On a popular daytime TV talk show in the UK, the host, Robert Kilroy, announces to the audience the wonders of a new antidepressant drug:63
Kilroy: This pill could solve all your problems. It is called Prozac. And it may mean the end of depression as we know it! [Kilroy approaches a female member of the audience and directs the microphone toward her]
Woman: I have been taking Prozac for two years.
Kilroy: And what difference has that made?
Woman: Brilliant!
Kilroy: Oh, she is smiling. [audience laughs] Her eyes are lighting up!
Woman: I feel as if I am back to normal. [she laughs]
Kilroy: You feel normal?
Woman: Yeah. [beaming a smile]
Kilroy: You feel like a better person?
Woman: Yeah, yeah. [smiling]
Kilroy: [turning to her husband] Has it worked? You look very dubious, my friend.
Husband: Apparently it has … but I can’t help being suspicious of it. [looks sad and uncomfortable] I don’t think she’s the woman I married.
Kilroy: Why?
Husband: I think she has changed. [audience goes silent]
Kilroy: In what way?
Husband: I don’t know. I don’t know, but there is something … there is something there that is … different.
Kilroy: Okay, so she is not the woman you married. Is she a better woman?
Husband: No.(husband looks down sadly) She is … different.
In chapters 4 and 5, we saw that antidepressants have effects. Mostly they have placebo and side effects. Yet an increasing amount of evidence now confirms that for a subset of people they have other effects too—effects we don’t yet fully understand. Like the woman on Kilroy’s chat show, sometimes these pills make us “different.” Sometimes they sedate and numb us. And sometimes they change us in more unpredictable ways.
As this chapter unfolds, we will see that no matter what effects antidepressants unleash, these effects do not “cure” us or return us to “normality.” Instead, if we are to make any sense of their effects at all, we must regard them as we do other mind-altering substances—as jettisoning us into an abnormal state of mind.
By taking this view, I tackle head-on one of the most powerful myths embraced by the psychiatric establishment: that psychiatric drugs are capable of “curing” us and are therefore distinct from recreational drugs that merely alter our state of mind. What I am going to explore now is whether this “curing view” of antidepressants, far from capturing how these pills actually work, is rather a tale of convenience resting upon no solid, scientific basis.
2
In most British clinics and hospitals, before a patient is given psychotherapy like CBT or psychodynamic therapy, they usually undergo what is called a clinical assessment. These are interviews usually lasting about fifty minutes during which a psychologist or therapist assesses whether a given patient is suitable for therapeutic work. During these interviews the practitioner notes down the patient’s problem, his or her personal and clinical history, and their understanding of the patient’s problem. The aim of this meeting is to gather information with which to advise the clinical team on what kind of psychological intervention is needed.
Some years back, a colleague of mine conducted one of these assessments with a 52-year-old man I shall call Toby. A few months before the assessment, Toby had lost his wife to a long-standing heart condition. Her death had left him devastated. For the first time in his life, he said, he could truly understand what it meant to be entirely alone. He couldn’t sleep, he could barely eat, and he was regularly incapacitated by heavy bouts of grief. After being consumed by his heartache for some weeks, he decided to visit his doctor for help. He was immediately prescribed antidepressants. After taking them for four weeks, however, some odd things started to happen. In the assessment, my colleague asked him precisely what these odd things were.
The first thing Toby mentioned was that he’d lost all capacity to cry. After a month on the pills, his tears had literally dried up. When my colleague asked him to elaborate, Toby responded that he no longer cried because he now experienced the memories of his wife in a different way. In short, the vivid “flashbacks” he used to have of his wife had now disappeared. He characterized these flashbacks as vivid bursts of recollection that would quite literally overwhelm him with the presence of his deceased wife, as if she were suddenly right there, alive and by his side.
His flashbacks would typically arrive at unexpected moments: when walking home he would suddenly see an image of her smiling and opening the front door; or when lying in bed he’d hear her voice or feel her hand stretching out for his own; or when on the train he’d glimpse her in the expression of a female stranger in a smile, a nod, or a look of concern. In these fleeting moments, his wife would become extraordinarily visible to him. And his body would respond with every sinew and fiber as if she were really there.
Yet she was not there. And that, he said, was what made these flashbacks so significant: their vividness meant that when they passed, he’d be left with a crushing sense of loss and grief. But since taking his pills, Toby told my colleague, these flashbacks had just stopped. Was this healthy? Was this natural? Toby now wanted to know.
