“When it comes to dead bodies in current psychotropic
trials, there are a greater number of them in the
active treatment groups than in the placebo groups.
This is quite different from what happens in pencillin
trials or trials of drugs that really work.”
—DAVID HEALY, PROFESSOR OF PSYCHIATRY AT
CARDIFF UNIVERSITY, WALES (2008)1
During the 1920s, owners of radios in the heartland of America regularly tuned into station KFKB, which had perhaps the most powerful signal in the country at that time, even though it emanated from tiny Milford, Kansas. “This is Dr. John R. Brinkley greeting his friends in Kansas and everywhere,” they’d hear, and Dr. Brinkley did indeed have a most amazing story to tell. In 1918, he had begun transplanting goat gonads into the testicles of older men worried about their declining virility, a fifteen-minute operation, he told KFKB listeners, that had been proven to “completely restore” sexual prowess. “A man is as old as his glands,” the good doctor would explain, and this rejuvenating surgery worked because the goat tissue “blends with and nourishes the human tissue, stimulating the human gland to new activity.”2
Although Brinkley’s medical credentials were of a dubious sort—he had a degree from Eclectic Medical University of Kansas City, a diploma mill—he was a masterful storyteller and something of an advertising genius. After his first few operations, he told his story to newspapers in Kansas, and soon they were publishing pictures of him cradling the first “goat-gland baby,” the offspring of an older man who had undergone the operation. Older men began pouring into Milford, each paying $750 for the procedure, and Brinkley cranked up his publicity machine. He hired three press agents to write ready-to-print newspaper features, which were then distributed to “publications interested in popularizing the latest developments from the laboratories of science.” Naturally, these planted articles included testimonials from satisfied customers, such as J. J. Tobias, chancellor of Chicago Law School, who—the articles said—liked to pound his chest and shout: “I’m a new man! It’s one of the great things of the century!” Brinkley established his own “Scientific Press” and reported a “90% to 95% success rate” for his surgery, which, he explained, returned the body to a proper hormonal “balance.” Once he began broadcasting his story on KFKB in 1923, he became so famous that three thousand letters arrived at his Mil-ford hospital each day, and by the late 1920s, he was perhaps the wealthiest “doctor” in the United States.
Eventually, Dr. Brinkley earned a place in medical history as one of the great charlatans of all time, when the American Medical Association targeted him as a quack. But when it came to marketing his goat-gonad surgery, he employed advertising techniques and a storytelling model that have stood the test of time. He published articles that appeared scientific, courted the press, claimed a very high success rate, offered a biological rationale for why the surgery worked, and provided reporters with quotes from satisfied customers. That—as Eli Lilly and other drug manufacturers can attest—is a tried-and-true formula for turning a psychiatric drug into a commercial success.
Fibs, Lies, and a Blockbuster Drug
Today, the fraudulent nature of the story told by Eli Lilly and psychiatry about Prozac when it came to market is fairly well known, having been documented by Peter Breggin, David Healy, and Joseph Glenmullen, among others. Breggin and Healy wrote their accounts after gaining access to Eli Lilly files while serving as expert witnesses in civil lawsuits, which allowed them to see data and internal memorandums that belied what the public had been told about the drug. At the risk of going over familiar ground, we need to revisit that story briefly, for it will help us see, with considerable clarity, how our societal delusions about the merits of the “second-generation” psychiatric drugs were formed. Eli Lilly’s marketing of Prozac proved to be a model that other companies followed as they brought their drugs to market, and it involved telling a false story in the scientific literature, hyping that story even more to the media, and hiding risks that could lead to disability and death for those who used the drugs.
The science of fluoxetine
Drug development begins in the laboratory, with investigation into a drug’s “mechanism of action,” and as we learned earlier, Eli Lilly scientists determind in the mid-1970s that fluoxetine caused serotonin to “pile up” in the synapse, which in turn triggered a series of physiological changes in the brain. Next, in animal studies, the drug was found to cause stereotyped activity in rats (repetitious sniffing, licking, etc.) and aggressive behavior in cats and dogs.3 In 1977, Eli conducted its first small trial in humans, but “none of the eight patients who completed the four-week treatment showed distinct drug-induced improvement,” Eli Lilly’s Ray Fuller told his colleagues in 1978. The drug also had caused “a fairly large number of reports of adverse reactions.” One patient had gone psychotic on the drug, and others had suffered from “akathisia and restlessness,” Fuller said.4
The trials of fluoxetine had barely begun and it was clear that Eli Lilly had a big problem. Fluoxetine didn’t appear to lift depression and it caused a side effect—akathisia—known to increase the risk of suicide and violence. After more reports of this kind came in, Eli Lilly amended its trial protocols. “In future studies, the use of benzodiazepines to control the agitation will be permitted,” Fuller wrote on July 23, 1979.5 The benzodiazepines would help suppress reports of akathisia, and likely boost efficacy results, as several trials of benzodiazepines for depression had shown them to be as effective as a tricyclic. Of course, as Eli Lilly’s Dorothy Dobbs later confessed in court, the use of benzodiazepines was “scientifically bad,” as it would “confound the results” and “interfere with the analysis of both safety and efficacy,” but it enabled the company to continue development of fluoxetine.6
Still, even with addition of the benzodiazepines, fluoxetine failed to perform well. During the early 1980s, the company conducted a phase III trial of the drug in Germany, and in 1985, the German licensing authority, Bundesgesundheitsamt (BGA), concluded that this drug was “totally unsuitable for the treatment of depression.”7 According to the patients’ “self ratings” (as opposed to the doctors’ ratings), the drug produced “little response or no improvement in the clinical picture of the patients,” the BGA noted.8 At the same time, it had caused psychosis and hallucinations, and increased some patients’ anxiety, agitation, and insomnia, “which as adverse effects exceed those which are considered acceptable by medical standards,” the BGA wrote.9 Most problematic of all, this drug treatment could prove fatal. “Sixteen suicide attempts were made, two of these with success,” the BGA said.10 A German Eli Lilly employee privately calculated that the incidence rate of suicidal acts for the fluoxetine patients was “5.6 times higher than under the other active medication, imipramine.”11
With Germany having rejected its application, Eli Lilly naturally worried that it would be unable to gain FDA approval for fluoxetine.* It needed to hide the suicide data, and in a 1994 civil lawsuit, Nancy Lord, an expert in clinical trial design, explained how the company did it. First, Eli Lilly instructed investigators to record various drug-related adverse events as “symptoms of depression.” As such, in the trial results submitted to the FDA, the problems were attributed to the disease rather than to fluoxetine. Second, when Eli Lilly scientists tabulated the data from case report forms, they changed individual reports of “suicidal ideation” to “depression.” Third, Lilly employees went through the German data “and pulled out [suicide] cases that they didn’t think were suicide.”12
