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Authors: James Davies

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While these changes could have been due to the placebo effect, they still seemed to her very real. She was doing things differently. There was a real down side, however, which she experienced when coming off her pills. “I feel like I've been drugged for two years,” she said, “and now I want to take a look at my checkbook.” She went on to report other uncharacteristic behavior which, from her non-drugged perspective, now seemed frankly bizarre. She had bought a puppy that she kept in an unfinished basement. While medicated she had not bothered to clean up the puppy's poo, reacting with that same “well, whatever” attitude she'd felt at work.
68

Sobo provides many other examples of drugs mitigating one problem but at the same time creating a plethora of others. He talks of a man who was usually very conscientious but quite anxious, quickly becoming on his pills completely indifferent to all the speeding tickets he started gathering. He also talks of a woman who began taking meds for a long-term phobia suddenly and uncharacteristically becoming blasé about her son's diagnosis of testicular cancer.

Turning to my experience, I can remember a dedicated student of mine taking meds to manage his examination terror. They lessened his fear, granted, but oddly his grades started to plummet—his fear of failure, it turns out, had been the only thing that'd got him to the library. Finally, and perhaps most dramatic, a colleague of mine once told me about a seventeen-year-old girl he had worked with psychotherapeutically. She had been given pills to help with her social phobia. And yes, her confidence had minimally increased. But so too had her libido. Within two weeks she had slept with six men.

So the real question we must ask is not whether pills are leading people to change their lives, but whether they are leading people to change them in the way that is natural to them. Are these manufactured states of mind guiding people to make the right moves or decisions? Or are they stacking up more problems for them in the future, like many other mood-altering substances can do? Is it right that pills should make us feel suddenly invincible, or blasé about our son's cancer, or sexually unbridled, or indifferent to staying in a dead-end job? Is it right that they should suddenly dry up our grief for someone we love?

Toward the end of my interview with Moncrieff, she agreed that antidepressants do have effects. Mostly they have placebo effects and side effects, yet for some patients they can have additional psychoactive effects such as numbing and sedating effects, which can in turn bring other unintended consequences. Moncrieff was therefore insistent that whatever effects they do have, they cannot be classed as curing effects. For her, to think of these pills as cures is a scientific and professional error. As she said: “The idea that there is a brain disease, or a chemical imbalance, or a faulty neural network that these pills correct is completely false and unsupported. You cannot therefore say that these drugs are having curative or remedial effects if the evidence doesn't support that point of view.”

As I left Moncrieff's office at University College London, I realized it was time to tackle the idea that mental disorders are rooted in brain malfunctions that can be corrected by chemical cures. Again and again the experts were telling me that this view was incorrect—Robert Spitzer, Walter Brown, Tim Kendall, Irving Kirsch, and now Joanna Moncrieff. So why was the popular and prevailing view so radically different? Why did so many people believe that the brain is at the heart of the problem?

It was time for me to find out for myself precisely what the science says. What role does our biology play in our mental distress? That's the matter I shall now address.

CHAPTER SEVEN

BIO-BABBLE?

O
n a sunny Saturday morning on August 12, 2003, six people entered a church in Pasadena, California, set up a suite of computers, and began sending e-mails around the country announcing that their hunger strike had begun. Their protest was about human rights abuses perpetrated by an institution the hunger strikers claimed had tortured them in their youth, by incarcerating them against their will, poisoning them, firing electrical currents into their brains, branding them insane, and affirming the improbability of their ever being fully sane again. To these protestors this institution is known as a system of legalized mental and emotional abuse. To most of the rest of us it is known as medical psychiatry.

In late 2011, I spoke to one of the striker's leaders, 56-year-old David Oaks. My aim was to discover why this group had taken such drastic steps to be heard. Oaks chose to answer my question by telling me his story.
69
As an undergraduate entering Harvard University in the mid-1970s, he had great difficulty adapting to his new environment. He had been raised in a working-class family on Chicago's South Side, and so found the world of privilege at Harvard so fundamentally alien to all he had known that he had struggled to find his place. He soon started experimenting with marijuana, which only deepened his feelings of estrangement and alienation. And as these difficult feelings spiraled, it was not long until he entered what he called an “altered state.”

Once a couple of people noticed this change in him, it wasn't long before he was sent to the college infirmary. There they classified his experiences according to the
DSM
's definition of schizophrenia. He was therefore prescribed heavy doses of Thorazine, a powerful antipsychotic drug. But the drug did not help him; in fact, it seemed only to deepen his confusion.

By the following semester, Oaks was admitted to the famous McLean Hospital, where it was decided that what he needed was heavy sedation. But Oaks did not want to be heavily medicated, so the authorities did what they are entitled to do if a psychiatric patient does not comply with treatment—they locked him in solitary confinement and subjected him to forced drugging. The medication with which they injected him was so powerful that he could barely eat, think, or move—let alone continue to uphold his spirited protest.

