Anatomy Of An Epidemic Quotes

In the United States, people with depression, bipolar, and schizophrenia are losing twelve to twenty years in life expectancy compared to people not in the mental health system.

With psychiatric medications, you solve one problem for a period of time, but the next thing you know you end up with two problems. The treatment turns a period of crisis into a chronic mental illness. - Amy Upham

If you expand the boundaries of mental illness, which is clealry what has happened in this country during the past twenty-five years, and you treat the people so diagnosed with psychiatric medications, do you run the risk of turning an anger-ridden teenager into a lifelong mental patient?

Rather than fix chemical imbalances in the brain, the drugs creat them.

Prior to being medicated, a depressed person has no known chemical imbalance.

...all I could think about was how both sets of parents had needed to make their decision, on whether to medicate their child, in a scientific vacuum. (p. 35)

Recovery on the med model requires you to be obedient, like a child," she explains. "You are obedient to your doctors, you are compliant with your therapist, and you take your meds. There's no striving toward greater intellectual concerns.

The “cure,” it seemed, had once again been proven to be “worse than the disease.

And what science had revealed was this: Prior to treatment, patients diagnosed with schizophrenia, depression, and other psychiatric disorders do not suffer from any known "chemical imbalance". However, once a person is put on a psychiatric medication, which, in one manner or another, throws a wrench into the usual mechanics of a neuronal pathway, his or her brain begins to function, as Hyman observed, abnormally.

Psychosis does not live in the head. It lives in the in-between of family members, and in the in-between of people," Salo explained. "It is in the relationship, and the one who is psychotic makes the bad condition visible. He or she 'wears the symptoms' and has the burden to carry them.

That experience allowed me to see this therapeutic principle in action," Stanton said. "You just can't organize yourself without a connection to another human being, and you can't make that connection if you embalm yourself with drugs.

Klonopin ruined my lie. It takes away your drive, and in the morning, you don't want to get out of bed, because you feel so groggy. I don't even know what it's like to feel normal. This is my world. Things don't get me as excited as most people because I'm in a constant state of sedation. It should never have been prescribed for long-term use.

We have been focusing on the role that psychiatry and its medications may be playing in this epidemic, and the evidence is quite clear. First, by greatly expanding diagnostic boundaries, psychiatry is inviting and ever-greater number of children and adults into the mental illness camp. Second, those so diagnosed are then treated with psychiatric medications that increase the likelihood they will become chronically ill. Many treated with psychotropics end up with new and more severe psychiatric symptoms, physically unwell, and cognitively impaired. This is the tragic story writ large in five decades of scientific literature.

That is where we stand as a nation today. Twenty years ago, our society began regularly prescribing psychiatric drugs to children and adolescents, and now one out of every fifteen Americans enters adulthood with a "serious mental illness." That is proof of the most tragic sort that our drug-based paradigm of care is doing a great deal more harm than good. The medicating of children and youth became commonplace only a short time ago, and already it has put millions onto a path of lifelong illness.

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 penicillin trials or trials of drugs that really work. -David Healy

In 1967, one in three American adults filled a prescription for a “psychoactive” medication, with total sales of such drugs reaching $692 million.

The GAO, in its June 2008 report, concluded that one in every sixteen young adults in the United States is now “seriously mentally ill.

We must realize that mental problems are just as real as physical disease, and that anxiety and depression require active therapy as much as appendicitis or pneumonia,” wrote Dr. Howard Rusk, a professor at New York University who penned a weekly column for the New York Times. “They are all medical problems requiring medical care.”12

I have always been told that a person has to accept that the illness is chronic," she says, at the end of our interview. "You can be 'in recovery,' but you can never be 'recovered.' But I don't want to be on disability forever, and I have started to question whether depression is really a chemical thing. What are the origins of my despair? How can I really help myself? I want to honor the other parts of me, other than the sick part that I'm always thinking about. I think that depression is like a weed that I have been watering, and I want to pull up that weed, and I am starting to look to people for solutions. I really don't know what the drugs did for me all these years, but I do know that I am disappointed in how things have turned out." Such is Melissa Sances's story. Today it is a fairly common one. A distressed teenager is diagnosed with depression and put on an antidepressant, and years later he or she is still struggling with the condition. But if we return to the 1950s, we will discover that the depression rarely struck someone as young as Melissa, and it rarely turned into the chronic suffering that she has experienced. Her course of illness is, for the most part, unique to our times.

...and she no longer is having her emotional responses to...stress numbed by medication. "I've been off the drugs for two years, and sometimes I find it very, very difficult to deal with my emotions. I tend to have these rages of anger. Did the drugs bring such a cloud over my mind, make me so comatose, that I never gained skills on how to deal with my emotions? Now I'm finding myself getting angrier than ever and getting happier than ever too. The circle with my emotions is getting wider. And yes, it's easy to deal with when you're happy, but how do you deal with it when you're mad? I'm working on not getting overly defensive, and trying to take things in stride.

