E. Fuller Torrey, through his Treatment Advocacy Center, is the country’s most prominent advocate for outpatient commitment laws, which typically force people with a diagnosis of a severe mental illness to take antipsychotic medications. He has posted a review of Anatomy of an Epidemic on his TAC website, scathing—naturally—in kind, and I think his review provides a rare opportunity: In essence, we can now examine it to see if it provides a convincing defense of outpatient commitment laws and society’s decision to force certain adults to take antipsychotics.
The logic behind outpatient commitment laws is that antipsychotic medication is a necessary good for people with a diagnosis of severe mental illness. The medications are known to be helpful, but—or so the argument goes—people with “severe mental illness” lack insight into their disease and this is why they reject the medication.
However, if the history of science presented in Anatomy of an Epidemic is correct, antipsychotic medications, over the long term, worsen long-term outcomes in the aggregate, and thus a person refusing to take antipsychotic medications may, in fact, have good medical reason for doing so. And if that is so, the logic for forced treatment collapses.
We need to go over Torrey’s review, step by step. This may be a bit exhausting, but since his critical review can ultimately be seen as a defense of his advocacy of forced treatment, I think it will be worthwhile. In the end, we will be able to judge whether his is an honest review, or dishonest in kind, and if it is the latter, that—by itself—will reveal much about the scientific merits of outpatient commitment laws.
Part One: Diagnostic Criteria and Schizophrenia Outcomes
In my foreword to Anatomy of an Epidemic, I told of how, when co-writing a series for the Boston Globe in 1998 on abuses of psychiatric patients in research settings, I stumbled upon two outcome studies that I found difficult to understand. Dr. Torrey opens his review by setting out to show that my curiosity about those studies was misplaced, and that my subsequent reporting on those studies was in error.
The first such study was by Harvard researchers, who reported in 1994 that outcomes for schizophrenia patients had worsened during the past two decades and were now no better than they had been a century earlier. This outcome belied what I understood to be true at that time, which was that psychiatry had made great progress in treating schizophrenia.
This is the only context for my citing this study in Anatomy of an Epidemic, as a finding that piqued my curiosity. I do not mention the study again in the book, and thus do not cite it in the chapter examining the evidence base for antipsychotics. However, Dr. Torrey claims that I do, writing that after I summarized the findings from this study in the preface, I “later added that the worsened outcomes (in recent decades) were due to the use of antipsychotic drugs.”
Since Dr. Torrey has focused attention on this study, let’s look at what the researchers found and their discussion of their findings.
In a survey of outcome studies over the past century, which were conducted around the world, the researchers reported that from 1895 to 1955, 35.4% of schizophrenia patients “improved;” that this improvement rate increased from 1956 to the 1970s to 48.5%; and then it declined. They concluded that since 1986 the “likelihood of a favorable outcome has diminished to only 36.4%, or a level that is statistically indistinguishable from that found in the first half of the century.”
In their discussion, the researchers reasoned that improved outcomes in the middle part of the century were due to both a change in diagnostic criteria that broadened the definition to include patients who were less ill at disease onset and then to the introduction of neuroleptics. They attribute the decline in outcomes, which began to show up in the late 1970s, to a decline in social services and, starting in 1980 with the publication of DSM-III, a narrowing of the diagnostic criteria for schizophrenia.
So the study has two parts: One tells of how outcomes have deteriorated in recent times, and are now no better than they were in the first half of the 20th century, before the arrival of antipsychotics, which seems to belie the common wisdom that the arrival of the drugs “revolutionized” the treatment of schizophrenia. At the same time, in their discussion, the researcher write that that neuroleptics helped improve outcomes, at least when they were first introduced.
As I wrote above, I mentioned this study in my foreword to explain how I got interested in this subject. The deterioration in modern outcomes, such that they were now no better than in the pre-antipsychotic era, surprised me. But I didn’t discuss this study at any length, precisely because I don’t think it provides evidence regarding the long-term efficacy of neuroleptics, one way or another.
