia

Schizophrenia today is regularly thought of as a lifelong, chronic illness, and that is an understanding that originated with the work of German psychiatrist Emil Kraepelin. In the late 1800s, he systematically tracked the outcomes of patients at an asylum in Estonia, and he observed that there was an identifiable group that reliably deteriorated into dementia. These were patients who, upon entry to the asylum, showed a lack of emotion. Many were catatonic, or lost hopelessly in their own worlds, and they often had gross physical problems. They walked oddly, suffered from facial tics and muscle spasms, and were unable to complete willed physical acts. In his 1899 textbook
Lehrbuch der Psychiatrie
, Kraepelin wrote that these patients suffered from
dementia praecox
, and in 1908, Swiss psychiatrist Eugen Bleuler coined the term “schizophrenia” as a substitute diagnostic term for patients in this dilapidated condition. However, as British historian Mary Boyle convincingly argued in a 1990 article, “Is Schizophrenia What It Was? A Re-analysis of Kraepelin’s and Bleuler’s Population,” many of Kraepelin’s
dementia praecox
patients were undoubtedly suffering from a viral disease,
encephalitis lethargica
, which in the late 1800s had yet to be
identified. This disease caused people to turn delirious, or to drop into a stupor, or to start walking in a jerky manner, and once Austrian neurologist Constantin von Economo described the illness in 1917, the
encephalitis lethargica
patients were no longer part of the “schizophrenia” pool, and after that happened, the patient group that remained was quite different from Kraepelin’s
dementia praecox
group. “The inaccessible, the stuporous catatonic, the intellectually deteriorated”—those types of schizophrenia patients, Boyle noted, largely disappeared. As a result, the descriptions of schizophrenia in psychiatric textbooks during the 1920s and 1930s changed. All of the old physical symptoms—the greasy skin, the odd gait, the muscle spasms, the facial tics—disappeared from the diagnostic manuals. What remained were the mental symptoms—the hallucinations, the delusions, and the bizarre thoughts. “The referents of schizophrenia,” Boyle wrote, “gradually changed until the diagnosis came to be applied to a population who bore only a slight, and possibly superficial, resemblance to Kraepelin’s.”
2

So now we have to ask: What is the natural spectrum of outcomes for
that
group of psychotic patients? Here, unfortunately, we run into a second problem. From 1900 until the end of World War II, eugenic attitudes toward the mentally ill were quite popular in the United States, and that social philosophy dramatically affected their outcomes. Eugenicists argued that the mentally ill needed to be sequestered in hospitals to keep them from having children and spreading their “bad genes.” The goal was to keep them confined in asylums, and in 1923, an editorial in the
Journal of Heredity
concluded, with an air of satisfaction, that “segregation of the insane is fairly complete.”
3
As a result, many people diagnosed with schizophrenia in the first half of the century were hospitalized and never discharged, but that social policy was then misperceived as outcomes data. The fact that schizophrenics never left the hospital was seen as proof that the disease was a chronic, hopeless illness.

However, after World War II, eugenics fell into disrepute. This was the very “science” that Hitler and Nazi Germany had embraced, and after Albert Deutsch’s exposé of the abysmal conditions in U.S. mental hospitals, in which he likened them to concentration camps, many states began talking about treating the mentally ill in
the community. Social policy changed and discharge rates soared. As a result, there is a brief window of time, from 1946 to 1954, when we can look at how newly diagnosed schizophrenia patients fared and thereby get a sense of the “natural outcomes” of schizophrenia prior to the arrival of Thorazine.
*

Here’s the data. In a study conducted by the NIMH, 62 percent of first-episode psychotic patients admitted to Warren State Hospital in Pennsylvania from 1946 to 1950 were discharged within twelve months. At the end of three years, 73 percent were out of the hospital.
4
A study of 216 schizophrenia patients admitted to Delaware State Hospital from 1948 to 1950 produced similar results. Eighty-five percent were discharged within five years, and on January 1, 1956—six years or more after initial hospitalization—70 percent were successfully living in the community.
5
Meanwhile, Hill side Hospital in Queens, New York, tracked 87 schizophrenia patients discharged in 1950 and determined that slightly more than half never relapsed in the next four years.
6
During this period, outcomes studies in England, where schizophrenia was more narrowly defined, painted a similarly encouraging picture: Thirty-three percent of the patients enjoyed a “complete recovery,” and another 20 percent a “social recovery,” which meant they could support themselves and live independently.
7

These studies provide a rather startling view of schizophrenia outcomes during this time. According to the conventional wisdom, it was Thorazine that made it possible for people with schizophrenia to live in the community. But what we find is that the majority of people admitted for a first episode of schizophrenia during the late 1940s and early 1950s recovered to the point that within the first twelve months, they could return to the community. By the end of three years, that was true for 75 percent of the patients. Only a small percentage—20 percent or so—needed to be continuously hospitalized. Moreover, those returning to the community weren’t living in shelters and group homes, as facilities of that sort didn’t yet exist. They were not receiving federal disability payments, as the SSI and SSDI programs had yet to be established. Those discharged from hospitals were mostly returning to their families, and judging by the social recovery data, many were working. All in all, there was reason for people diagnosed with schizophrenia during that postwar period to be optimistic that they could get better and function fairly well in the community.

It is also important to note that the arrival of Thorazine did not improve discharge rates in the 1950s for people newly diagnosed with schizophrenia, nor did its arrival trigger the release of chronic patients. In 1961, the California Department of Mental Hygiene reported on discharge rates for all 1,413 first-episode schizophrenia patients hospitalized in 1956, and it found that 88 percent of those who weren’t prescribed a neuroleptic were discharged within eighteen months. Those treated with a neuroleptic—about half of the 1,413 patients—had a
lower
discharge rate; only 74 percent were discharged within eighteen months. This is the only large-scale study from the 1950s that compared discharge rates for first-episode patients treated with and without drugs, and the investigators concluded that “drug-treated patients tend to have longer periods of hospitalization…. The untreated patients consistently show a somewhat lower retention rate.”
8

The discharge of
chronic
schizophrenia patients from state mental hospitals—and thus the beginning of deinstitutionalization—got under way in 1965 with the enactment of Medicare and Medicaid. In 1955, there were 267,000 schizophrenia patients in state and county mental hospitals, and eight years later, this number had barely budged. There were still 253,000 schizophrenics residing in the hospitals.
9
But then the economics of caring for the mentally ill changed. The 1965 Medicare and Medicaid legislation provided federal subsidies for nursing home care but no such subsidy for care in state mental hospitals, and so the states, seeking to save money, naturally began shipping their chronic patients to nursing homes. That was when the census in state mental hospitals began to noticeably drop, rather than in 1955, when Thorazine was introduced. Unfortunately, our societal belief that it was this medication that
emptied the asylums, which is so central to the “psychopharmacology revolution” narrative, is belied by the hospital census data.

Through a Lens Darkly

In 1955, pharmaceutical companies were not required to prove to the FDA that their new drugs were effective (that requirement was added in 1962), and thus it fell to the NIMH to assess the merits of Thorazine and the other new “wonder drugs” coming to market. Much to its credit, the NIMH organized a conference in September 1956 to “consider carefully the entire psychotropic question,” and ultimately the conversation at the conference focused on a very particular question: How could psychiatry adapt, for its own use, a scientific tool that had recently proven its worth in infectious medicine: the placebo-controlled, double-blind, randomized clinical trial?
10

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