All of these shenanigans, Lord told a court in 1994, made the entire testing process scientifically “worthless.” Yet even with these statistical manipulations, Eli Lilly still struggled to present a convincing case for fluoxetine in its application to the FDA. It had conducted placebo-controlled trials at eight sites, and in four of them, the fluoxetine patients had fared no better than the placebo group, and in the others, fluoxetine was only slightly better than a placebo.13 Meanwhile, when Peter Breggin reviewed Lilly’s documents, he discovered that imipramine had proven to be more effective than fluoxetine in six of seven trials.14 The FDA, in its March 28, 1985, review of one large trial, made the same observation: “Imipramine was clearly more effective than placebo, whereas fluoxetine was less consistently better than placebo.”15 At best, fluoxetine’s efficacy was of a very marginal sort, and FDA reviewer Richard Kapit also worried about its safety. At least thirty-nine patients treated with fluoxetine had gone psychotic in the short trials, and slightly more than 1 percent had become manic or hypomanic. Other side effects included insomnia, nervousness, confusion, dizziness, memory dysfunction, tremors, and impaired motor coordination. Fluoxetine, Kapit concluded, “may negatively affect patients with depression.”16 The FDA also understood that Eli Lilly had tried to hide many of these problems, the company having engaged in “large-scale underreporting” of the harm that fluoxetine could cause, according to reviewer David Graham.17
While the trials may have been scientifically worthless, they nevertheless proved to be an accurate forecast of what happened after Prozac was brought to market. There were numerous anecdotal accounts of Prozac-treated patients committing horrendous crimes or killing themselves, and so many adverse-events reports flowed into the FDA’s MedWatch program that Prozac quickly became America’s most complained about drug. By the summer of 1997, the FDA had received thirty-nine thousand such reports about Prozac, far outstripping the number received by any other drug for that nine-year period (1988–1997). The MedWatch filings told of hundreds of suicides, and of a long list of vexing side effects, which included psychotic depression, mania, abnormal thinking, hallucinations, hostility, confusion, amnesia, convulsions, tremors, and sexual dysfunction.18 The FDA estimates that only 1 percent of all adverse events are reported to MedWatch, which suggests that roughly 4 million Americans during that nine-year period had a bad or even fatal reaction to Prozac.19
The story told in the medical journals
Obviously, the record chalked up by fluoxetine in the clinical trials was not one that would support a successful launch in the marketplace. The public was not likely to embrace a medication that German’s licensing authority, in its initial review, had deemed “totally unsuitable” as a treatment for depression. If Prozac was going to be successful, the psychiatrists that Eli Lilly had paid to run the trials needed to tell a very different story in the medical journals and to the public.
The first account of a U.S. trial of fluoxetine appeared in the Journal of Clinical Psychiatry in 1984. This novel agent, wrote James Bremner, from Northwest Psychopharmacology Research in Washington, “provides effective antidepressant activity with fewer and less troublesome side effects than imipramine…. None of the adverse events reported by fluoxetine patients were considered to be drug related.” Fluoxetine, he added, “proved more effective than the tricyclic antidepressant.”20 Next, John Feigner, from the University of California at San Diego, reported that fluoxetine was at least equal in efficacy to imipramine (and probably superior to the tri-cyclic) and that “no serious side effects were observed” in his twenty-two fluoxetine patients during a five-week study.21 A theme had been sounded—a very safe and improved antidepressant had been developed—and Eli Lilly’s investigators stuck to it in the years that followed. “Fluoxetine was better tolerated than imipramine,” California psychiatrist Jay Cohn reported in 1985.22 “This drug,” said Eli Lilly’s Joachim Wernicke, in another article in the Journal of Clinical Psychiatry, “has very few serious side effects.”23 Finally, in the 1985 report on its large phase III trial, Eli Lilly announced that “fluoxetine produced greater improvement than placebo on all major efficacy parameters.”24
While these reports did tell of a new drug that was superior to the old class of antidepressants, this still was not a narrative of a “breakthrough” medication. There was no sense of why this drug worked better, but as FDA approval for fluoxetine neared, a new “fact” began to appear in the scientific reports. In a 1987 article in the British Journal of Psychiatry, Sidney Levine wrote that “studies have shown that [serotonin] deficiency plays an important role in the psychobiology of depressive illness.”25 While this was not what had actually been found—Levine had apparently missed the 1984 NIMH report that “elevations or decrements in the functioning of serotonergic systems per se are not likely to be associated with depression”—this article set the stage for fluoxetine to be touted as a drug that fixed a chemical imbalance. Two years later, University of Louisville psychiatrists surveyed the fluoxetine literature in order to provide “prescribing guidelines for the newest antidepressant,” and they wrote that “depressed patients have lower than normal concentrations of [serotonin metabolites] in their cerebrospinal fluid.” A delusional belief was now spreading through the medical literature, and perhaps not surprisingly, the Kentucky psychiatrists concluded that fluoxetine, which theoretically raised serotonin levels, was “an ideal drug for the treatment of depression.”26
This trail of reports in medical journals provided Eli Lilly with the sound bites it needed to advertise its drug to doctors. The company flooded medical journals with ads that featured good-looking people who radiated happiness, the ads touting Prozac as equal in efficacy to imipramine, and better tolerated. Science had proven that psychiatry had a new and much improved pill for depression, which appeared to correct a chemical imbalance in the brain.
The story told to the public
The story that had been told in psychiatric journals was certain to resonate with the public. However, at this point, the market for antidepressants was still moderate in size. When Prozac was approved, Wall Street analysts predicted that it could generate $135 to $400 million in annual sales for Eli Lilly. But the drug companies, the APA, and the leaders of the NIMH were keen on expanding the market for antidepressants, and the NIMH’s DART “public awareness” campaign turned out to be the perfect vehicle for doing so.
After the NIMH announced its plans for DART in 1986, it had studied the public’s beliefs about depression. A survey revealed that only 12 percent of American adults would take a pill to treat it. Seventy-eight percent said they “would live with it until it passed,” confident they could handle it on their own. This was an attitude consistent with what the NIMH had preached only fifteen years earlier, when Dean Schuyler, head of the depressive section, had told the public that most depressive episodes “will run their course and terminate with virtually complete recovery without specific intervention.” There was epidemiological wisdom in the public’s belief that depression would pass, but the NIMH—once Shervert Frazier and other biological psychiatrists took the helm—was intent on delivering a different message.