During one particularly agonizing night locked up in solitary confinement, David became so overwhelmed with shame and disgust at the way he'd been handled that he made a lifelong pledge: “I remember looking out through one of those impenetrable metal window screens,” David Oaks recalled emotionally, “and there and then I pounded on the screen with my fist, vowing to do something for human rights once I got out.”

Thirty-five years have now passed since that harrowing episode, but Oaks has more than honored that vow. After his discharge from hospital (which he secured by threatening legal action unless they released him), he graduated from Harvard University in 1977 with honors. Since then he has dedicated his life to protecting the rights of psychiatric patients, or as he would call them “psychiatric survivors.”

He first worked with the Mental Patients Liberation Front, organizing rallies during the early 1980s against the American Psychiatric Association's sanctioning of electroshock therapy. He also wrote for the influential
Madness Network News
, becoming one of America's foremost advocates for psychiatric patients' rights. In the 1990s he helped found Support Coalition, now called MindFreedom, of which he is now executive director. Over the years, this organization has gone from strength to strength, recently being accredited by the United Nations as a nongovernmental organization with consulting status.

David Oaks's history of patient advocacy and activism is the backdrop against which we find him protesting with five other hunger strikers in that church in Pasadena. Each of the other strikers could also tell their own tales of woe—some were force-fed drugs they didn't want, others were given ECT against their will, and most had suffered from the stigma and crippling side effects of their psychiatric treatment. So together they all sat in that church, refusing solid food until their demands were met.

So what were their demands? What did the hunger strikers exactly want? David Oaks was forthright about this: “We wanted something very simple—we wanted the American Psychiatric Association and two other major organizations to answer some basic questions. We wanted them to provide evidence for what we had been led to believe as patients: that the major mental illnesses are actually biologically-based brain diseases; that psychiatric diagnosis is objective; that there are chemical imbalances that can be corrected by psychiatric drugs; and that psychiatric drugs actually cure us rather than temporarily alter us like recreational drugs do.”

After sending these requests from their overheating computers, the hunger strikers sat back and waited … and waited … and … well … waited some more. Two of the organizations (National Alliance for the Mentally Ill (NAMI) and the Office of the Surgeon General of the United States) completely ignored the hunger strikers' requests, acting as though the whole event was just not taking place. “Their total silence could've made the situation very sticky,” recalled Oaks, “if the American Psychiatric Association had not finally clicked that they actually needed to respond.”

And respond they did. It came in the form of a brief 247-word PR statement declaring that the APA was committed to promoting “the highest quality care for individuals with mental illness,” and further adding that in recent years, “there has been substantial progress in understanding the neuroscientific basis of many mental illnesses.” The APA therefore did not provide the evidence that Oaks and his fellow protesters had specifically asked for. Instead, the APA told the strikers if they wanted to learn about the biology of mental distress, then there were three good psychiatric textbooks that they should consult for the evidence they sought.

This somewhat dismissive response would soon backfire for the APA, because what they did not know was that the protestors had organized a scientific panel to assess the APA's response. This panel was comprised of fifteen senior academics and clinicians from the United States and Europe, including Professor Mary Boyle (University of East London), Professor David Cohen (University of Texas), Dr. Patricia E. Deegan (Boston University), Professor Tom Greening (UCLA), and Dr. Peter Breggin (founder of the ICSPP). “These guys worked incredibly hard,” said Oaks energetically, “and yes, they went away and scoured those textbooks for any relevant studies and citations, etc.”

So what did the scientific panel find? Did the textbooks provide the evidence the protesters asked for? “In short,” said Oaks, “they did not.” Instead, the scientific panel found the books littered with confessions of failure, such as: “The precise causes (etiology) of mental disorders are not known;” and “Few lesions or physiologic abnormalities define the mental disorders, and for the most part their causes remain unknown;” and “Although reliable criteria have been constructed for many psychiatric disorders, validation of the diagnostic categories as specific entities has not been established;” and “In the areas of pathophysiology and etiology, psychiatry has more uncharted territory than the rest of medicine.”
70

Given that these statements hardly supported the APA's earlier claim that modern psychiatry had made “substantial progress in understanding the neuroscientific basis of many mental illnesses,” the scientific panel sent these and other statements back to the APA, stating that they had neither found, nor once again been given, the evidence they wanted. When the APA responded, now for the second time, it was clear they had become irritated: “It is unfortunate that in the face of … [psychiatry's] remarkable scientific and clinical progress,” they wrote, “[that] a small number of individuals and groups persist in questioning the reality and clinical legitimacy of disorders that affect the mind, brain, and behavior.” The APA then reaffirmed that there is “research” and “compelling evidence” showing that
some
disorders have a strong genetic component, and that schizophrenia reveals reproducible abnormalities of brain structure.