However, there is a non-drug explanation for the improvement of outcomes in the 1950s. In the first half of the century, up until the end of World War II, eugenic attitudes toward the mentally ill in the United States, which were also seen in Britain and other European countries, dramatically affected the outcomes of people hospitalized with a diagnosis of schizophrenia. Eugenicists argued that people with schizophrenia were genetically defective, and thus they needed to be segregated from the population—i.e. kept in mental hospitals—to keep them from breeding. This idea began to take hold in the late 1890s, and once it did, discharge rates plunged. Those low discharge rates in the eugenics era would be seen as evidence that patients didn’t improve, and thus the low improvement rate up until 1945 was in large part due to this social policy.
After World War II, eugenics came to be associated with Nazi Germany and the “science” that led to the Holocaust, and thus seen as a discredited, even shameful science. The need to keep schizophrenia patients in mental hospitals for eugenic reasons began to evaporate, and that led, in the wake of World War II, to new discussions within psychiatry and our society about providing care to patients in the community. Discharge rates for first-episode schizophrenia patients immediately began to climb. For instance, a study of first-episode psychotic patients admitted to Warren State Hospital in Pennsylvania from 1946 to 1950 found that 62 percent were discharged within 12 months, and that by the end of three years, 73% were living out of the hospital. Similarly, a study of 216 schizophrenia patients admitted to Delaware State Hospital from 1948 to 1950 found that six years later, 70% were successfully living in the community. These are very high “improvement” rates, and they predate the arrival of the first antipsychotic, Thorazine, in asylum medicine.
Moreover, once Thorazine was introduced in the mid 1950s, there was one large study that looked at how the new antipsychotics affected discharge rates for first-episode patients, and it did not find that the drugs were helpful in this regard. In 1961, the California Department of Mental Hygiene reported on the discharge rates for 1,413 first-episode schizophrenia patients hospitalized in 1956, and it found that 88% of those who weren’t prescribed a neuroleptics—about half of the 1,413 patients—were discharged within 18 months. Those treated with a neuroleptic had a lower discharge rate; only 74 percent were discharged within 18 months.
Thus, if we look closely at changing discharge rates during the middle part of the century, we see that they rose for first-episode patients following World War II, when eugenic attitudes became discredited, and that the arrival of neuroleptics in asylum medicine did not increase this rate. This change in social attitude, along with broadened diagnostic criteria, is what led to the improvement in outcomes following World War II. This change in social attitude grew in the 1950s and 1960s. Deinstitutionalization, as a social policy, took hold and that led to improved discharge rates in those decades.
As anyone can see, the study does raise a question. Why are outcomes today no better than they were in the first half of the century? Doesn’t this finding belie the common wisdom that antipsychotics kicked off a psychopharmacological revolution, a great advance in care. This was a study that understandably piqued my curiosity, which is how I presented it in my book, and yet Dr. Torrey, eager to discredit Anatomy of an Epidemic, states that I cited it as evidence that antipsychotics worsen long-term outcomes.
Call this dishonesty moment number one in his review.
Next, in my foreword to to Anatomy of an Epidemic, I also wrote of how my curiosity about the merits of our drug-based paradigm of care was triggered by studies conducted by the World Health Organization, which twice found that outcomes in three developing countries, India, Columbia, and Nigeria were “considerably better” than in the United States and other developed countries. That also seemed odd—why should outcomes in poor countries like India and Nigeria be better than in the U.S. and other rich countries?
In Anatomy of an Epidemic, I then reported on the WHO findings in the chapter on antipsychotics. This, I noted, was data from a cross-cultural study, in which medication use varied. I presented the WHO data as one piece in a larger body of evidence regarding the long-term merits of antipsychotics.
Here are the findings from the WHO study that included, as part of its reporting on outcomes, the patients’ use of antipsychotics.
- Outcomes were best in the three developing countries, where only 16% of patients were regularly maintained on antipsychotics (versus 61% of patients in the developed countries.)
- The best outcomes of all were seen in Agra, India, where only 3% of patients were maintained on the drugs. The worse outcomes of all—in terms of the highest percentage of patients who were constantly ill—were reported in Moscow, and it was there that medication usage was highest.
- In a 1997 followup (15 to 25 years after the initial study), the patients in the developing countries were still faring much better. “The outcome differential” held up for “general clinical state, symptomatology, disability, and social functioning,” the researchers noted.