The purpose of DART, the NIMH explained in 1988, was “to change public attitudes so that there is greater acceptance of depression as a disorder rather than a weakness.” The public needed to understand that it regularly went “underdiagnosed and under-treated,” and that it could “be a fatal disease” if left untreated. There were 31.4 million Americans who suffered from at least a mild form of depression, the NIMH said, and it was important that they get diagnosed. The public needed to be made aware that anti-depressants produced recovery rates of “70% to 80% in comparison with 20% to 40% for placebo.” The NIMH vowed to continue DART indefinitely in order to “inform” the public of these “facts.”27
The NIMH officially launched DART in May 1988, five months after Prozac landed on pharmacy shelves. The NIMH enlisted “labor, religious, educational groups” and businesses to help it spread its message, and of course pharmaceutical companies and NAMI had been on board from the start. The NIMH ran advertisements in the media, and Eli Lilly helped pay for the printing and distribution of 8 million DART brochures titled “Depression: What You Need to Know.” This pamphlet informed readers, among other things, of the particular merits of “serotonergic” drugs for the disease. “By making these materials on depressive illness available, accessible in physicians’ offices all over the country, important information is effectively reaching the public in settings which encourage questions, discussion, treatment, or referral,” said NIMH director Lewis Judd.28
The remaking of the American mind was under way. This selling of depression, which was being done under the guise of a “public education” campaign, turned into one of the most effective marketing efforts ever devised. Newspapers picked up on this story, sales of Prozac began to soar, and then, on December 18, 1989, the green-and-white pill officially gained celebrity status when New York magazine put it on its cover. BYE, BYE BLUES, the headline screamed. A NEW WONDER DRUG FOR DEPRESSION. In the article, one “anonymous” user of Prozac said that on a scale of 1 to 100, he now felt “over 100.” Thanks to this new miracle pill, the magazine concluded, psychiatrists felt that their “profession has been buoyed.”29
Other such glowing stories quickly followed. On March 26, 1990, Newsweek’s cover featured the green-and-white capsule floating Nirvana-like over a beautiful landscape. PROZAC: A BREAKTHROUGH DRUG FOR DEPRESSION the magazine announced. Physicians were now writing 650,000 prescriptions for the pill each month, and “nearly everyone has something nice to say about the new treatment,” Newsweek said. Patients were loudly exclaiming, “I never felt better!”30 Three days later, Natalie Angier of the New York Times, who arguably was the nation’s most popular science writer, explained that antidepressants “work by restoring the balance of neurotransmitter activity in the brain, correcting an abnormal excess or inhibition of the electrochemical signals that control mood, thoughts, appetite, pain and other sensations.” This new drug, Dr. Francis Mondimore told Angier, “is not like alcohol or Valium. It’s like antibiotics.”31 Television shows weighed in with a similar message, and on 60 Minutes, Lesley Stahl told the inspiring story of a woman, Maria Romero, who, after a decade of horrible depression, had been reborn on Prozac. “Somebody, something left my body and another person came in,” Romero said. Stahl happily explained the biological cure that was at work: “Most doctors believe that chronic depression like Romero’s is caused by a chemical imbalance in the brain. To correct it, the doctor prescribed Prozac.”32
Scientology to the Rescue
Fairly early on, there was a moment when this wonder-drug story threatened to fall apart. The problem, of course, was that fluoxetine did in fact stir suicidal and violent thoughts in some people, and during the summer of 1990, the issue of Prozac’s safety burst into the news. And it was then, at that critical moment, that Scientology proved so useful to Eli Lilly and the psychiatric establishment.
By 1990, so many people had suffered bad reactions to fluoxetine that a national Prozac Survivors Support Group had formed. Many harmed by the drug had taken their complaints to lawyers, and two lawsuits in particular grabbed the public’s attention. First, on July 18, newspapers reported that a Long Island woman, Rhoda Hala, was suing Eli Lilly because, after going on Prozac, she had slashed her wrists and “other parts of her body hundreds of times.”33 Two weeks later, newspapers reported on a lawsuit related to a mass murder committed by a crazed Kentucky man. Five weeks after starting the drug, Joseph Wesbecker walked into a Louisville printing plant where he had worked and opened fire with an AK-47 assault rifle, killing eight and wounding twelve. The Citizens Commission on Human Rights quickly issued a press release urging Congress to ban this “killer drug,” and that’s when Eli Lilly pounced. These lawsuits, Eli Lilly loudly announced, “are being drummed up by the Scientology group, which has a history of criticizing the use of psychiatric drugs.”34
This was the start of Eli Lilly’s campaign to save its blockbuster drug. “Lilly can go down the tubes if we lose Prozac,” wrote chief medical officer Leigh Thompson, in a harried 1990 memo.35 The company quickly honed a four-point message for the media: This was an issue being raised by Scientologists; extensive clinical trials had shown that Prozac was a safe drug; the suicidal and homicidal events were “in the disease, not the drug;” and “people who could be helped are being scared away from treatment, and that’s the real public menace.”36 The company ran media-training sessions for the academic psychiatrists it hired as consultants, getting them to practice their delivery of this message. “Frankly, I was unimpressed with the performance of our outside professionals,” company vice-president Mitch Daniels complained to Thompson after one such practice session in April 1991. The company would “mandate” that the academic psychiatrists perform better “in their future training sessions,” he said.37
An article that appeared in the Wall Street Journal on April 19, 1991, showed that Eli Lilly’s training sessions had paid off. “Scientology,” the paper informed its readers, was a “quasi-religious/business/paramilitary organization” that was “waging war on psychiatry.” The group had attacked Prozac’s safety even though “doctors unaffiliated with Lilly” had found, during the clinical trials, that there was “a lower tendency toward suicidal thinking with Prozac than with other antidepressants, or with the starch capsules given to a control group.” It was, Leigh Thompson said, a “demoralizing revelation to watch twenty years of solid research by doctors and scientists shouted down in twenty-second sound bites by Scientologists and lawyers.” Indeed, the Wall Street Journal reported, Eli Lilly, in response to concerns about Prozac’s safety, had asked “suicide experts” to re-scrutinize the trial data, but they had “concluded that nothing in the clinical trials linked suicidal thinking—common in depression patients—to Prozac.” It was the disease, not the drug, and that was the tragedy, explained Jerrold Rosenbaum, a Harvard psychiatrist at Massachusetts General Hospital. “The public’s fear of Prozac as a result of this campaign has itself become a potentially serious public-health problem as people stay away from treatment.”38
Rosenbaum, naturally, was one of Eli Lilly’s “outside professionals.” As the Boston Globe later reported, he “sat on a marketing advisory panel for Lilly before Prozac was launched,” his relationship to Eli Lilly a “cozy” one.39 But the Wall Street Journalpresented him as an independent expert, one of the nation’s top depression doctors, and so readers could only draw one conclusion: This was an issue conjured up by noxious Scientologists, rather than a legitimate concern. Other newspapers and magazines framed the issue in that way, with Time, in May of that year, publishing a scathing cover story on Scientology, calling it a “criminal organization” that attracted “psychopaths.”40
On September 20, 1991, the FDA did convene a hearing on whether Prozac elevated the risk of suicide, but the advisory panel, which was dominated by physicians with ties to pharmaceutical companies, showed little interest in seriously investigating this question. Although more than two dozen citizens testified on the harm that the drug could cause, the panel made sure that the scientific discussion was limited to presentations that supported Eli Lilly’s position that fluoxetine was perfectly safe. As the Wall Street Journal reported, the scientific data presented at the hearing proved that “fluoxetine doesn’t lead to increased suicide or suicidal thinking, and, in fact, show that the drug helps alleviate these conditions.” The entire controversy, one Lilly supporter told the Journal, was a “complete fiction” that had been “organized and funded by an anti-psychiatric group.”41
At that moment, Eli Lilly and all of psychiatry had achieved a public relations victory of lasting importance. The wonder-drug aura around Prozac had been restored, and the public and the media had been conditioned to associate criticism of psychiatric drugs with Scientology. The debate over the merits of these drugs now seemed to feature the nation’s top scientists and doctors on one side and religious kooks on the other, and if that were so, the public could be certain where the truth lay. Other SSRIs came to market, sales of Prozac hit the $1 billion mark in 1992, and then, in 1993, Brown University psychiatrist Peter Kramer, in his book Listening to Prozac, pushed the wonder-drug story up a notch. Prozac, he wrote, was making some patients “better than well.” An era of “cosmetic psychopharmacology” was dawning, Kramer suggested, with psychiatry likely to have pills in the near future that could give normal people whatever personality they wanted. His book spent twenty-one weeks on the New York Times bestseller list, and soon Newsweek was warning readers that it was time for society to start grappling with the ethical questions raised by psychiatry’s new powers. “The same scientific insights into the brain that led to the development of Prozac are raising the prospect of nothing less than made-to-order, off-the-shelf personalities,” Newsweek explained in 1994. Will those who refuse to “give their brain a makeover,” the magazine asked, be left behind?