The three books were The Emperor’s New Drugs: Exploding the Antidepressant Myth by Irving Kirsch; Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America by Robert Whitaker; and Unhinged: The Trouble with Psychiatry—A Doctor’s Revelations About a Profession in Crisis by Daniel Carlat.

But none of these drugs had been developed after scientists had identified any disease process or brain abnormality that might have been causing these symptoms.

For the past twenty-five years, the psychiatric establishment has told us a false story. It told us that schizophrenia, depression, and bipolar illness are known to be brain diseases, even though—as the MindFreedom hunger strike revealed—it can’t direct us to any scientific studies that document this claim. It told us that psychiatric medications fix chemical imbalances in the brain, even though decades of research failed to find this to be so. It told us that Prozac and the other second-generation psychotropics were much better and safer than the first-generation drugs, even though the clinical studies had shown no such thing. Most important of all, the psychiatric establishment failed to tell us that the drugs worsen long-term outcomes.

Wallace Laboratories hired Salvador Dalí to help stoke Miltown fever, paying the great artist $35,000 to create an exhibit at an AMA convention that was meant to capture the magic of this new drug.

The cocktail she took usually included a mood stabilizer, an antidepressant, and a benzodiazepine for anxiety, although the exact combination was always changing. One drug would make her sleepy, another would give her tremors, and none of the cocktails seemed to bring her emotional tranquility. Then, in 2001, she was put on an anti-psychotic, Zyprexa, which, in a sense, worked like a charm. "You know what?" she says today, amazed by what she is about to confess. "I loved the stuff. I felt like I finally found the answer. Because what do you know. I have no emotions. It was great. I wasn't crying anymore.

The off-drug patients also suffered less from depression, blunted emotions, and retarded movements. Indeed, they told Carpenter and McGlashan that they had found it "gratifying and informative" to have gone through their psychotic episodes without having their feelings numbed by the drugs. Medicated patients didn't have that same learning experience, and as a result Carpenter and McGlashan concluded, over the long term they "are less able to cope with subsequent life stresses.

I do wonder what might have happened if [at age sixteen] I could have just talked to someone, and they could have helped me learn about what I could do on my own to be a healthy person. I never had a role model for that. They could have helped me with my eating problems, and my diet and exercise, and helped me learn how to take care of myself. Instead, it was you have this problem with your neurotransmitters, and so here, take this pill Zoloft, and when that didn’t work, it was take this pill Prozac, and when that didn’t work, it was take this pill Effexor, and then when I started having trouble sleeping, it was take this sleeping pill,” she says, her voice sounding more wistful than ever. “I am so tired of the pills.

Twenty-four percent of the patients treated with Saint-John’s-wort had a “full response,” 25 percent of the Zoloft patients, and 32 percent of the placebo group. “This study fails to support the efficacy of H perforatum in moderately severe depression,” the investigators concluded, glossing over the fact that their drug had failed this test too.29

Today, according to the NIMH, bipolar illness affects one in every forty adults in the United States, and so, before we review the outcomes literature for this disorder, we need to try to understand this astonishing increase in its prevalence.9 Although the quick-and-easy explanation is that psychiatry has greatly expanded the diagnostic boundaries, that is only part of the story. Psychotropic drugs—both legal and illegal—have helped fuel the bipolar boom.

The history of psychiatry and its treatments can be a contentious issue in our society, so much so that when you write about it, as I did in an earlier book, Mad in America, people regularly ask about how you became interested in the subject. The assumption is that you must have a personal reason for being curious about this topic, as otherwise you would want to stay away from what can be such a political minefield. In addition, the person asking the question is often trying to determine if you have any personal bias that colors your writing.

The number of episodes, and it’s a very rich literature [documenting this], is associated with more cognitive deficits,” he said. “We are building more episodes, more treatment resistance, more cognitive dysfunction, and there is data showing that if you have four depressive episodes, unipolar or bipolar, it doubles your late-life risk of dementia. And guess what? That isn’t even the half of it…. In the United States, people with depression, bipolar, and schizophrenia are losing twelve to twenty years in life expectancy compared to people not in the mental health system.

This new marketplace for drugs proved profitable for all involved. Drug industry revenues topped $1 billion in 1957, the pharmaceutical companies enjoying earnings that made them “the darlings of Wall Street,” one writer observed.19 Now that physicians controlled access to antibiotics and all other prescription drugs, their incomes began to climb rapidly, doubling from 1950 to 1970 (after adjusting for inflation). The AMA’s revenues from drug advertisements in its journals rose from $2.5 million in 1950 to $10 million in 1960, and not surprisingly, these advertisements painted a rosy picture. A 1959 review of drugs in six major medical journals found that 89 percent of the ads provided no information about the drugs’ side effects.20