In his review, Dr. Torrey seeks to discredit this finding. First, he notes that he and others have argued that the difference in outcomes was due to a difference in the type of schizophrenia suffered by people in the developing countries. Second, and this is more important, he implies that the authors of the WHO studies, in response to such criticism, in 2008 backed away from their initial findings.
The WHO authors, he says, wrote that “we do not argue that the prognosis of schizophrenia in developing countries is groupwise uniformly milder.” The WHO investigators admitted, he says, that “the proportions of continuous unremitting illness . . . did not different significantly across the two types [developed and developing) of settings.”
When you read that sentence, you are led to understand that the authors of the WHO study no longer believe that outcomes in the developing countries were truly better. It seems that they now agree with their critics, which is that the better outcomes were an artifact of diagnostic differences. If that is true, it would mean that this cross-cultural study should not be seen as an instance in which patients, who were treated in settings where antipsychotics were less frequently used, had better outcomes. That is how I presented the study, and so if the researchers did indeed conclude what Dr. Torrey said they did, my presentation of that study would be in error.
So let’s look at what the authors, Jablensky and Sartorius, actually wrote in their 2008 article.
There were two WHO studies that compared outcomes in developing and developed countries, they noted. The first was known as the WHO International Pilot Study of schizophrenia, which found “markedly better outcomes of schizophrenia patients in India and Nigeria at 2-year and 5-year follow-ups.” However, at that time, the researchers concluded that the divergent outcomes—in this first study—might be the result of a difference in patient groups. Thus, they mounted a rigorous second study, known as the DOSMeD study, to investigate that possibility. This study followed all new onset cases of psychosis within a geographical area for two years.
In 1992, the WHO investigators reported their findings, and as part of their report, they divided patients into schizophrenia subtypes and compared outcomes in the subgroups. But it didn’t matter. No matter how the data were cut ande sliced, outcomes in the developing countries were much better. “The findings of a better outcome in developing countries was confirmed,” they wrote.
Now, in their recent 2008 paper, Sartorius and Jablensky, rather than back away from their 1992 findings, vigorously defended them.
They noted the following results from the DOSMeD study:
- High rates of complete clinical remission were significantly more common in developing country areas (37%) than in developed countries (15.5%).
- Patients in developing countries experienced significantly longer periods of unimpaired functioning in the community, although only 16% of them were on continuous antipsychotic medications (compared with 61% in the developed countries.)
- In the study, one of the best predictors of outcome was “type of setting (developed vs. developing country.)”
- Elevated rates of early death (standardized mortality ratios) are more common in developed countries than developing ones.
So, where did Torrey’s misleading quote come from? In their 2008 report, Sartorius and Jablensky did observe that the percentage of patients with a “continuous unremitting illness” in the poor countries was 11.1 %, which was not significantly less than the percentage with this course in the rich countries (17.4%). In other words, there was a small percentage of patients in both settings that had a very bad course, but this did not reflect overall outcomes.
Dr. Torrey, in his review, was intent on discrediting the findings from this WHO study, which reported superior outcomes in poor countries where only a small percentage of patients were regularly maintained on antipsychotics. To do so, he implied that the WHO investigators now agreed with the critics of the study, when that is not true.
Call this dishonesty moment number two in his review.
Part Two: Schizophrenia Outcomes and Medication
In this part of his review, Dr. Torrey takes aim at two longer-term studies (Courtenay Harding’s and Martin Harrow’s) and my reporting on those studies. He also takes aim at the results reported for patients treated with open-dialogue therapy in Western Lapland, Finland, and my reporting of that program.
Courtenay Harding’s Vermont Longitudinal Study
I wrote one paragraph on this study in Anatomy of an Epidemic. Here it is:
In the late 1950s and early 1960s, Vermont State Hospital discharged 269 chronic schizophrenics, most of whom were middle-aged, into the community. Twenty years later, Courtenay Harding interviewed 168 patients from this cohort (those who were still alive), and found that 34 percent were recovered, which meant they were “asymptomatic and living independently, had close relationships, were employed or otherwise productive citizens, were able to care for themselves and led full lives in general.” This was a startling good outcome for patients who had been seen as hopeless in the 1950s, and those who had recovered, Harding told the APA Monitor, had one thing in common: They all “had long since stopped taking medications.” She concluded that it was a “myth” that schizophrenia patients “must be on medications all their lives,” and that, in fact, “it may be a small percentage who need medication indefinitely.”