Gushed neuropsychiatrist Richard Restak: “For the first time in human history, we will be in a position to design our own brains.”42
As the Prozac story unfolded in the media, surely the ghost of John Brinkley was smiling somewhere. He had transfixed listeners to his radio show with tales of the wonders of transplanted goat gonads, and now here was a storytelling process that had transformed a drug “totally unsuited” for treating depression into a miracle compound, with psychiatrists publicly wringing their hands over their new godlike powers to shape the human mind. Should they worry about making people “better than well”? Would our society lose something precious if everybody were happy all the time? The widespread medicating of the American mind was now under way, and—as a very quick review will reveal—it was this same storytelling process that supported the launch of Xanax as a drug for panic disorder and the atypical antipsychotics for schizophrenia. Once those “second-generation” drugs became blockbusters, the drug companies and academic psychiatrists began touting psychiatric drugs of all kinds for use in children, this storytelling sweeping millions of American youth into the “mental illness” bin.
Xanax (alprazolam) was approved by the FDA as an anti-anxiety agent in 1981, and then Upjohn set out to get it approved for panic disorder, which had been newly identified as a discrete condition for the first time in DSM-III (1980). As a first step, it hired former NIMH director Gerald Klerman to co-chair its “steering committee” for the testing process, and it paid Daniel Freedman, editor of the Archives of General Psychiatry, to be an assistant to its “division of medical affairs.”43 This was just part of the company’s efforts to co-opt academic psychiatry: “The most senior psychiatrists in the world were flooded with offers of consultancies” from Upjohn, said Isaac Marks, an expert in anxiety disorders at the Institute of Psychiatry in London.44
Klerman and Upjohn designed Upjohn’s Cross National Collaborative Panic Study in a manner that could be expected to produce a poor placebo response. Patients who had been on benzodiazepines were allowed into the study, which meant that many in the placebo group would in fact be going through the horrors of benzodiazepine withdrawal, and thus could be expected to be extremely anxious during the first weeks of the trial. Nearly one-fourth of the placebo patients had traces of benzodiazepines in their blood when the treatment period began.45
Benzodiazepines are known to work quickly, and that proved true in this study. At the end of four weeks, 82 percent of the alprazolam patients were “moderately improved” or “better,” versus 43 percent of the placebo group. However, during the next four weeks, the placebo patients continued to improve, while the alprazolam patients did not, and by the end of the eighth week, there “was no significant difference between the groups” on most of the rating scales, at least among the patients who remained in the study. The alprazolam group also experienced a variety of troubling side effects: sedation, fatigue, slurred speech, amnesia, and poor coordination. One of every twenty-six alprazolam patients suffered a “serious” reaction to the drug, such as mania or aggressive behavior.46
At the end of eight weeks, the patients were tapered from their medication for four weeks and then followed while medication-free for another two weeks. The results were predictable. Thirty-nine percent of those withdrawn from alprazolam “deteriorated significantly,” their panic and anxiety skyrocketing to such an extent they had to start taking the medication again. Thirty-five percent of the alprazolam patients suffered “rebound” panic and anxiety symptoms more severe than when the study began, and an equal percentage suffered a host of debilitating new symptoms, including confusion, heightened sensory perceptions, depression, a feeling that insects were crawling over them, muscle cramps, blurred vision, diarrhea, decreased appetite, and weight loss.47
In sum, at the end of fourteen weeks, the drug-exposed patients were worse off than the placebo group: They were more phobic, more anxious, more panic stricken, and doing worse on a “global scale” that assessed overall well-being. Forty-four percent had been unable to get off the drug, on their way to a lifetime of addiction. In every way, the results painted a powerful portrait of the benzo trap: This was a drug that worked for a short time, then its efficacy over a placebo petered out, and yet when patients tried to go off the drug, they became quite sick and many couldn’t kick the habit. The first few weeks of relief came at a very high long-term cost, with those stuck on the drug—as previous benzodiazepine studies had shown—likely to end up physically, emotionally, and cognitively impaired.
The Xanax Study
In Upjohn’s study of Xanax, patients were treated with the drug or placebo for eight weeks. Then this treatment was slowly withdrawn (weeks 9 through 12), and during the last two weeks patients didn’t receive any treatment. The Xanax patients fared better during the first four weeks, which is the result that the Upjohn investigators focused on in their journal articles. However, once the Xanax patients began withdrawing from the the drug, they suffered many more panic attacks than the placebo patients, and at the end of the study were much more symptomatic. Source: Ballenger, C “Alprazolam in panic disorder and agoraphobia.” Archives of General Psychiatry 45 (1988): 413–22. Pecknold, C “Alprazolam in panic disorder and agoraphobia.” Archives of General Psychiatry 45 (1988): 429–36.