There was also something else that the pills had changed. Before taking them, in those early weeks after his wife’s death he’d regularly experience, almost on a daily basis, a dull ache growing in his chest. This would build and build, sometimes building all day until the pressure, unable to be contained anymore, would finally burst out through a deluge of tears. But, again, since taking his pills this internal pressure was somehow behaving differently. Instead of finding an outlet through his tears, he said it almost now seemed to get stuck in his head, agitating his thoughts and making him act in uncharacteristic ways.
One of these uncharacteristic behaviors involved religiously counting the number of lampposts he passed as he walked down the street. Another involved endlessly tracing the contours of distant objects with his index finger. For Toby, these acts had reached obsessive levels, but they did not end there. He’d also become addicted to online card games, which he now played deep into the night. He’d never played these games before, let alone stayed up late on his computer. He had always preferred other activities in the late evening, like reading. But he rarely read nowadays, as serious concentration was almost impossible.
As he spoke to my colleague he wondered openly whether this pent-up pressure was generating these “obsessive activities.” Of course he couldn’t be sure, although he was worried that the pills had somehow cut off his emotions and forced him into his own head.
During the initial assessment, my colleague dutifully noted all of Toby’s insightful reflections. That was his task. That’s how assessments work. What his task didn’t involve was exploring if the pills were responsible for the changes in Toby’s behavior. Assessments do not afford the opportunity for that kind of enquiry. After all, if you choose to open Pandora’s box you’d better do it in therapy where you have time to manage what may fly out, rather than in a time-restricted assessment where you don’t.
But what if my colleague had more time? What if he and Toby had met in a different environment, one that allowed for a more frank conversation about whether the pills Toby was taking had affected him in the way he feared?
As such a question is hypothetical, it requires a hypothetical answer. That’s what I’d like to provide now—an imaginative scenario of how things may have panned out had my colleague had more time. The purpose of imagining an exchange that never took place is to try and learn a little more about how the pills Toby was taking actually work and how they may have been affecting his life.
3
Please imagine the following exchange taking place in a drop-in center, where Toby has stopped by to ask my colleague for some advice.
Toby: I’m not sure what’s happening to me. My emotions have become so flat. Is this normal? Are the pills responsible for this?
Colleague: It’s difficult to be 100 percent certain what’s responsible, because these changes may have occurred even if you’d not taken the pills. But on the other hand, we do know that antidepressants have effects. Mostly they have placebo effects and side effects. We also know that, for certain people, they can have sedating or numbing effects—perhaps the very effects that have interfered with your grieving.
Toby: So you’re saying that if the pills have affected me, they’ve sedated rather than healed or cured me?
Colleague: Right. We misunderstand antidepressants when we think of them as curing us.
Toby: Could you elaborate? I am not sure what you mean.
Colleague: Well, antidepressants work differently from many drugs used in other branches of medicine. Take antibiotics and antiviral drugs, for example. When these enter the body, they attack the viruses or bacteria at the root of the illness. In this sense they cure us by literally killing the problem. The same can be said for chemotherapy, which is sent into the blood to destroy the cancer cells. But antidepressants don’t work in that way, because when we’re talking about emotional problems there is rarely an underlying pathology, virus, or disease to be cured [as I’ll discuss in the next chapter]. Rather, these drugs, when they do have effects, therefore work more like substances that temporarily alter your state of mind, such as caffeine, coffee, or cannabis.64
Toby: So these pills don’t cure us, they change us?
Colleague: Yes, they throw some of us temporarily into a foreign state of mind—into an altered version of who we are. This means they do not return us to normal health as medical pills aim to do. Rather, they alter our consciousness.
Toby: It sounds like you are saying these pills manufacture a new state of mind, perhaps even an unnatural state.
Colleague: Well, just think about it for a moment, Toby. Do you believe it’s natural to stop crying after a terrible loss? I mean just like that? Grieving commonly goes on for a long time and drifts away only very slowly and intermittently. It’s rare for it to just stop dead in its tracks, as it has done with you. Now, of course, some people may argue that you suddenly stopped because you were “cured” of an excessive emotional response. But that would be a silly argument, least of all because it assumes that grief is something we need to be “cured” from. No, it makes far more sense to say that in a situation like yours the pills have simply numbed your natural reaction to a deeply painful event.
Toby: You mean they’ve interfered with my normal responses?
Colleague: In your case, it may be so. After all, research shows that if you give Prozac to a group of healthy individuals, after a while about half of them will experience emotional blunting.65 So the question is what’s happening to these healthy people? The pills certainly aren’t “curing” them, because these people are healthy and have nothing to be cured from.
