What Americans Aren’t Told About Psychiatric Medications | Robert Whitaker

[RUSH TRANSCRIPT BELOW] For the past half century, Americans have been told that psychiatric drugs fix chemical imbalances in the brain. But this is nothing but a myth, says journalist Robert Whitaker.

Whitaker is the publisher of MadInAmerica.com and is known for his influential critiques of modern psychiatry and psychiatric drug treatment.

It was hypothesized that depression was due to too little serotonin and that schizophrenia was caused by too much dopamine—and that drugs could fix that, just like insulin for diabetes. But that was never backed up by evidence, Whitaker said.

“That was the story that was used to sell a whole second generation of psychiatric drugs and dramatically expand the psychiatric enterprise worldwide,” he said.

In 1999, Whitaker co-wrote a series of articles for the Boston Globe on psychiatric research and became a finalist for the 1999 Pulitzer Prize for Public Service, thereby establishing his reputation in this field. Later, he served as director of publications at Harvard Medical School.

“We have this story that we’re making great progress in diagnosing and treating mental disorders,” he told me.

U.S. spending on treating mental disorders has risen substantially over the past decades, from tens of billions in the late 1980s to more than $100 billion per year today. But there is no evidence, he says, that these drugs improve long-term outcomes. On the contrary, there is plenty of evidence that psychiatric drugs can actually make things worse, he says.

“They actually cause chemical imbalances, increase the chronicity of disorders, increase functional impairment, and you see rising disability rates wherever you see this paradigm of care adopted,” he says.

Certain antipsychotics for schizophrenia, for instance, can actually reduce brain tissue, particularly in the first year, and that’s been associated with cognitive decline and a worsening of symptoms.

Evidence shows that other countries, including developing nations, that have not adopted this same approach have seen much better outcomes, he says.

In this episode, he breaks down his findings from decades of studying this issue. Whitaker is the author of “Mad in America” and “Anatomy of an Epidemic.”

Views expressed in this video are opinions of the host and the guest, and do not necessarily reflect the views of The Epoch Times.

RUSH TRANSCRIPT

Jan Jekielek:

Robert Whitaker, such a pleasure to have you on American Thought Leaders.

Robert Whitaker:

Well, thanks for inviting me. It’s a pleasure to be here.

Mr. Jekielek:

What would you say is the biggest myth around mental health or psychiatry today?

Mr. Whitaker:

I think the myth that has become most well known is the story that the drugs fix chemical imbalances in the brain. So, for example, depression was due to too little serotonin, and drugs that upsurge energy activity in the brain therefore normalize it, like insulin for diabetes. And that was the story that was used to sell a whole second generation of psychiatric drugs and dramatically expand the psychiatric enterprise worldwide, if you look at the number of people getting treated. 

The thing was, even as they were pitching that, and it really began to be pitched in the United States in the late 1980s and early 1990s, a drug called Prozac came to market in 1988. It was presented to the public as an incredibly novel drug, a breakthrough medication because it fixes a serotonin imbalance in the brain. 

The irony is that was a hypothesis, this idea of chemical imbalances, that was born in the 1960s based on an understanding of how the drugs acted on the brain. So, for example, the first generation of antidepressants both blocked the normal removal of serotonin from that tiny gap, the synaptic gap between neurons. And so they said, oh, look, it’s boosting serotonin reactivity. Maybe depression is due to too little serotonin. That’s in 1965. 

Well, they then had to investigate whether people with depression actually have too little serotonin before they go on the drugs. Now, as early as the 1970s, they had to find methods for making that investigation. But even by the early 1970s or late 1970s, people were saying, we aren’t really finding this. In 1984, I believe it was, the NIMH [National Institute of Mental Health] did a big study on this question. And they said, we’re not finding any lesion in the serotonergic system that is abnormal in any way. 

In 1998, I believe it was, the American Psychiatric Association’s own textbook said that that story, that idea, the chemical imbalance theory of depression, was no longer valid. They said, we’ve investigated it many ways and we just haven’t found that serotonin is abnormally low in people with depression.