The Upjohn investigators published three articles in the Archives of General Psychiatry in May 1988, and anyone who carefully reviewed the data could see the harm caused by alprazolam. But in order for Xanax to be successfully marketed, Upjohn needed its investigators to draw a different sort of conclusion, and so they did, particularly in the abstracts of the three articles. First, they focused their attention on the four-week results (rather than the eight-week outcomes at the end of the treatment period), announcing that “alprazolam was found to be effective and well-tolerated.”48 Next, they noted that 84 percent of the alprazolam patients had finished the eight-week study, which was evidence that “patient acceptance of alprazolam was high.” Although their alprazolam patients regularly exhibited such problems as “slurred speech, amnesia” and other signs of “impaired mentation,” they still concluded that the drug had “few side effects and is well tolerated.”49 Finally, while they acknowledged that some alprazolam patients fared poorly when the drug was withdrawn, they reasoned that it had been used for too short a period and the withdrawal done too abruptly. “We recommend that patients with panic disorder be treated for a longer period, at least six months,” they said.50
In London, Isaac Marks and several of his colleagues at the Institute of Psychiatry subsequently pointed out how transparently ridiculous this all was. In a letter to the Archives of General Psychiatry, they observed that since the alprazolam patients “were in a worse state than patients receiving placebo” at the end of the study, the finding by the Upjohn investigators that the drug was effective and well tolerated could only be seen as “biased and arguable.”51 The entire affair, Marks subsequently wrote, “is a classic demonstration of the hazards of research funded by industry.”52
Yet the fact that the alprazolam patients came to such a bad end, with many on a path to a lifelong addiction, did not deter Upjohn, Klerman, the APA, and the NIMH from touting Xanax’s benefits to the American public. The same marketing machinery that had made Prozac a bestseller was rolled out again. Upjohn sponsored a symposium at the APA’s 1988 meeting where the “expert panel” highlighted the four-week results. Robert Pasnau, who had been head of the APA in 1987, sent a glossy booklet on the Consequences of Anxiety to APA members, an “educational” effort paid for by Upjohn. Both Shervert Frazier and Gerald Klerman penned a “Dear Doctor” letter that Upjohn included in the promotional literature it sent to doctors about Xanax as a treatment for panic disorder. Upjohn also gave $1.5 million to the APA so that it could mount a DART-like campaign to “educate” psychiatrists, health-care workers, and the public about panic disorder, which was said to be “under-recognized and undertreated.”53 Finally, the NIMH chipped in too, identifying panic disorder as a priority concern and sponsoring a conference in 1991 on it, with its panel of experts designating “high potency benzodiazepines”—this would be Xanax—as one of the two “treatments of choice.”54
The FDA approved Xanax as a treatment for panic disorder in November 1990, and many newspapers and magazines ran the usual features. IN A PANIC? HELP IS ON THE WAY, a St. Louis Post-Dispatch headline announced. Treatment, the paper said, helped 70 to 90 percent of those with the debilitating condition, which afflicted “4 million adults in this country.”55 The Associated Press explained that “a biochemical malfunctioning in the brain is believed to be one of the causes of panic attacks. Xanax can block the attacks by interacting with several different systems in the brain.”56 In the Chicago Sun-Times, Dr. John Zajecka at Rush Medical College in Chicago announced that “Xanax is the fastest acting and least toxic” of medications for the disorder.57 Once again, a very effective, safe drug had arrived on the market, and in 1992, Xanax became the fifth most frequently prescribed medication in the United States.58
Not so atypical
Even as Xanax was on the way to market as a treatment for panic disorder, Janssen was conducting tests of risperidone, a new drug for schizophrenia. By this time, the methods that pharmaceutical firms were employing to create new “blockbuster” psychotropics were becoming quite well practiced, with nearly everyone employing the Prozac model of drug development, and so Janssen, like Eli Lilly and Upjohn, designed trials that were biased in favor of its drug. In particular, Janssen compared multiple doses of risperidone to a high dose of haloperidol (Haldol), as it could then be relatively certain that one of the risperidone doses would have a good safety profile in comparison to the old “standard” neuroleptic. As FDA reviewers noted, these studies were “incapable” of providing any meaningful comparison of the two drugs.59 In the FDA’s letter of approval to Janssen, Robert Temple, director of the Office of Drug Evaluation, made this clear:
We would consider any advertisement or promotion labeling for RISPERDAL false, misleading, or lacking fair balance under section 502 (a) and 502 (n) of the ACT if there is presentation of data that conveys the impression that risperidone is superior to haloperidol or any other marketed antipsychotic drug product with regard to safety or effectiveness.60
However, while the FDA could prohibit Janssen from placing advertisements touting its drug as superior to haloperidol, it did not have authority over what the academic psychiatrists hired by Janssen could say. This was the commercial beauty of the “partnership” that had emerged between psychiatry and the pharmaceutical industry during the 1980s—the academic doctors could make claims, both in their medical journals and to the public, that the FDA considered false in kind. In this case, they published more than twenty articles in psychiatric journals touting risperidone as equal or superior to haloperidol in reducing positive symptoms of schizophrenia (psychosis) and superior to haloperidol in improving negative symptoms (lack of emotion). The academic doctors reported that risperidone reduced hospital stays, improved the patient’s ability to function socially, and reduced hostility. “Risperidone has important advantages compared with haloperidol,” they wrote in the Journal of Clinical Psychiatry. “When administered in an effective dose range, risperidone produced greater improvements on all five dimensions of schizophrenia.”61
Once again, this was a scientific story of a new and improved treatment, and in their interviews with the media, Janssen’s investigators told of a wonder drug. This new agent, the Washington Post reported, “represents a glimmer of hope for a disease that until recently had been considered hopeless.” Risperidone, it explained, did not “cause sedation, blurred vision, impaired memory or muscle stiffness, side effects commonly associated with an earlier generation of antipsychotic drugs.”62 The New York Times, quoting Richard Meibach, Janssen’s clinical research director, reported that “no major side effects” had appeared in the two-thousand-plus patients treated with risperidone in the clinical trials.* The drug was thought to “relieve schizophrenia symptoms by blocking excessive flows of serotonin or dopamine, or both,” the paper said.63
The atypical revolution was on. Risperdal apparently restored sanity by balancing multiple neurotransmitters in the brain, and it seemed to cause no side effects of any note. In 1996, Eli Lilly brought Zyprexa (olanzapine) to market, and the public story of the wonders of atypicals got ramped up another notch.