No, all that’s happened is that the pills have dulled their normal reactions. These people have been thrown into a new state of mind manufactured by the drugs they’ve taken. So these drugs can sometimes produce effects beyond side effects and placebo effects, but often not the effects drug companies advertise—not healing, improving, or curative effects, as they say, but mind-numbing effects.66
Toby: But if the drugs I’ve taken have just numbed me, some people would ask what’s wrong with that. Why shouldn’t I just take that result and run! People use substances all the time to alter their moods. The use of alcohol is perhaps the most obvious example.
Colleague: Well, I see your point at one level. But the obvious answer is that numbing things isn’t curing things, or even, in the long run, helping things. It’s just providing a temporary and superficial distraction, and one that may store up problems later along the line.
You mentioned alcohol, so I’ll illustrate what I mean with that example. Let’s say I am really nervous about a party I’ve been invited to on Saturday night. And perhaps I am nervous because I think everyone there will be smarter than me, more attractive, more interesting, and what have you. Anyway, I get there and no one is talking to me, so I grab a drink and gulp it down. After a few minutes I relax a little and start up a conversation. And because I’m feeling a little better, a little more confident, I have another drink, and then another and another. Soon I am swaying all over the place, bumping into things, hiccupping, and chatting to everyone. Fine, so I am no longer nervous. But I am not my usual self either.
You see, although the alcohol has had an effect, it has not uprooted the reason I felt insecure in the first place. It’s merely altered my state of mind so that I no longer experience my insecurity. It has replaced my feeling of inadequacy with a feeling of “what the heck,” a feeling that is neither a natural nor permanent product of my personality but a manufactured result of the alcohol I’ve drunk.
Toby: So the alcohol hasn’t really changed anything fundamentally?
Colleague: Right. It’s no more “cured” you of your insecurity than caffeine “cures” you of your tiredness. It’s merely changed your state of mind while under its influence. And that’s precisely how antidepressants work for some people—not curing us, but changing us. For you, your instinct was to cry, but the drugs seem to have cut that short. Your life is the same, your loss is the same, but your reaction to life events has now been altered. And so this raises a serious question about whether you’ve now just become like the guy at the party who’s simply anaesthetized his problem. And if so, psychologically speaking, is being sedated to your pain really the best thing for you in the long run?
Toby: What do you mean?
Colleague: Let me give you an example. I once worked with someone who hated his job at an accountancy firm so much that he became very depressed. He consulted his doctor and was prescribed Prozac. After a while things began to change a little for the better. At least that’s how he initially felt. He started to take less offense at his boss’s criticisms, he stopped stressing so much about deadlines, and he began to relax a little more socially with his colleagues. In total, he developed that “what the heck” attitude which some people on the drug report. So the question is, was he helped? Had the drugs made his life any better?
Well, from one angle, I suppose they had: he was now slightly more tolerant of work and less conflicted about going in every day. Yet from another angle he wasn’t helped at all, because once he stopped taking Prozac his old dislike of work returned. Worse still, once off the drug he wondered whether he’d actually drugged himself into staying in a job he should’ve left years ago. Perhaps his depression was an alarm that signaled he needed to change his life. But rather than listening to the alarm, he just turned it off with Prozac—pulling up the covers and going back to sleep.
Toby: So by dulling his suffering with pills, you are saying he failed to get up and make the changes he needed?
Colleague: That’s what this man believed. By taking the pills he had merely tranquilized himself, and when he came off them he returned to a problem he should have confronted a long time ago.
Toby: And maybe that’s what’s happened to me? I’ve taken a drug that’s interfered with my natural responses, and this may stack up problems for me in the future?
Colleague: This is of course a possibility. So at the very least I think it is something we should take seriously and explore …
4
The vision of antidepressants I have just articulated is not the vision embraced by mainstream psychiatry. In fact, as I’ve learned from experience, the above vision of antidepressants makes many conservative psychiatrists turn as red as tomatoes. But why is this so? What gets them so upset? The obvious answer is that it flatly contradicts their mainstream view, which is broadly consistent with that of the pharmaceutical industry.
So to understand that mainstream view and how it differs from the one above, let us talk for a moment to Dr. Joanna Moncrieff, a psychiatrist and senior researcher in the Department of Mental Health Science at University College London.