In studies of first-episode bipolar patients, investigators at McLean Hospital, the University of Pittsburgh, and the University of Cincinnati Hospital found that at least one-third had used marijuana or some other illegal drug prior to their first manic or psychotic episode.10 This substance abuse, the University of Cincinnati investigators concluded, may “initiate progressively more severe affective responses, culminating in manic or depressive episodes, that then become self-perpetuating.”11 Even the one-third figure may be low; in 2008, researchers at Mt. Sinai Medical School reported that nearly two-thirds of the bipolar patients hospitalized at Silver Hill Hospital in Connecticut in 2005 and 2006 experienced their first bout of “mood instability” after they had abused illicit drugs.12 Stimulants, cocaine, marijuana, and hallucinogens were common culprits. In 2007, Dutch investigators reported that marijuana use “is associated with a fivefold increase in the risk of a first diagnosis of bipolar disorder” and that one-third of new bipolar cases in the Netherlands resulted from it.13

Unfortunately, sitting rests the parts of the body that don’t need much of it while working the parts that desperately do. Specifically, it disengages the lower extremities while utilizing the spine. (This is in sharp contrast to squatting, which disengages the spine while utilizing the lower extremities.) Because sitting positions the spine vertically, it provides no rest or relief from the gravitational forces that compress it. Without a periodic therapeutic reprieve through the day, the relentless load overwhelms the entire structure, joints and muscles alike. To maintain an erect seated posture, some muscle groups in the back have to continually contract. Since this requires a great deal of energy, the muscles quickly become fatigued. (That is why slumping is more comfortable: It takes less energy to maintain.) When the muscles tire, you rely on the backrest more and your muscles less. The less you rely on your muscles, the weaker and more dysfunctional they become. The weaker and more dysfunctional they become, the more you rely on the backrest. The more you rely on the backrest, the more you tend to slump. The more you slump, the more pronounced the debilitating C-shaped curvature becomes. This weakens the muscles in your back even further, which causes them to overload the joints they serve. Sitting in chairs affects even the areas seemingly at rest (particularly the hips and knees). Because sitting keeps the joints static for long periods, the muscles that serve them become fixed in a short, tight position. When at last you do get up and move, the muscles impose more stress on these joints, thereby increasing their susceptibility to wear and tear. The prolonged stasis also prevents the joints from being lubricated with nourishing synovial fluid. Once depleted, the hips and knees, like the spine, deteriorate and erode. Is it any wonder that the areas most traumatized by sitting, namely, the lower back, hips, and knees, are also the most arthritic and disabled areas of the body in the world today? The real mystery is why so few people have made the connection between prolonged sitting and the epidemic of chronic pain. In fact, they need only look to their own bodies for an abundance of evidence.

As many speakers noted, this tool wasn’t particularly well suited for assessing outcomes of a psychiatric drug. How could a study of a neuroleptic possibly be “double-blind”? The psychiatrist would quickly see who was on the drug and who was not, and any patient given Thorazine would know he was on a medication as well. Then there was the problem of diagnosis: How would a researcher know if the patients randomized into a trial really had “schizophrenia”? The diagnostic boundaries of mental disorders were forever changing. Equally problematic, what defined a “good outcome”? Psychiatrists and hospital staff might want to see drug-induced behavioral changes that made the patient “more socially acceptable” but weren’t to the “ultimate benefit of the patient,” said one conference speaker.11 And how could outcomes be measured? In a study of a drug for a known disease, mortality rates or laboratory results could serve as objective measures of whether a treatment worked. For instance, to test whether a drug for tuberculosis was effective, an X-ray of the lung could show whether the bacillus that caused the disease was gone. What would be the measurable endpoint in a trial of a drug for schizophrenia? The problem, said NIMH physician Edward Evarts at the conference, was that “the goals of therapy in schizophrenia, short of getting the patient ‘well,’ have not been clearly defined.

Anti psychotics—a class of drugs previously seen as extremely problematic in kind, useful only in severely ill patients—were the top revenue-producing class of drugs in 2008, ahead even of the cholesterol-lowering agents.12 Total sales of all psychotropic drugs in 2008 topped $40 billion.

Now, once a business gets a customer into its store, it wants to keep that customer and get that customer to buy multiple products, and that’s when the psychiatric “drug trap” kicks in.

The prescribing of psychotropic drugs to two-year-olds and three-year-olds began to become more commonplace about a decade ago, and sure enough, the number of severely mentally ill children under six years of age receiving SSI has tripled since then, rising from 22,453 in 2000 to 65,928 in 2007.

An epidemic had come of age, and history reveals that it rose in lockstep with the prescribing of stimulants and antidepressants to children.

As early as 1992, when the prescribing of SSRIs to children was just getting started, University of Pittsburgh researchers reported that 23 percent of boys eight to nineteen years old treated with Prozac developed mania or maniclike symptoms, and another 19 percent developed “drug-induced” hostility.

Should they remain on the drugs for years, they are at high risk of becoming chronically depressed. They may also develop—as the American Psychiatric Association warns in one of its textbooks—an “apathy syndrome,” which “is characterized by a loss of motivation, increased passivity, and often feelings of lethargy and ‘flatness.