As had become customary, Eli Lilly employed trials that were “biased by design” against haloperidol, the FDA concluded. As a result, its large phase III trial, which wasn’t placebo controlled, provided “little useful efficacy data.” As for olanzapine’s safety profile, twenty patients treated with the drug during the trials died, 22 percent suffered a “serious” adverse event (higher than in the haloperidol patients), and two-thirds failed to complete the studies. Olanzapine, the data suggested, made patients sleepy and fat, and caused such problems as Parkinsonian symptoms, akathisia, dystonia, hypotension, constipation, tachycardia, diabetes, seizures, leaking breasts, impotence, liver abnormalities, and white blood cell disorders. Furthermore, warned the FDA’s Paul Leber, since olanzapine blocked receptors for many types of neurotransmitters, “no one should be surprised if, upon marketing, events of all kinds and severity not previously identified are reported in association with olanzapine’s use.”64
That was the story told by the trial data. The story that Eli Lilly wanted to appear in the medical journals and newspapers was that Zyprexa was better than Janssen’s Risperdal, and so that’s the story that its hired guns told. Psychiatrists from academic medical schools announced that olanzapine worked in a more “comprehensive” manner than either risperidone or haloperidol. It was a well-tolerated agent that led to global improvement—it reduced positive symptoms, caused fewer motor side effects than other antipsychotics, and improved negative symptoms and cognitive function.65 This second atypical was better than the first, and the Wall Street Journal ran with that angle. Zyprexa, it announced, “has substantial advantages” over other current therapies. “The real world,” explained John Zajecka, from Rush Medical College, “is finding that Zyprexa has fewer extrapyramidal side effects than Risperdal.”66 Zyprexa is “a potential breakthrough of tremendous magnitude,” Stanford University psychiatrist Alan Schatzberg told the New York Times.67
The only question now seemed to be whether Zyprexa was truly better than Risperdal, and after AstraZeneca brought a third atypical to market, Seroquel, the media settled on the notion that collectively the new atypicals were a dramatic improvement over the older drugs. They were, Parade told its readers, “far safer and more effective in treating negative symptoms, such as difficulty in reasoning and speaking in an organized way.”68 The newer drugs, the Chicago Tribune announced, “are safer and more effective than older ones. They help people go to work.”69 Wrote the Los Angeles Times, “It used to be that schizophrenics were given no hope of improving. But now, thanks to new drugs and commitment, they’re moving back into society like never before.”70 NAMI chimed in, too, publishing a book titled Breakthroughs in Antipsychotic Medications, which helpfully explained that these new drugs “do a better job of balancing all of the brain chemicals, including dopamine and serotonin.”71 On and on it went, and finally NAMI’s executive director, Laurie Flynn, told the press that the promised land had at last been reached: “These new drugs truly are a breakthrough. They mean we should finally be able to keep people out of the hospital, and it means that the long-term disability of schizophrenia can come to an end.”72
Lancet Asks a Question
That was the sequence of storytelling that led to the explosive rise in the use of psychiatric drugs in the United States. First, American psychiatrists touted Prozac as a wonder drug, next they hailed Xanax as a safe and effective therapy for panic disorder, and finally they informed the public that atypical antipsychotics were “breakthrough” medications for schizophrenia. In this way, they rejuvenated the market for psychiatric medications, even though the clinical studies of the new drugs had not told of any therapeutic advance.
At least in scientific circles, the “wonder drug” glow around the second-generation psychotropics has long since disappeared. As we learned earlier, the SSRIs were reported in 2008 to provide a meaningful clinical benefit only to severely depressed patients. Xanax is now understood to be much more addictive than Valium, with various investigators determining that two-thirds of people who take it for any length of time have trouble getting off it.73 As for the top-selling atypicals, the hyping of these drugs is now viewed as one of the more embarrassing episodes in psychiatry’s history, as one government-funded study after another failed to find that they were any better than the first-generation antipsychotics. In 2005, the NIMH’s “CATIE Trial” determined that there were “no significant differences” between the atypicals and their predecessors, and even more troubling, in this study neither the new drugs nor the old ones could really be said to work. Seventy-four percent of the 1,432 patients were unable to stay on the medications, mostly because of their “inefficacy or intolerable side effects.”74 A study by the U.S. Department of Veterans Affairs came to a similar conclusion about the relative merits of atypicals and the older drugs, and then, in 2007, British psychiatrists reported that schizophrenia patients, if anything, had a better “quality of life” on the old drugs than on the new ones.75 All of this led two prominent psychiatrists to write in the Lancet that the story of the atypicals as breakthrough medications could now be “regarded as invention only,” a tale concocted “by the drug industry for marketing purposes and only now being exposed.” Yet, they wondered, “how is it that for nearly two decades we have, as some have put it, ‘been beguiled’ into thinking they were superior?”76
History, as readers of this book can attest, reveals the answer to that question. The seed for the atypicals story was planted in the early 1980s, when the APA embraced “biological psychiatry” as a story that could be successfully marketed to the public. This was also a story that the field, as a whole, desperately wanted to believe in, and soon Nancy Andreasen and others were telling of a revolution that was under way, with mental illnesses finally giving up their biological secrets, even though nobody could precisely explain what those secrets were. That story gained steam, prepping the public to believe that therapeutic advances were on the way, and as pharmaceutical companies brought new medications to market, they hired the top psychiatrists in the country to tell of how these new wondrous drugs “balanced” brain chemistry. And it was that co-opting of academic medicine that gave the story its credibility. This was a story told by Harvard Medical School psychiatrist Jerrold Rosenbaum, by former NIMH director Gerald Klerman, and by Stanford University psychiatrist Alan Schatzberg.
Of course we, as a society, believed it.
As we have seen, American psychiatry has told the public a false story over the past thirty years. The field promoted the idea that its drugs fix chemical imbalances in the brain when they do no such thing, and it grossly exaggerated the merits of the second-generation psycho tropics. In order to keep that tale of scientific progress afloat (and to protect its own belief in that tale), it has needed to squelch talk about the harm that the drugs can cause.
Psychiatry’s policing of its own ranks began in earnest in the late 1970s, when Loren Mosher was ousted from the NIMH for having run his Soteria experiment. The next prominent psychiatrist to end up on psychiatry’s hit list was Peter Breggin. Although he is known today for his “antipsychiatry” writings, he, too, had once been on the fast track at the NIMH. After finishing his residency at a Harvard Medical School hospital, Breggin went to the NIMH in 1966 to work on developing community mental health centers. “I was still the young hotshot guy,” he recalled, in an interview. “I thought I would be the youngest professor of psychiatry in the history of Harvard Medical School. That was the trajectory I was on.”77 However, he saw that the future belonged to biological psychiatry, as opposed to the social psychiatry that interested him, and he left the NIMH to go into private practice. Soon he began writing about the hazards of electroshock and psychiatric drugs, which, he argued, “worked” by disabling the brain. After a number of heated battles with the APA’s leaders, Breggin appeared in 1987 on Oprah Winfrey’s television show, where he spoke about tardive dyskinesia and how that dysfunction was evidence that neuroleptics damaged the brain. His comments so infuriated the APA that it sent a transcript of the show to NAMI, which in turn filed a complaint with the Maryland State Commission on Medical Discipline, asking that it take away Breggin’s medical license on the grounds that his statements had caused schizophrenia patients to stop taking their medications (and thus caused harm). Although the commission decided not to take any action, it did conduct an inquiry (rather than summarily dismissing NAMI’s complaint), and the message to everyone in the field was, once again, quite clear.