Now here is what Dr. Torrey writes. “As Whitaker describes it . . . ‘34 percent were recovered’ which he claims is a ‘startling good outcome.’ Whitaker attributes this outcome (emphasis added) to the fact that ‘they had all long since stopped taking their medications.’ ”
We can call this dishonesty moment number three in his review. I did not attribute the 34% recovery rate to the fact that they had “all long since stopped taking their medications,” as that would indicate that I had drawn that conclusion. Instead, I repeated what Dr. Harding had said in an interview with the APA Monitor about the recovered patients. Equally revealing is what he omits from his discussion of Dr. Harding’s study: he does not mention her conclusion that the conventional wisdom regarding the need for schizophrenia patients to stay on antipsychotics all their life is a “myth.”
Martin Harrow’s Longitudinal Study
As Dr. Torrey correctly notes (for once), I do consider Martin Harrow’s report on the long-term outcomes of people diagnosed with schizophrenia and milder psychotic disorders to be of great importance. His was a prospective study of 200 psychotic patients, whom he followed for 20 years, and it is the only such study in the scientific literature.
Dr. Torrey dismisses the study as “completely unremarkable,” and so let’s take a close look at it to see if that is a fair assessment of his findings.
In the study, everyone was treated conventionally in the hospital with antipsychotics and then discharged. Harrow then periodically assessed how they were doing over the next 20 years. At each followup, he looked at whether they were symptomatic, whether they were working, and a variety of other outcome measures. He also charted their use of antipsychotics and other psychiatric medications. At the end of 15 years, he still had 145 patients in his study (64 with schizophrenia and 81 with milder disorders. In one of his article, he also reported outcomes for a schizophrenia-spectrum group, which included the schizophrenia patients and a few others with schizoaffective disorder.)
Here is a summary of Harrow’s findings, taken from both his 2007 report on their 15-year outcomes, and his 2012 report on their 20-year outcomes. (See slides for a graphic presentation of this data.)
1. Recovery rates in the schizophrenia group
At the end of two years, the schizophrenia patients who had stopped taking antipsychotics were doing slightly better on a “global assessment scale” than those taking an antipsychotic. Then, over the next 30 months, the collective fates of the two groups began to dramatically diverge. The off-med group began to improve significantly, and by the end of 4.5 years, 39% were in recovery. In contrast, outcomes for the medicated group worsened during this 30-month period. As a group, their global functioning declined slightly, and at the 4.5-year mark, only six percent were in recovery, and few were working.
That stark divergence in outcomes remained for the next ten years. At the 15-year followup, 40 percent of the schizophrenia patients off antipsychotics (25 of the 64 patients) were in recovery, compared to five percent of those taking antipsychotics. (To be in recovery, a person had to have no positive or negative symptoms; couldn’t have been hospitalized in the previous year; and adequate work and social functioning.)
2. Spectrum of outcomes in the schizophrenia group
Harrow divided long-term outcomes for the 64 schizophrenia patients into three categories: recovered, fair, and uniformly poor. Of the 25 patients who stopped taking antipsychotics, 10 recovered (40%), 11 had fair outcomes (44%), and 4 (16%) had uniformly poor outcomes. In contrast, only 2 of the 39 patients who stayed on antipsychotics recovered (5%); 18 had fair outcomes (46%), and 19 (49%) had uniformly pair outcomes. In sum, medicated patients had one-eighth the recovery rate of unmedicated patients, and a threefold higher rate of faring miserably over the long term.
3. Global outcomes for schizophrenia patients by prognostic type.
At the start of the study, Harrow grouped his schizophrenia patients into two subgroups: those with a good prognosis and those with a bad prognosis. Although he didn’t provide the global data for these two subtypes, he did report this finding: “In addition, global outcome for the group of patients with schizophrenia who were on antipsychotics were compared with the off-medication schizophrenia patients with similar prognostic status. Starting with the 4.5-year followup and extending to the 15-year follow-up, the off-medication subgroup tended to show better global outcomes at each follow-up.”