Psychiatry’s thought leaders shaped our society’s understanding of mental disorders, and once they began serving as paid speakers, the pharmaceutical companies sent money their way through multiple channels.

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.

American psychiatry has told the public a false story over the past thirty years.

In her 1968 book, The Epidemiology of Depression, Charlotte Silverman, who directed epidemiology studies for the NIMH, noted that community surveys in the 1930s and 1940s had found that fewer than one in a thousand adults suffered an episode of clinical depression each year. Furthermore, most who were struck did not need to be hospitalized. In 1955, there were only 7,250 “first admissions” for depression in state and county mental hospitals. The total number of depressed patients in the nation’s mental hospitals that year was around 38,200, a disability rate of one in every 4,345 people.

In 1972, Samuel Guze and Eli Robins at Washington University Medical School in St. Louis reviewed the scientific literature and determined that in follow-up studies that lasted ten years, 50 percent of people hospitalized for depression had no recurrence of their illness. Only a small minority of those with unipolar depression—one in ten—became chronically ill, Guze and Robins concluded.

The minimal efficacy of imipramine and other antidepressants led some investigators to wonder whether the placebo response was the mechanism that was helping people feel better. What the drugs did, several speculated, was amplify the placebo response, and they did so because they produced physical side effects, which helped convince patients that they were getting a “magic pill” for depression. To test this hypothesis, investigators conducted at least seven studies in which they compared a tricyclic to an “active” placebo, rather than an inert one. (An active placebo is a chemical that produces an unpleasant side effect of some kind, like dry mouth.) In six of the seven, there was no difference in outcomes.21

Finally, in 2008, Irving Kirsch, a psychologist at the University of Hull in the United Kingdom, found that in the trials of Prozac, Effexor, Serzone, and Paxil, symptoms in the medicated patients dropped 9.6 points on the Hamilton Rating Scale of Depression, versus 7.8 points for the placebo group. This was a difference of only 1.8 points, and the National Institute for Clinical Excellence in Britain had previously determined that a three-point drug-placebo difference was needed on the Hamilton scale to demonstrate a “clinically significant benefit.” It was only in a small subgroup of patients—those most severely depressed—that the drugs had been shown to be of real use. “Given these data, there seems little evidence to support the prescription of antidepressant medication to any but the most severely depressed patients, unless alternative treatments have failed to provide benefit,” Kirsch and his collaborators concluded.

In the short span of forty years, depression had been utterly transformed. Prior to the arrival of the drugs, it had been a fairly rare disorder, and outcomes generally were good. Patients and their families could be reassured that it was unlikely that the emotional problem would turn chronic. It just took time—six to twelve months or so—for the patient to recover. Today, the NIMH informs the public that depressive disorders afflict one in ten Americans every year, that depression is “appearing earlier in life” than it did in the past, and that the long-term outlook for those it strikes is glum.

Several countries also observed that following the arrival of the SSRIs, the number of their citizens disabled by depression dramatically increased. In Britain, the “number of days of incapacity” due to depression and neurotic disorders jumped from 38 million in 1984 to 117 million in 1995, a threefold increase.62 Iceland reported that the percentage of its population disabled by depression nearly doubled from 1976 to 2000. If antidepressants were truly helpful, the Iceland investigators reasoned, then the use of these drugs “might have been expected to have a public health impact by reducing disability, morbidity, and mortality due to depressive disorders.”63 In the United States, the percentage of working-age Americans who said in health surveys that they were disabled by depression tripled during the 1990s.

All drugs have a risk-benefit profile, and the usual thought within medicine is that a drug should provide a benefit that outweighs the risks. A drug that curbs psychotic symptoms clearly provides a marked benefit, and that was why antipsychotics could be viewed as helpful even though the list of negatives with these drugs was a long one. Thorazine and other first-generation neuroleptics caused Parkinsonian symptoms and extraordinarily painful muscle spasms. Patients regularly complained that the drugs turned them into emotional “zombies.” In 1972, researchers concluded that neuroleptics “impaired learning.”30 Others reported that even if medicated patients stayed out of the hospital, they seemed totally unmotivated and socially disengaged. Many lived in “virtual solitude” in group homes, spending most of the time “staring vacantly at television,” wrote one investigator.31 None of this told of medicated schizophrenia patients faring well, and here was the quandary that psychiatry now faced: If the drugs increased relapse rates over the long term, then where was the benefit? This question was made all the more pressing by the fact that many patients maintained on the drugs were developing tardive dyskinesia (TD), a gross motor dysfunction that remained even after the drugs were withdrawn, evidence of permanent brain damage. All of this required psychiatry to recalculate the risks and benefits of antipsychotics, and in 1977 Jonathan Cole did so in an article provocatively titled “Is the Cure Worse Than the Disease?” He reviewed all of the long-term harm the drugs could cause and observed that studies had shown that at least 50 percent of all schizophrenia patients could fare well without the drugs. There was only one moral thing for psychiatry to do: “Every schizophrenic outpatient maintained on antipsychotic medication should have the benefit of an adequate trial without drugs.” This, he explained, would save many “from the dangers of tardive dyskinesia as well as the financial and social burdens of prolonged drug therapy.”32