Moncrieff is today considered one of the most exciting figures in antidepressant research, earning a reputation almost as notorious as Irving Kirsch’s for upsetting the status quo. As I sat with Moncrieff in her university office, sipping coffee and talking louder than usual to be heard over the drilling outside, she was more than eager to explain to me the difference between the vision of drugs largely embraced by the psychiatric establishment (a vision called the “disease-centered model”), and the vision of antidepressants outlined above (a vision she calls the “drug-centered model”). She traced their differences in the following way:
“In the disease-centered model,” began Moncrieff, “people are assumed to have a mental disease, a problem in their brain. And drugs are thought to be effective because they rectify or reverse that underlying brain problem in some way. This is the dominant model in psychiatry and the one that best serves psychiatric interests.
“But the drug-centered model,” Moncrieff continued, “offers an entirely different way of understanding how these drugs work. It rather emphasizes that drugs are drugs; they are chemical substances that are foreign to the human body but which affect the way people think and feel. They have psychoactive properties, just like recreational drugs do, which alter the way the body functions at a physiological level. So the drug-centered model does not say that psychiatric drugs heal brain problems, like the disease model claims; it rather says they alter people’s states of mind in ways that may or may not be helpful.”
The interesting thing about the drug-centered model is that while there are growing numbers of psychiatric nurses, psychotherapists, and clinical psychologists who accept this version of how psychiatric drugs work, at the heart of the psychiatric establishment there is still considerable resistance to this view. “There are many psychiatrists who find the drug-centered model extremely challenging and simply don’t want to hear it,” said Moncrieff candidly. “This is because it fundamentally undermines the notion upon which modern psychiatry is based: the idea that mental disorders are brain-based diseases which psychiatric drugs can remedy in the same way medical drugs remedy physical problems.”
Moncrieff’s own academic research has shown that this current and widespread resistance to the drug-centered model has not always been so strong. “Prior to the 1950s, psychiatric drugs weren’t understood to act upon underlying diseases like they are today. They were seen as drugs that would pep you up. They were accepted as sticking plasters or uplifters that might at best be able to suppress symptoms for a period, but never were they seen as reversing a disease state.”
But this all changed, Moncrieff explained to me, when in the 1950s the drug-centered model began to be discredited. “This happened because the pills being used at that time [tranquilizers like Valium and Librium] were discovered to have terrible withdrawal effects. It also became obvious that these pills had been doled out to millions of people who were unhappy with their lives, particularly women who were trapped in miserable marriages. So once people started to realize that these pills had been used to suppress appropriate emotional responses to unhappy situations, that whole drug-centered model of taking pep pills to pick you up fell into disrepute.”
Moncrieff therefore sees the rise of the disease-centered model as filling a vacuum left by the demise of the drug-centered model. “With the growing popularity of the older antidepressants during the 1960s, ’70s, and ’80s, the diseased-centered model began to take over,” continued Moncrieff. “This was especially the case in the 1990s, when the new SSRI antidepressants came on the scene. The drug companies were trying to capture that huge market of people who once took tranquilizers. But because the old model of how drugs work had been tarnished, they needed a new model to reassert their value and necessity. So now these drugs were cast as curing us rather than changing us.
“And that’s where the idea of the chemical imbalance came in. It was perfect because it implied that these drugs actually corrected a defect in the brain. If you have a brain disorder, a chemical imbalance, and this pill is going to correct that imbalance, then obviously you must take it. Few questioned whether this new way of thinking totally obscured what these drugs really do. And this unthinking acceptance of the disease-centered view has dominated mainstream psychiatry for the last twenty or thirty years.”
5
Having now heard my imaginary exchange with Toby and my real one with Moncrieff, I imagine that some of you could now be feeling a little confused. After all, only two chapters ago we saw how Irving Kirsch’s research revealed that antidepressants work almost no better than placebo pills. And yet, in this current chapter, we have understood antidepressants as altering how we feel and behave. So is there a contradiction here? Can Moncrieff’s view—that pills change us—be reconciled with Kirsch’s view that they help us little better than sugar pills? I decided to put this question to Moncrieff.
“I actually think our work is complimentary, not contradictory,” Moncrieff answered decisively. “I agree with Kirsch that the majority of benefit from these pills is due to the placebo effect. But also remember that Kirsch’s research shows that active drugs can sometimes work fractionally better than placebos, especially with people who are severely depressed. And that’s where the drug-centered model comes in. It can explain this small difference in terms of the psychoactive effects real drugs have. Either they produce uncomfortable side effects that convince people they’re on the real drug (which in turn makes the placebo effect greater) or some of these drugs are so sedative that they put people into such a fog that they can no longer feel depressed or anything else.”