In other words, in every subgroup of patients (by prognostic type), those off medication had better long-term outcomes (in the aggregate).
4. Psychotic symptoms in the schizophrenia-spectrum and schizophrenia-only group
At the two-year follow-up, about 35% of the “schizophrenia spectrum” group were off antipsychotics, and that percentage remained fairly stable throughout the next 15 years. There was no significant differences in severity of psychotic symptoms between the on-med and off-med groups at two years, but starting with the 4.5-year followup and continuing through year 20, those “who were not on antipsychotic medications were significantly less psychotic than those on antipsychotics.
Among the schizophrenia patients, at the 10-year follow-up, 23% off antipsychotics were experiencing psychotic symptoms, versus 79% of those still on the drugs. At the 15-year followup, 28% of those off antipsychotics had psychotic symptoms, versus 64% of those on the medications.
5. Anxiety symptoms in the schizophrenia-spectrum group
At the two-year followup, about 50% of those on antipsychotics and a similar percentage of those off medications were experiencing “high anxiety.” However, over the next 30 months, high anxiety symptoms soared in the on-antipsychotics group, such that nearly 75% were experiencing this distress by year 4.5, whereas anxiety markedly declined for those off antipsychotics, such that only about 20% were experiencing this distress by year 4.5. This dramatic difference in anxiety symptoms remained throughout the study, with more than half of those on antipsychotics still suffering from high anxiety at the end of 20 years.
6. Cognitive function in the schizophrenia-spectrum group
The researchers assessed cognitive function at each followup, with one test assessing ability to access general information, and the other abstract thinking. At three of the six follow-ups, those off antipsychotics showed significantly better cognitive functioning, and in the other three follow-ups, there was a general trend favoring those off antipsychotics.
7. Sustained periods of recovery in the schizophrenia-spectrum group.
Of the 24 schizophrenia patients who remained continuously on antipsychotics throughout the 20 years, only 4 (17%) “ever entered into a period meeting the operational definition of recovery during any of the six follow-ups.” The reasons they failed to do so was either because they were psychotic or not working, Harrow noted. In contrast, there were 15 in the group of 70 who were off antipsychotics by the two-year follow-up and remained off the drugs throughout the remaining 18 years. Thirteen of these 15 patients (87%) “experienced two or more periods of recovery,” which meant they were both asymptomatic and working more than 50% of the time.
8. Global outcomes of all 145 patients
Harrow provided global adjustment data for all four groups in his study: schizophrenia on meds, schizophrenia off psychiatric medications, milder disorders on psychiatric meds, milder disorders off. At the end of 15 years, the global outcomes for the four groups lined up like this, from best to worst: Milder disorders off meds, schizophrenia off meds, milder disorders on meds, and schizophrenia on meds.
As could be expected, Dr. Torrey does not report of any of these outcomes in detail. I’ll let readers of this blog decide whether such findings are—as Dr. Torrey writes— “completely unremarkable.”
In his discussion of the Harrow study, Dr. Torrey also makes this claim: “Whitaker . . . using tortured logic, asserts that the Harrow study proves that long-term antipsychotic use causes brain damage and is responsible for many of the symptoms of schizophrenia, when in fact the study does nothing of the kind.”
Here is my challenge to Dr. Torrey. I wrote about the Harrow study on pages 115 to 118 of Anatomy of An Epidemic. He should point to the passage on those pages where I asserted that the Harrow study “proves that long-term antipsychotic use causes brain damage and is responsible for many of the symptoms of schizophrenia.” If he can not point to such an assertion, then he should print this correction on his Treatment for Advocacy web page: “I lied about what Robert Whitaker wrote about the Harrow study.” He could then explain to his readers why he felt motivated to lie in this way.
But for our purposes, we can chalk this up as dishonesty moment number four in his review.
The Open Dialogue Program in Finland
In the solutions section of Anatomy of an Epidemic, I wrote about the good outcomes for psychotic patients in Western Lapland, a region in Finland, that—since 1992—has used antipsychotic drugs in a selective manner. Two-thirds of their first-episode patients have not been exposed to antipsychotics five years after initial diagnosis, and 80% are either working or back in school. These are extraordinarily good results, but Dr. Torrey dismisses them out of hand: “Most revealing and remarkable, however, is the fact that more than 40 years after the treatment program began, there are almost no publications describing its results and nobody in Finland or elsewhere has tried to replicate it. Robert Whitaker appears to be the person most impressed by it.