At autopsy, the brains of twenty schizophrenics had 70 percent more D2 receptors than normal. At first glance, it seemed that the cause of schizophrenia had been found, but Seeman cautioned that all of the patients had been on neuroleptics prior to their deaths. “Although these results are apparently compatible with the dopamine hypothesis of schizophrenia in general,” he wrote, the increase in D2 receptors might “have resulted from the long-term administration of neuroleptics.”20 A variety of studies quickly proved that the drugs were indeed the culprit. When rats were fed neuroleptics, their D2 receptors quickly increased in number.21 If rats were given a drug that blocked D1 receptors, that receptor subtype increased in density.22 In each instance, the increase was evidence of the brain trying to compensate for the drug’s blocking of its signals. Then, in 1982, Angus MacKay and his British colleagues reported that when they examined brain tissue from forty-eight deceased schizophrenics, “the increases in [D2] receptors were seen only in patients in whom neuroleptic medication had been maintained until the time of death, indicating that they were entirely iatrogenic [drug-caused].”23 A few years later, German investigators reported the same results from their autopsy studies.24 Finally, investigators in France, Sweden, and Finland used positron emission topography to study D2-receptor densities in living patients who had never been exposed to neuroleptics, and all reported “no significant differences” between the schizophrenics and “normal controls.

Prior to treatment, patients diagnosed with schizophrenia, depression, and other psychiatric disorders do not suffer from any known “chemical imbalance.” However, once a person is put on a psychiatric medication, which, in one manner or another, throws a wrench into the usual mechanics of a neuronal pathway, his or her brain begins to function, as Hyman observed, abnormally.

Over the next couple of years, Cole and the rest of psychiatry settled on a trial design for testing psychotropic drugs. Psychiatrists and nurses would use “rating scales” to measure numerically the characteristic symptoms of the disease that was to be studied. Did a drug for schizophrenia reduce the patient’s “anxiety”? His or her “grandiosity”? “Hostility”? “Suspiciousness”? “Unusual thought content”? “Uncooperativeness”? The severity of all of those symptoms would be measured on a numerical scale and a total “symptom” score tabulated, and a drug would be deemed effective if it reduced the total score significantly more than a placebo did within a six-week period. At least in theory, psychiatry now had a way to conduct trials of psychiatric drugs that would produce an “objective” result. Yet the adoption of this assessment put psychiatry on a very particular path: The field would now see short-term reduction of symptoms as evidence of a drug’s efficacy. Much as a physician in internal medicine would prescribe an antibiotic for a bacterial infection, a psychiatrist would prescribe a pill that knocked down a “target symptom” of a “discrete disease.” The six-week “clinical trial” would prove that this was the right thing to do. However, this tool wouldn’t provide any insight into how patients were faring over the long term. Were they able to work? Were they enjoying life? Did they have friends? Were they getting married? None of those questions would be answered. This was the moment that magic-bullet medicine shaped psychiatry’s future. The use of the clinical trial would cause psychiatrists to see their therapies through a very particular prism, and even at the 1956 conference, New York State Psychiatric Institute researcher Joseph Zubin warned that when it came to evaluating a therapy for a psychiatric disorder, a six-week study induced a kind of scientific myopia. “It would be foolhardy to claim a definite advantage for a specified therapy without a two- to five-year follow-up,” he said. “A two-year follow-up would seem to be the very minimum for the long-term effects.

A year later, Maurice Rappaport at the University of California in San Francisco announced results that told the same story, only more strongly so. He had randomized eighty young newly diagnosed male schizophrenics admitted to Agnews State Hospital into drug and non-drug groups, and although symptoms abated more quickly in those treated with antipsychotics, both groups, on average, stayed only six weeks in the hospital. Rappaport followed the patients for three years, and it was those who weren’t treated with antipsychotics in the hospital and who stayed off the drugs after discharge that had—by far—the best outcomes. Only two of the twenty-four patients in this never-exposed-to-antipsychotics group relapsed during the three-year follow-up. Meanwhile, the patients that arguably fared the worst were those on drugs throughout the study. The very standard of care that, according to psychiatry’s “evidence base,” was supposed to produce the best outcomes had instead produced the worst. “Our findings suggest that antipsychotic medication is not the treatment of choice, at least for certain patients, if one is interested in long-term clinical improvement,” Rappaport wrote. “Many unmedicated-while-in-hospital patients showed greater long-term improvement, less pathology at follow-up, fewer rehospitalizations, and better overall functioning in the community than patients who were given chlorpromazine while in the hospital.

In 1967, one in three American adults filled a prescription for a “psychoactive” medication, with total sales of such drugs reaching $692 million.42

Since the arrival of Thorazine, the disability rate due to psychotic illness has increased fourfold in our society.