A recent study published in the British Journal of Psychiatry by a team of researchers from Oxford University strongly confirms the view that most psychoactive effects are neither useful nor beneficial.67 To reach this conclusion, the researchers assessed thirty-eight patients who had taken SSRI antidepressants for periods between three and forty-eight months (the median length being twenty-three months). The researchers then undertook in-depth interviews with all of the patients to find out how the pills affected them. The results they uncovered are so at odds with the modern myth of the “happy pill” that it is worth paraphrasing them almost in full:
· • Most participants described a general reduction in the intensity of all the emotions that they experienced, using words like “dulled,” “numbed,” “flattened,” or completely “blocked” to capture how they felt.
· • A few participants described feeling no emotions at all, while others reported their emotional experience had become more “cognitive” or “intellectual.”
· • A few participants described how the emotions that were at times present seemed “unreal,” “fake,” or “artificial.” And almost all participants, paradoxically, described a reduction in their positive emotions, including a reduction in emotions like happiness, enjoyment, excitement, anticipation, passion, love, affection, and enthusiasm.
· • Most participants also described feeling emotionally detached or disconnected from their surroundings. Most also described this detachment as extending to a detachment from other people. Specifically, they felt reduced sympathy and empathy, and felt detached during social interactions. Many participants also described an emotional detachment from their friends and family, including their partners or children.
· • Almost all participants described not caring about things that used to matter to them. They cared less about themselves, about other people, and about the consequences of their actions. Not caring could have both helpful and unhelpful consequences: it could reduce the sense of pressure and stress, but it could also increase the likelihood that important tasks were neglected.
· • Many participants described a general feeling of indifference to things in life that used to matter to them. Some felt they just did not care as much about the consequences to themselves of their behavior. A few participants went further, mentioning thoughts of self-harm or suicide that they related to their emotional detachment and numbness. One participant had started to self-harm in an effort to feel emotion. Many participants reported not caring as much about others, being less sensitive or courteous toward other people, having reduced concern for others’ feelings, and reduced concern about other people’s opinions of them. Some participants described being less concerned or even unable to care about responsibilities in their everyday lives.
· • All participants experienced a reduction of intensity or frequency of negative emotions. Most considered that at some stage the reduction in negative emotions was beneficial to them, bringing relief from distressing negative emotions like emotional distress, anger, irritability, aggression, anxiety, worry, or fear. Although this reduction was usually at some stage a relief, many participants also reported it impaired their quality of life. Participants described the need to be able to feel negative emotions when appropriate, such as grief or concern. Some were unable to respond with negative emotions, such as being unable to cry when this would have been appropriate or respond appropriately to bad news.
· • Some participants felt their personality had changed in some way. They felt they were not the person that they used to be. Participants also reported that specific aspects of their personality and, in particular, emotional aspects had been changed or lost. Some participants believed that at times their antidepressant had made them behave out of character. One participant believed that the medication had changed their personality permanently, having a lasting effect beyond finishing their medication.
When reading this study of how antidepressants make people feel, Toby’s reaction to his pills suddenly seems less idiosyncratic. In fact, because Moncrieff is so familiar with research like the above, when I told her about Toby’s experience she was completely unsurprised. “We know these pills can have this sort of numbing effect, creating a kind of emotional disengagement,” she said, “and sometimes this disengagement can also lead to a kind of dis-inhibition. Because people aren’t in touch with their normal range of emotions, they can start to do odd things, like the man Toby you’re describing.”
This final point about pills making us do “odd things” crops up again and again in the clinical research. Like Toby, or the woman on Kilroy’s show, or the people surveyed in the research we’ve just seen, these pills can severely knock us off center. To illustrate the nature of this, let’s have a quick look at some examples of such drug-induced behavior, as explored by Dr. Simon Sobo in his work. Sobo is a psychiatrist who has spent years documenting the strange and unwanted effects these pills can unleash.
Among the various examples Sobo provides is a female patient of his who worked as a computer consultant. She had very low self-esteem generally, and at work felt she wasn’t as capable with computers as her five male colleagues. She needed constant reassurance, and when things went wrong she’d punish herself with violent self-accusations.
Yet on an SSRI antidepressant, things changed. She acknowledged that she wasn’t as good with computers as her colleagues, but that she wasn’t that bad either. More important, she realized she was necessary to her team. She was the only one with sufficient social skills to handle their clients. She was now also able to ask questions at conferences without feeling foolish.
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.