“I think the interesting thing is that Loren [Mosher] and I took on scientifically the two sides of the issue,” Breggin said. “Loren took on the issue that there is a better treatment than drugs for schizophrenia. I took on the treatments—the drugs, electroshock, and psychosurgery. And what this showed is that it didn’t matter which end you wanted to take, they were willing to destroy your career. That is the lesson.”
The career setback that Irish psychiatrist David Healy experienced was, in some ways, reminiscent of Mosher’s fall from grace. During the 1990s, he earned a reputation as one of the field’s leading historians, his writings focusing on the psychopharmacology era. He had served as secretary of the British Association for Psychopharmacology, and in early 2000, he accepted an offer from the University of Toronto’s Centre for Addiction and Mental Health to head up its mood and anxiety program. Up until that moment, he was very much part of the psychiatric establishment, just as Mosher had been. However, for several years he had been interested in the question of whether SSRIs could stir suicide, and he had recently completed a “healthy volunteers” study. Two of the twenty volunteers had become suicidal after they were exposed to an SSRI, which clearly showed that the drug could cause such thoughts. Not long after he accepted the Toronto job, he presented his results at a meeting of the British Association for Psychopharmacology. There, one of the most prominent figures in American psychiatry warned him to knock it off. “He told me that my career would be destroyed if I kept on showing results like the ones I’d just shown, that I had no right to bring out hazards of the pills like these,” Healy said.78
In November of 2000, only a few months before he was scheduled to start his new job at the University of Toronto, Healy gave a talk on the history of psychopharmacology at a colloquium organized by the school. In his presentation, Healy spoke about problems that had arisen with neuroleptics since their introduction in the 1950s, briefly reviewed the data showing that Prozac and other SSRIs elevated the risk of suicide, and then observed in passing that outcomes for affective disorders are worse today than they were a century ago. This, he observed, shouldn’t be happening if “our drugs really worked.”79
Although the audience subsequently rated his talk as the colloquium’s best for content, by the time Healy arrived back in Wales, the University of Toronto had rescinded the job offer. “While you are held in high regard as a scholar of the history of modern psychiatry, we do not feel your approach is compatible with the goals for development of the academic and clinical resources that we have,” wrote the Centre’s head psychiatrist, David Goldbloom, in an e-mail.80 Once more, others in the field could draw only one lesson. “The message is that it is a bad idea to speak out, and that the idea that treatments might not work or might not be best managed by being entrusted to doctors is beyond the pale,” Healy said in an interview.81
Numerous others can attest to the fact that it is a “bad idea” to speak out. Nadine Lambert, a psychologist at the University of California at Berkeley, conducted a long-term study of children treated with Ritalin and found that, as young adults, they had elevated rates of cocaine abuse and cigarette smoking. After she reported her results at a 1998 NIH conference, the National Institute on Drug Abuse stopped funding her work. In 2000, when Joseph Glenmullen, a clinical instructor in psychiatry at Harvard Medical School, authored Prozac Backlash, which detailed the many problems associated with the use of SSRIs, Eli Lilly mounted a campaign to discredit him. A public-relations firm gathered critical comments from several prominent psychiatrists, who derided Glenmullen as a “nobody” in the field, and then it mailed these “reviews” to various newspapers. “It’s a dishonest book, it’s manipulative, it’s mischievous,” said Harvard Medical School psychiatrist Jerrold Rosenbaum, even though he was a colleague of Glenmullen’s. The press release naturally did not mention that Rosenbaum was an Eli Lilly consultant.82 Next up on the chopping block: Gretchen LeFever, a psychologist at East Virginia Medical School. After she published research showing that an overly high number of children in Virginia schools were being diagnosed with ADHD, an anonymous “whistle-blower” charged her with scientific misconduct. Her federal research funds were cut off and her computers were seized, and while she was subsequently cleared of any misconduct, her career had still been derailed.
Said Healy: “The thought-control aspect of things in psychiatry today is like old-style Eastern European social control.”
Hiding the Evidence
The third aspect to the storytelling process that has led to our societal delusion about the merits of psychiatric drugs is easy to document. Imagine what our beliefs would be today if, over the past twenty years, we had opened our newspapers and read about the following findings, which represent but a sampling of the outcome studies we reviewed earlier in the book:
1990: In a large, national depression study, the eighteen-month stay-well rate was highest for those treated with psychotherapy (30 percent) and lowest for those treated with an antidepressant (19 percent). (NIMH)
1992: Schizophrenia outcomes are much better in poor countries like India and Nigeria, where only 16 percent of patients are regularly maintained on antipsychotics, than in the United States and other rich countries, where continual drug usage is the standard of care. (World Health Organization)
1995: In a six-year study of 547 depressed patients, those who were treated for the disorder were nearly seven times more likely to become incapacitated than those who weren’t, and three times more likely to suffer a “cessation” of their “principal social role.” (NIMH)
1998: Antipsychotic drugs cause morphological changes in the brain that are associated with a worsening of schizophrenia symptoms. (University of Pennsylvania)
1998: In a World Health Organization study of the merits of screening for depression, those diagnosed and treated with psychiatric medications fared worse—in terms of their depressive symptoms and their general health—over a one-year period than those who weren’t exposed to the drugs. (WHO)
1999: When long-term benzodiazepine users withdraw from the drugs, they become “more alert, more relaxed, and less anxious.” (University of Pennsylvania)
2000: Epidemiological studies show that long-term outcomes for bipolar patients today are dramatically worse than they were in the pre-drug era, with this deterioration in modern outcomes likely due to the harmful effects of antidepressants and antipsychotics. (Eli Lilly; Harvard Medical School)
2001: In a study of 1,281 Canadians who went on short-term disability for depression, 19 percent of those who took an antidepressant ended up on long-term disability, versus 9 percent of those who didn’t take the medication. (Canadian investigators)
2001: In the pre-drug era, bipolar patients did not suffer cognitive decline over the long term, but today they end up almost as cognitively impaired as schizophrenia patients. (Sheppard Pratt Health System in Baltimore)
2004: Long-term benzodiazepine users suffer cognitive deficits “moderate to large” in magnitude. (Australian scientists)
2005: Angel dust, amphetamines, and other drugs that induce psychosis all increase D2 HIGH receptors in the brain; antipsychotics cause this same change in the brain. (University of Toronto)
2005: In a five-year study of 9,508 depressed patients, those who took an antidepressant were, on average, symptomatic nineteen weeks a year, versus eleven weeks for those who didn’t take any medication. (University of Calgary)
2007: In a fifteen-year study, 40 percent of schizophrenia patients off antipsychotics recovered, versus 5 percent of the medicated patients. (University of Illinois)
2007: Long-term users of benzodiazepines end up “markedly ill to extremely ill” and regularly suffer from symptoms of depression and anxiety. (French scientists)