One-Year Outcomes in WHO Screening Study for Depression The WHO investigators reported that a higher percentage of the unmedicated group recovered, and that “continuing depression” was highest in those treated with an antidepressant. Source: Goldberg, D. “The effects of detection and treatment of major depression in primary care.” British Journal of General Practice 48 (1998): 1840–44.

Several countries also observed that following the arrival of the SSRIs, the number of their citizens disabled by depression dramatically increased. In Britain, the “number of days of incapacity” due to depression and neurotic disorders jumped from 38 million in 1984 to 117 million in 1995, a threefold increase.62 Iceland reported that the percentage of its population disabled by depression nearly doubled from 1976 to 2000. If antidepressants were truly helpful, the Iceland investigators reasoned, then the use of these drugs “might have been expected to have a public health impact by reducing disability, morbidity, and mortality due to depressive disorders.”63 In the United States, the percentage of working-age Americans who said in health surveys that they were disabled by depression tripled during the 1990s.64

Today, as provost of Harvard University, Steve Hyman is mostly engaged in the many political and administrative tasks that come with leading a large institution. But he is a neuroscientist by training, and in 1996 to 2001, when he was the director of the NIMH, he wrote a paper, one both memorable and provocative in kind, that summed up all that had been learned about psychiatric drugs. Titled “Initiation and Adaptation: A Paradigm for Understanding Psychotropic Drug Action,” it was published in the American Journal of Psychiatry, and it told of how all psychotropic drugs could be understood to act on the brain in a common way.46 Antipsychotics, antidepressants, and other psychotropic drugs, he wrote, “create perturbations in neurotransmitter functions.” In response, the brain goes through a series of compensatory adaptations. If a drug blocks a neurotransmitter (as an antipsychotic does), the presynaptic neurons spring into hyper gear and release more of it, and the postsynaptic neurons increase the density of their receptors for that chemical messenger. Conversely, if a drug increases the synaptic levels of a neurotransmitter (as an antidepressant does), it provokes the opposite response: The presynaptic neurons decrease their firing rates and the postsynaptic neurons decrease the density of their receptors for the neurotransmitter. In each instance, the brain is trying to nullify the drug’s effects. “These adaptations,” Hyman explained, “are rooted in homeostatic mechanisms that exist, presumably, to permit cells to maintain their equilibrium in the face of alterations in the environment or changes in the internal milieu.” However, after a period of time, these compensatory mechanisms break down. The “chronic administration” of the drug then causes “substantial and long-lasting alterations in neural function,” Hyman wrote. As part of this long-term adaptation process, there are changes in intracellular signaling pathways and gene expression. After a few weeks, he concluded, the person’s brain is functioning in a manner that is “qualitatively as well as quantitatively different from the normal state.” His was an elegant paper, and it summed up what had been learned from decades of impressive scientific work. Forty years earlier, when Thorazine and the other first-generation psychiatric drugs were discovered, scientists had little understanding of how neurons communicated with one another. Now they had a remarkably detailed understanding of neurotransmitter systems in the brain and of how drugs acted on them. And what science had revealed was this: Prior to treatment, patients diagnosed with schizophrenia, depression, and other psychiatric disorders do not suffer from any known “chemical imbalance.” However, once a person is put on a psychiatric medication, which, in one manner or another, throws a wrench into the usual mechanics of a neuronal pathway, his or her brain begins to function, as Hyman observed, abnormally.

Readers of this book, having come this far in the text, cannot be surprised to learn that outcomes for bipolar disorder have dramatically worsened in the pharmacotherapy era. The only surprising thing is that this failure was so openly discussed at the APA meeting. Given what the scientific literature revealed about the long-term outcomes of medicated schizophrenia, anxiety, and depression, it stood to reason that the drug cocktails used to treat bipolar illness were not going to produce good long-term results. The increased chronicity, the functional decline, the cognitive impairment, and the physical illness—all of these can be expected to show up in people treated with a cocktail that often includes an antidepressant, an antipsychotic, a mood stabilizer, a benzodiazepine, and perhaps a stimulant, too. This was a medical train wreck that could have been anticipated, and unfortunately, as we trace the history of this story, the details will seem all too familiar.