But after asking the APA, now for a third time, to provide its “compelling evidence,” not a single specific reference or piece of scientific research was provided to back up their claims. As Oaks told me with a twinkle in his eye, “They could not give us what we wanted because what we wanted does not exist. We knew that, they knew that, but I think they realized coming clean publicly would be a PR disaster.”

Toward the end of our interview, I asked what Oaks felt the hunger strike had achieved. “It did not change psychiatry, that's for sure. Biopsychiatry is now more powerful than ever in its entire history. But we did consider it a success to the extent we got our message out there. Many media outlets covered the story, like the
Washington Post
, the
LA Times
, and the BBC. And people saw firsthand how the APA operates—concealing information, distorting the facts, and unwilling to be held to account. We even won a real concession: the APA's final statement conceded that psychiatry cannot yet readily point to any ‘discernible pathological lesions or genetic abnormalities' in mental disorders.
71
Now, that is something you won't hear them admit every day.”

Oaks is not opposed to all psychiatric treatment. He recognizes that in some cases drugs may help the most severely distressed in society. What he objects to is the treatment and sectioning of patients against their will, psychiatry's dubious financial dependency on the pharmaceutical industry, psychiatry's medicalization of our most basic everyday problems, and finally the psychiatric myth that our emotional troubles are rooted in biochemical imbalances or genetic dispositions.

As this current chapter is primarily interested in the biology of mental distress, it is now time to focus more closely on that final statement about genes and biochemical imbalances. Are they indeed at the root of our mental ill-health, as much of the public have been led to suppose?

2

In the early 1960s, a young medical researcher from the wrong side of Brooklyn stumbled upon an idea that would launch a paradigm shift in psychiatry. The researcher was called Joseph Schildkraut, and the idea he advanced was rather simple: fluctuations in our moods may be due to chemical imbalances in our brains. To be sure, Schildkraut was not the first person to entertain this compelling idea. It had been floating around the psychiatric community in one form or another since the mid-1950s when the first antidepressants started to be used. But for some reason when Schildkraut published his hypothesis in the
American Journal of Psychiatry
in 1965, his views took the community by storm.
72

In fact, his paper, which has since become one of the most cited papers in psychiatric history and which was ungainly entitled “The Catecholamine Hypothesis of Affective Disorders,” is now regarded as the first and clearest articulation of what is now widely called the chemical imbalance theory of mental illness.

What prompted Schildkraut to write this paper was a confluence of many things. One spur of particular note was that, while working as a researcher at the National Institute of Mental Health, Schildkraut had become fascinated with the observation that certain depressed people who did not respond well to talk therapy often seemed to improve when given certain drugs. But he, like others at that time, was uncomfortable with the “drug-centered” view I discussed in the last chapter: the idea that psychiatric drugs were merely soothing tonics that have mood-altering effects like recreational drugs do. Schildkraut was rather convinced they must have a more curative effect.

It was this conviction that led him to try and explain the biology of this “curative effect” in his 1965 article. His method was to review data from many different pharmacological studies, mainly conducted on animals, which seemed to suggest depression was due to a brain deficiency in a chemical called norepinephrine. His theory was that the two types of antidepressant in most widespread use at the time (the tricyclics and the monoamineoxidase inhibitors [MAOIs]) worked by increasing the amount of norepinephrine available in the central nervous system—the implication being that depression was an outcome of some kind of norepinephrine deficiency.

Now the first thing to say about Schildkraut's theory was that he himself called it at the time “at best a reductionist simplification” that could neither be rejected nor confirmed “on the basis of data currently available.” In other words, Schildkraut explicitly acknowledged that the chemical imbalance theory was just that—a theory for which the science of the day offered no clear support. This meant that his now famous article actually
proved
nothing at all. All it did was postulate an idea. An idea that, it would soon turn out, would come to captivate an entire new generation. As the medical historian David Healy puts it:

Despite the fact that such a hypothesis could have been proposed earlier and despite the many flaws inherent in it, this particular statement in 1965 came to dominate the field, set research agendas, and direct drug company efforts for the following two decades. It crystallized a split in psychiatry between biological and psychodynamic branches, each group having its own journals, its own meetings, and de facto very little to do with each other.
73

Let's now fast-forward three years to 1967. At this time, Schildkraut's theory was taken in an unexpected direction by a British psychiatrist called Alec Coppen. What Coppen argued, in a paper published in the
British Journal of Psychiatry
entitled “The Biochemistry of Affective Disorders,” was that norepinephrine is not the only chemical implicated in mood irregularities. Others were crucial too, especially a neurotransmitter chemical called serotonin. But again, after reviewing all the relevant studies available at that time, Coppen, like Schildkraut before him, was still cautious with his conclusions, adding the following caveat at the end of his article:

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