If Dr. Torrey had checked the notes section of my book, he would have found a number of citations documenting the good outcomes in Western Lapland since 1992, when that district began using antipsychotics in a selective manner. Here are five such published reports, and if Dr. Torrey likes, I can point him to others:
1. V. Lehtinen, “Two-year outcome in first-episode psychosis treated according to an integrated model,” European Psychiatry 15 (2000):312-20.
2. J. Seikkula. “Five year experience of first-episode non-affective psychosis in open-dialogue approach,” Psychotherapy Research 16 (2006): 214-28.
3. J. Seikkula. “A two-year follow-up on open dialogue treatment in first episode psychosis,” Society of Clinical Psychology 10 (2000):20-29.
4. J. Seikkula. “Open dialogue, good and poor outcome,” J of Constructivist Psychology 14 (2002):267-86.
5. J. Seikkula. “Open dialogue approach: treatment principles and preliminary results of a two-year follow-up on first episode schizophrenia.” Ethical Human Sciences Services 5 (2003):163-82.
There are also now groups in the United States and elsewhere seeking to “replicate” the open-dialogue model, and if Dr. Torrey likes, I could point him to a conference that will be held in Finland in late August devoted to this topic. Many others, who have read the published articles, apparently are “impressed” by the success of Open Dialogue Therapy.
Part Three: What SSI and SSDI Rates Say
In this part of his review, Dr. Torrey states that while the number of individuals on disability for SSI and SSDI has “indeed increased alarmingly,” he argues that this is because these programs “have become alternatives to welfare for poor and unemployed individuals who have any kind of psychiatric problem.”
I agree this is partly true. But, as I detail in Anatomy of an Epidemic, our drug-based paradigm of care is fueling this epidemic too. One, the widespread use of stimulants and antidepressants has helped create a “bipolar boom” and the disability numbers are soaring, in large part, because of an extraordinary influx of bipolar patients. Two, a review of the long-term outcomes data for antipsychotics, anti-anxiety agents, and antidepressants reveals that these drugs, in the aggregate, increase the risk of long-term disability.
Part Four: The Dopamine Receptor Story
This section of Dr. Torrey’s review has its interesting moments. He writes that if antipsychotics do indeed cause an increase in dopamine receptors (as I report in Anatomy of an Epidemic,) then “Whitaker is correct that this could potentially be a serious problem, but at this point in time the reality of the problem in humans is unknown.” Although antipsychotics have been shown to cause an increase in dopamine receptors in rats, he writes, it “still is not clear whether or not this also occurs in humans.”
But as Dr. Torrey well knows, there is in fact good evidence that it does indeed occur in humans.
As Philip Seeman first reported in Nature in 1978, the brains of schizophrenia patients at autopsy have 50 percent more dopamine receptors than controls. But at that time, Seeman and his collaborators were uncertain whether this increase in dopamine receptors was due to the disease, or caused by the antipsychotics. During the next decade, investigators in the United States, England and Germany investigated this question, and all determined that neuroleptics led to an increase in brain dopamine receptors.
“From our data,” German investigators wrote in 1989, “we conclude that changes in [receptor density] values in schizophrenics are entirely iatrogenic [drug caused.]”
Finally, in 2002, Seeman reported that, in a study that utilized positron emission tomography, he had documented this increase in dopamine receptors in living patients. This study, he reported, “demonstrates for the first time, using in vivo neuroreceptor imaging, that dopamine D2 receptor binding is increased after long-term treatment with antipsychotics in humans.”
Here is why this is so important. This increase in D2 receptors is thought to make patients more biologically vulnerable to psychosis. The increase may lead to severe relapses when patients abruptly withdraw from antipsychotics, and the worry is that it also leads to tardive psychosis—a deepening of psychotic symptoms—over the long term (when patients stay on the drugs.) In his 2002 paper, Seeman also found that those patients that had the “highest degree of D2 receptor upregulation” subsequently developed “severe and persistent tardive dyskinesia.”