In studies of first-episode bipolar patients, investigators at McLean Hospital, the University of Pittsburgh, and the University of Cincinnati Hospital found that at least one-third had used marijuana or some other illegal drug prior to their first manic or psychotic episode.10 This substance abuse, the University of Cincinnati investigators concluded, may “initiate progressively more severe affective responses, culminating in manic or depressive episodes, that then become self-perpetuating.”11 Even the one-third figure may be low; in 2008, researchers at Mt. Sinai Medical School reported that nearly two-thirds of the bipolar patients hospitalized at Silver Hill Hospital in Connecticut in 2005 and 2006 experienced their first bout of “mood instability” after they had abused illicit drugs.12 Stimulants, cocaine, marijuana, and hallucinogens were common culprits. In 2007, Dutch investigators reported that marijuana use “is associated with a fivefold increase in the risk of a first diagnosis of bipolar disorder” and that one-third of new bipolar cases in the Netherlands resulted from it.13 Antidepressants have also led many people into the bipolar camp, and to understand why, all we have to do is return to the discovery of this class of drugs. We see tuberculosis patients treated with iproniazid dancing in the wards, and while that magazine report was probably a bit exaggerated, it told of lethargic patients suddenly behaving in a manic way. In 1956, George Crane published the first report of antidepressant-induced mania, and this problem has remained present in the scientific literature ever since.14 In 1985, Swiss investigators tracking changes in the patient mix at Burghölzli psychiatric hospital in Zurich reported that the percentage with manic symptoms jumped dramatically following the introduction of antidepressants. “Bipolar disorders increased; more patients were admitted with frequent episodes,” they wrote.15 In a 1993 practice guide to depression, the APA confessed that “all anti-depressant treatments, including ECT [electroconvulsive therapy], may provoke manic or hypomanic episodes.”16

A few years later, researchers at Yale University School of Medicine quantified this risk. They reviewed the records of 87,290 patients diagnosed with depression or anxiety between 1997 and 2001 and determined those treated with antidepressants converted to bipolar at the rate of 7.7 percent per year, which was three times greater than for those not exposed to the drugs.17 As a result, over longer periods, 20 to 40 percent of all patients initially diagnosed with unipolar depression today eventually convert to bipolar illness.18 Indeed, in a recent survey of members of the Depressive and Manic-Depressive Association, 60 percent of those with a bipolar diagnosis said they had initially fallen ill with major depression and had turned bipolar after exposure to an antidepressant.19 This is data that tells of a process that routinely manufactures bipolar patients. “If you create iatrogenically a bipolar patient,” explained Fred Goodwin, in a 2005 interview in Primary Psychiatry, “that patient is likely to have recurrences of bipolar illness even if the offending antidepressant is discontinued. The evidence shows that once a patient has had a manic episode, he or she is more likely to have another one, even without the antidepressant stimulation.”20 Italy’s Giovanni Fava put it this way: “Antidepressant-induced mania is not simply a temporary and fully reversible phenomenon, but may trigger complex biochemical mechanisms of illness deterioration.”21

All of this told of harm done, of a drug that made a child depressed, lonely, and filled with a sense of inadequacy, and when researchers looked at whether Ritalin at least helped hyperactive children fare well academically, to get good grades and thus succeed as students, they found that it wasn’t so. Being able to focus intently on a math test, it turned out, didn’t translate into long-term academic achievement. This drug, Sroufe explained in 1973, enhances performance on “repetitive, routinized tasks that require sustained attention,” but “reasoning, problem solving and learning do not seem to be [positively] affected.”26 Five years later, Herbert Rie was much more negative. He reported that Ritalin did not produce any benefit on the students’ “vocabulary, reading, spelling, or math,” and hindered their ability to solve problems. “The reactions of the children strongly suggest a reduction in commitment of the sort that would seem critical for learning.”27 That same year, Russell Barkley at the Medical College of Wisconsin reviewed the relevant scientific literature and concluded “the major effect of stimulants appears to be an improvement in classroom manageability rather than academic performance.”28 Next it was James Swanson’s turn to weigh in. The fact that the drugs often left children “isolated, withdrawn and overfocused” could “impair rather than improve learning,” he said.29 Carol Whalen, a psychologist from the University of California at Irvine, noted in 1997 that “especially worrisome has been the suggestion that the unsalutary effects [of Ritalin] occur in the realm of complex, high-order cognitive functions such as flexible problem-solving or divergent thinking.”30 Finally, in 2002, Canadian investigators conducted a meta-analysis of the literature, reviewing fourteen studies involving 1,379 youths that had lasted at least three months, and they determined that there was “little evidence for improved academic performance.”31

For the APA and pharma companies, the emergence of NAMI could not have come at a more opportune moment. This was a parents’ group eager to embrace biological psychiatry, and both the APA and pharmaceutical firms pounced. In 1983, the APA “entered into an agreement with NAMI” to write a pamphlet on neuroleptic drugs, and soon the APA was encouraging its branches across the country “to foster collaborations with local chapters of the National Alliance for the Mentally Ill.”61 The APA and NAMI joined together to lobby Congress to increase funding for biomedical research, and the beneficiary of that effort, the NIMH—which saw its research budget soar 84 percent during the 1980s—thanked the parents for it. “The NIMH in a very meaningful sense is NAMI’s institute,” Judd told NAMI president Laurie Flynn in a 1990 letter.62 By that time, NAMI had more than 125,000 members, most of whom were middle-class, and it was busily seeking to “educate the media, public officials, healthcare providers, educators, the business community, and the general public about the true nature of brain disorders,” said one NAMI leader.63 NAMI brought a powerful moral authority to the telling of the broken-brain story, and naturally pharmaceutical companies were eager to fund its educational programs, with eighteen firms giving NAMI $11.72 million from 1996 to 1999.64

Thanks to Scientology, the powers that be in psychiatry had the perfect storytelling foil, for they could now publicly dismiss criticism of the medical model and psychiatric drugs with a wave of the hand, deriding it as nonsense that arose from people who were members of a deeply unpopular cult, rather than criticism that arose from their own research. As such, the presence of Scientology in the storytelling mix served to taint all criticism of the medical model and psychiatric drugs, no matter what its source.