2007: In a large study of children diagnosed with ADHD, by the end of the third year “medication use was a significant marker not of beneficial outcome, but of deterioration.” The medicated children were also more likely to engage in delinquent behavior; they ended up slightly shorter, too. (NIMH)
2008: In a national study of bipolar patients, the major predictor of a poor outcome was exposure to an antidepressant. Those who took an antidepressant were nearly four times as likely to become rapid cyclers, which is associated with poor long-term outcome. (NIMH)
A check of newspaper archives reveals that the psychiatric establishment has thoroughly succeeded in keeping this information from the public. I searched for accounts of these studies in the New York Times archives and in the LexisNexis database, which covers most U.S. newspapers, and I couldn’t find a single instance where the results were accurately reported.*
Newspapers, of course, would have been happy to publish these study results. However, medical news is typically generated in this way: The scientific journals, the NIH, medical schools, and pharmaceutical companies issue press releases touting certain findings as important, and reporters then sift through the releases to identify the ones they deem worthy of writing about. If no press releases are issued, or there is no other effort by the medical community to publicize the findings, then no stories appear. We can even document this blackout process at work in the NIMH’s handling of Martin Harrow’s outcomes study. In 2007, the year he published his results in the Journal of Nervous and Mental Disease, the NIMH issued eighty-nine press releases, many on inconsequential matters. But it did not issue one on Harrow’s findings, even though his was arguably the best study of the long-term outcomes of schizophrenia patients that had ever been done in the United States.83 It’s fair to say that if the results had been the reverse, the NIMH would have sounded the press-release gong and newspapers across the country would have touted the findings.
Although reports about most of the studies listed above simply never appeared in newspapers, there were a couple of instances when psychiatrists were forced to say something to reporters about one of the studies, and each time they spun the results. For example, when the NIMH announced the three-year results from its MTA study of ADHD treatments, it did not inform the public that stimulant usage during the third year was a “marker of deterioration.” Instead, it put out a press release with this headline: IMPROVEMENT FOLLOWING ADHD TREATMENT SUSTAINED FOR MOST CHILDREN. That headline told of drugs that had been beneficial, and while the text of the release did state that “continuing medication was no longer associated with better outcomes by the third year,” it also included a canned quote from lead author Peter Jensen stating that there was still plenty of reason to keep children on Ritalin. “Our results suggest that medication can make a long-term difference for some children if it’s continued with optimal intensity, and not started or added too late in a child’s clinical course.”84
If we want to get another look at this spinning process, we can turn to a 1998 New York Times article that briefly told of the WHO study on schizophrenia outcomes in rich and poor countries. After interviewing psychiatrists about the study, the Times reporter wrote that “schizophrenics generally responded better to treatment in less developed countries than in more technologically developed countries.”85 Responded better to treatment—readers could only assume that schizophrenia patients in India and Nigeria responded better to antipsychotics than patients in the United States and other rich countries did. They had no way to know that “treatment” for 84 percent of the schizophrenia patients in the poor countries consisted of being off the drugs.
In July 2009, I also searched the NIMH and NAMI websites for some mention of the studies listed above, and I found zilch. For instance, the NIMH website did not discuss the remarkable decline in bipolar outcomes in modern times, even though Carlos Zarate, who coauthored the 2000 article that documented this decline, was head of the NIMH’s mood and anxiety disorders research unit in 2009. Similarly, NAMI’s website didn’t provide any information about Harrow’s study, even though it provides reason for parents of schizophrenic children to be optimistic. Forty percent of those off medications recovered over the long term! But that finding directly contradicted the message that NAMI has promoted to the public for decades, and NAMI’s website is sticking to that message. Antipsychotics, it informs the public, “correct an imbalance in the chemicals that enable brain cells to communicate with each other.”86
Finally, the entire outcomes history documented in this book is missing from the 2008 edition of the APA’s Textbook of Psychiatry, which means that medical students training to be psychiatrists are kept in the dark about this history.87 The book does not discuss “supersensitivity psychosis.” It does not mention that antidepressants may be depressogenic agents over the long term. It does not report that bipolar outcomes are much worse today than they were forty years ago. There is no discussion of rising disability rates. There is no talk about the cognitive impairment that is seen in longtime users of psychotropic drugs. The textbook authors are clearly familiar with many of the sixteen studies listed above, but, if they do mention them, they don’t discuss the relevant facts about medication usage. The long-running study by Harrow, the textbook states, reveals that there are some schizophrenia patients who “are able to function without the benefit of continuous antipsychotic treatment.” The authors of that sentence didn’t mention the stunning difference in recovery rates for the unmedicated and medicated groups; instead they crafted a sentence that told of the benefit of continuous antipsychotic treatment. In a similar vein, while the textbook briefly discusses the WHO study on the better outcomes of schizophrenia patients in poor countries like India and Nigeria, it does not mention that patients in those countries weren’t regularly maintained on antipsychotics. In a section on benzodiazepines, the authors acknowledge that there are concerns about their addictive properties, but then state that long-term outcomes for those who stay on benzodiazepines are generally good, as most patients “maintain their therapeutic gains.”
There is a story that psychiatry doesn’t dare tell, which shows that our societal delusion about the benefits of psychiatric drugs isn’t entirely an innocent one. In order to sell our society on the soundness of this form of care, psychiatry has had to grossly exaggerate the value of its new drugs, silence critics, and keep the story of poor long-term outcomes hidden. That is a willful, conscious process, and the very fact that psychiatry has had to employ such storytelling methods reveals a great deal about the merits of this paradigm of care, much more than a single study ever could.
* At the end of 1989, Eli Lilly obtained approval to market fluoxetine in Germany, but with a label that warned of the elevated risk of suicide.
* In fact, eighty-four patients treated with risperidone had suffered a “serious adverse event,” which the FDA defined as a life-threatening event or one that required hospitalization.
* There were newspaper reviews of my book Mad in America that mentioned the WHO study of better schizophrenia outcomes in poor countries where patients were not regularly maintained on the drugs, and since then, this information has become somewhat known. In addition, I mentioned Martin Harrow’s fifteen-year schizophrenia study in a talk I gave at Holy Cross College in February 2009, and that led to a February 8, 2009, article in the Worcester Telegram and Gazette (Mass.) that discussed Harrow’s work. That was the first time that news of his study had appeared in any American newspaper.