So, in this instance, give Dr. Torrey credit for acknowledging that a drug-induced increase in dopamine receptors could be a troubling thing indeed. But when he writes that it is “not clear whether or not this occurs in humans,” we have a new moment of dishonesty in his review to tally up.
Miscellany:
I could point to many other instances from Dr. Torrey’s review in which he hasn’t accurately represented what I wrote in the book, or has misrepresented the research literature. But detailing all such problems would take several thousand words more, and so I will let those pass.
However, there is one final bit of miscellany in his review that I want to address, and it has to do with Loren Mosher’s ouster from the NIMH.
Dr. Torrey states that Loren Mosher was not ousted from his position at NIMH as head of the Center for Schizophrenia Studies because he had led the Soteria experiment, but because the field “was moving strongly in a biological direction” and thus Mosher held views of schizophrenia that were at odds with this new wave in psychiatry. Dr. Torrey then writes this of my reporting on Dr. Mosher’s ouster from the NIMH:
“What is perhaps most surprising in Whitaker’s book, given his past career as a respected journalist, is his willingness to uncritically accept anything he has been told as long as it fits his thesis and his wish to blame antipsychotics for everything except global warming.”
The story of Dr. Mosher’s fall from grace at the NIMH is, in fact, easily documented, and it indeed is associated with the Soteria project. As internal written records reveal, the psychiatric establishment began attacking Dr. Mosher the minute he reported good outcomes for his Soteria patients. The study had “serious flaws,” the NIMH review committee snapped. “The credibility of the pilot study is very low,” it wrote. Evidence of superior outcomes for the Soteria patients is “not compelling.” And so on, and then, after the initial reports appeared the committee hit Mosher with the lowest blow of all: It would approve further funding for the Soteria project only if he was replaced by another investigator, who would then work with the committee to redesign the experiment.
“The message was clear,” Mosher said, when I interviewed him years later about the Soteria project. “If we were getting outcomes this good, then I must not be an honest scientist.”
When I reported this story in Mad in America, I obtained the written documents that detailed this response to Loren Mosher’s Soteria experiment. Those documents laid bare the hostility of the biological faction within psychiatry toward his study, and toward Mosher personally because of it. So rather than accept this story “uncritically,” as Dr. Torrey suggests, I dotted my I’s and crossed by T’s. In fact, this was the same reporting path–a reliance on documents–that led me to write Mad in America and Anatomy of an Epidemic. If I had been willing to “uncritically accept anything had been told,” then I would have written about the wonders of the “psychopharmacological revolution.”
Dr. Torrey’s Review as a Foil for Assessing the Merits of Outpatient Commitment Laws
The fact that Dr. Torrey has written a scathing review of Anatomy of an Epidemic, asserting that I “made so many errors it is difficult to know where to begin,” is—in its guise as a book review–of little import. I had exchanged a couple of emails with him before his review appeared, and I knew this was coming. You cannot write a book like Anatomy of an Epidemic, which so directly challenges conventional beliefs, and not expect to be attacked, and it should not be surprising when the attacker misrepresents what you wrote, or twists things in order to try to publicly discredit you. Indeed, in the two years since my book was published, I have gotten quite used to reviews of this type, with defenders of the faith eager to inform readers that all is well in the world of psychiatric medications.
But here is why the review could be considered important to us as a society. We are embracing the increased use of outpatient commitment laws that force people to take antipsychotic medications, and we do so under the belief that these drugs are a necessary good for those people. This is an extraordinary thing for a society to do, to force people to take medications that alter their minds and experience of the world.
Yet, here is the story told in Anatomy of an Epidemic: If we look closely at Harrow’s study and a long list of other research, there is good reason to believe that these medications increase psychotic symptoms over the long-term, increase feelings of anxiety, impair cognitive function, cause tardive dyskinesia with some frequency, and dramatically reduce the likelihood that people will fully recover and be able to work. If this is so, how can we, as a society, defend our increasing embrace of forced treatment laws?
We can now ask this key question about Dr. Torrey’s review of Anatomy of an Epidemic. Given that he is a foremost proponent of outpatient commitment laws, what are we—as a society—to make of the fact that, in order to attack the book, he had to do so in a dishonest way?