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

Leung’s feature-length film on the history of AIDS, House of Numbers: Anatomy of an Epidemic. Leung asked an uncomfortable, chafing Dr. Fauci for his best evidence linking HIV to immune deficiency disease. With two decades and ten billion dollars to prepare his answer, Dr. Fauci’s best explanation was the classic Fauci soft shoe.

those quitting a benzodiazepine. In addition to rebound anxiety, patients could experience insomnia, seizures, tremors, headaches, blurred vision, a ringing in the ears, extreme sensitivity to noise, a feeling that insects were crawling over them, nightmares, hallucinations, extreme depression, depersonalization, and derealization (a sense that the external world is unreal). Withdrawal, one patient told Heather Ashton, was like “living death … I thought I had gone mad.

The prescribing of Ritalin and antidepressants took off in the late 1980s and early 1990s, and as this occurred, the bipolar epidemic erupted.

SSRIs also cause a multitude of troubling side effects. These include sexual dysfunction, suppression of REM sleep, muscle tics, fatigue, emotional blunting, and apathy. In addition, investigators have reported that long-term use is associated with memory impairment, problem-solving difficulties, loss of creativity, and learning deficiencies.

To date, no study has found any long-term benefit of attention-deficit medication on academic performance, peer relationships, or behavior problems, the very things we want to improve…. The drugs can also have serious side effects, including stunting growth.

The theories that patients with depression lack serotonin and that patients with schizophrenia have too much dopamine have long been refuted. The truth is just the opposite. There is no chemical imbalance to begin with, but when treating mental illness with drugs, we create a chemical imbalance.

The prescribing of stimulants to ADHD youth began to take off in the 1980s, and today, thirty years later, studies have failed to show that this treatment helps children grow up and thrive. In a 2012 op-ed published in the New York Times, Alan Sroufe, a professor of psychology at the University of Minnesota’s Institute of Child Development, told of this bottom-line finding: “To date, no study has found any long-term benefit of attention-deficit medication on academic performance, peer relationships, or behavior problems, the very things we want to improve…. The drugs can also have serious side effects, including stunting growth.

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 penicillin trials or trials of drugs that really work.” —DAVID HEALY, PROFESSOR OF PSYCHIATRY AT CARDIFF UNIVERSITY, WALES (2008)1

Thus, in 1955, 1 in every 468 Americans was hospitalized due to a mental illness. In 1987, there were 1.25 million people receiving an SSI or SSDI payment because they were disabled by mental illness, or 1 in every 184 Americans.

consequently a more rapid return to work?” Dewa wondered.60 In a similar vein, University of Iowa psychiatrist William Coryell and his NIMH-funded colleagues studied the six-year “naturalistic” outcomes of 547 people who suffered a bout of depression, and they found those who were treated for the illness were three times more likely than the untreated group to suffer a “cessation” of their “principal social role” and nearly seven times more likely to become “incapacitated.” Moreover, while many of the treated patients saw their economic

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 penicillin trials or trials of drugs that really work.” —DAVID HEALY, PROFESSOR OF PSYCHIATRY AT CARDIFF UNIVERSITY, WALES (2008)

Sometimes I thought I would die and other times wished I had.”11 Although the FDA held a hearing on the matter, it did not impose any legal control on benzodiazepines similar to what had been placed on amphetamines and barbiturates, and so the public’s belief that the drugs were relatively nonaddictive and harmless survived until 1975, when the U.S. Justice Department demanded that they be classified as schedule IV drugs

But here is the conundrum. Given this great advance in care, we should expect that the number of disabled mentally ill in the United States, on a per-capita basis, would have declined over the past fifty years. We should also expect that the number of disabled mentally ill, on a per-capita basis, would have declined since the arrival in 1988 of Prozac and the other second-generation psychiatric drugs. We should see a two-step drop in disability rates. Instead, as the psychopharmacology revolution has unfolded, the number of disabled mentally ill in the United States has skyrocketed. Moreover, this increase in the number of disabled mentally ill has accelerated further since the introduction of Prozac and the other second-generation psychiatric drugs. Most disturbing of all, this modern-day plague has now spread to the nation’s children.

Yet, fueled by pharmaceutical advertisements, the belief lived on, and it caused Irish psychiatrist David Healy, who has written a number of books on the history of psychiatry, to quip in 2005 that this theory needed to be put into the medical dustbin, where other such discredited theories can be found. “The serotonin theory of depression,” he wrote, with evident exasperation, “is comparable to the masturbatory theory of insanity.

If we value the pursuit of knowledge, we must be free to follow wherever that search may lead us.” —ADLAI STEVENSON (1952)