Mr. Jekielek:

You know, if I may jump in just for a moment, that is astonishing because I suspect that today, I mean, I certainly took this as an obvious fact for years and so do many people, and I suspect even psychiatrists and doctors that are prescribing psychiatric medication. 

Mr. Whitaker:

So this is what was happening in the research literature and actually in psychiatry’s own textbooks when the people that really knew were summarizing the sort of the history of investigation into the low serotonin theory. And then, for example, there’s a famous guy, Stephen Stahl, who writes a book called, Essential Psychopharmacology. It is sort of the book for brand new psychiatrists. And he said, you know, we’ve looked for these and we have not found them. The monoamine thesis, serotonin is a monoamine, it’s just not real. So he said that in 2002. 

You can find Kenneth Kendler in 2004, who was an editor of Psychological Medicine, a big researcher in this field, and he said this: we have hunted for big simple neurochemical explanations for mental disorders and have not found them. But the public, that’s not what the public was told. The public was told, and you can follow the public pronouncements of the American Psychiatric Association [APA], which was that they had found this, and you saw a website saying that depression is due to too little serotonin; the drugs fix that like insulin for diabetes. So what happened is there was a valid hypothesis. It was investigated, not found to be true. 

However, that story, the American Psychiatric Association and the pharmaceutical companies understood was a great way to promote treatment, the selling of drugs, and also elevate the prestige of psychiatry because they now had, like other areas of medicine, a pathology they could talk about, which meant they were real doctors and they had an antidote to a pathology. Now, that’s a story that’s going to greatly boost the legitimacy and the respect society has for a discipline, right? Because they made this great medical advance, which fits into a larger narrative in Western society. 

But yes, that’s the biggest myth, and it’s a profound myth, but it’s because telling people there’s something wrong inside your head with your chemistry, and you need this drug to fix that abnormality, when in fact, it was a hypothesis born from understanding how the drugs act on the brain, investigated, and basically fell flat early on in the 70s, 80s, and 90s, and was discarded by the late 1990s within the American Psychiatric Association’s own textbook.

But we weren’t told, when I say we, we the public weren’t told that. In the United States, you can advertise your drugs on TV, right? So there were advertisements that showed you take this antidepressant and it fixed the chemical imbalance, and then the next thing you know, you’re walking on a beach with a beautiful woman or a beautiful man, right? So we had that part of telling the story. 

But we also had a guild, meaning the American Psychiatric Association, pronouncing, telling the American public that this was what caused depression and our drugs fixed it. And you can chart those sentiments. You can see that they were telling this on their website. They even put out a press release in 2005, 2006 saying that psychiatrists are experts in fixing chemical imbalances in the brain. 

So that’s a long-winded story to tell of how this very simple saying—it’s sort of a way to sell drugs basically—got started in the United States and then spread like a meme around the world until the next thing you know, people around the world were talking about chemical imbalances. But it never had scientific discovery behind it, not the low serotonin theory of depression. 

Mr. Jekielek:

Before I ask you about what these drugs actually do or what we know they do, why don’t you tell me a little bit about yourself and your background and how you got into this space? 

Mr. Whitaker:

My background was as a newspaper reporter. Starting in 1988, I began covering medicine and science for a newspaper called the Times Union in Albany, New York. I actually left daily journalism in 1994, and two things happened. First, I became director of publications at Harvard Medical School. This was at a time when people were talking about evidence-based medicine. We have to adopt evidence-based medicine. One of the thoughts about evidence-based medicine is that doctors can be deluded about the merits of their therapies based on their clinical perceptions. Okay, so you have to have science telling you what really is the best way to do things. That was very prominent in the early 1990s.

The second thing that happened was this: I co-founded a publishing company in 1994 called CenterWatch that looked at the business of clinical trials. The business was dramatic in the clinical testing of new drugs. The point of looking at it from a business perspective is that the spending on clinical trials was dramatically increasing in the late 1980s and 1990s, and it became a field of opportunity. Both academic centers wanted to get pharmaceutical money for testing the drugs. Individual doctors said, hey, listen, I have patients. I can enroll my patients in your clinical trials. So we were actually writing—and I think this is important—about the business opportunities of getting involved in clinical trials of new drugs. 

The problem was, as I began reporting on that, I began understanding that having such a financial environment for the testing of drugs was corrupting the testing of drugs and corrupting what the public was told about the actual results from those trials. Those adverse effects were being hidden, and the efficacy was being exaggerated, that sort of thing. That corruption that I began to write about was most noticeable in psychiatry. That’s how I became interested in psychiatry, because the clinical trials of their new drugs were particularly biased by design, particularly. notable for an exaggerated sense of efficacy and safety as they were promoted to the public. 

And the way I knew that is I used freedom of information requests to get what the FDA [U.S. Food and Drug Administration] said about these new drugs when the companies were making an application for, say, the new atypicals. And what you saw there with that freedom of information request was that the actual study data was very mixed. The efficacy was pretty marginal. And there were a lot of adverse events that the FDA investigators were saying you were going to see. But that wasn’t part of the message given to the public. 

So I then went to the Boston Globe, for whom I’d written before, and said, I’ll do a series on abuses of psychiatric patients in research settings because there were also some NIMH trials that were quite abusive towards the patients, and we can talk about. Now, one of the keys here, as you asked me this question, is at this time, I still believed in the chemical imbalance story, so much so that one of the things in the Boston Globe series that we wrote looked at studies in schizophrenia patients in which they took people who were doing fairly well on antipsychotics, and then they conducted what are known as relapse studies.

They took half the people who were maintained on the drug and half the people who were taken off the drug with great regularity. Those who were taken off the drug relapsed at a higher rate. And so we said, and when I called people up, they said, yes, antipsychotics fix a dopamine imbalance in the brain like insulin for diabetes. Would you fund studies that took a drug away from people that supposedly fixed a pathology to see how quickly they became sick again? You would never withdraw insulin from a diabetic to see how fast they became sick again. 

So I tell this story to explain that I was a believer in the chemical imbalance story. I was a believer in, therefore, that model of progress that we now had drugs that fixed known chemical imbalances. What happened, though, was this. That narrative that I was a believer in was a narrative of modern, amazing progress. And by the way, in my opinion, if they had actually discovered the molecule that caused madness and could fix it, or the molecule that caused depression and could fix it, I would say that’s the greatest medical discovery in history, given how complex the human brain is, right? 

But what happened was, as that series was being published, I came upon two studies that belied that narrative of progress. One was a study by Harvard researchers, published in 1994, which looked at longer-term outcomes for schizophrenia patients. They said these outcomes had declined since the 1970s, not improved, and were now no better than they had been in the first third of the 20th century. Now, we look back at the first third of the 20th century as these dark ages, right? So how can it be that with these modern drugs that fix chemical imbalances, we are no better off than when they put people in showers and did all sorts of harsh somatic treatments? Okay, that was number one. 

The second was I then stumbled upon studies done by the World Health Organization [WHO] cross-cultural studies that compared outcomes in three developing countries—India, Colombia, and Nigeria—to longer-term outcomes in the U.S. and 500 developed countries. Now, everybody was diagnosed with schizophrenia by Western doctors in the studies. What they found after the first study was that the outcomes in the developing countries were much, much better than in the developed countries. So much so that they concluded that living in a developed country is a strong predictor that you won’t have a good outcome if you’re diagnosed with schizophrenia. 

And I was saying, what? We’re so proud of our medicine. Why would you do better if you’re in India or Nigeria than in the U.S. with all our modern medicine? It was a conundrum, basically, a question I wanted to investigate further.So what the World Health Organization investigators did at that time, after the first such study, hypothesized that maybe the reason for the much better outcomes in the developing countries is that the patients are more medication compliant. They take their antipsychotics with great regularity. 

Now, that’s a valid hypothesis. If the drugs are supposed to be so helpful and so essential to treating the disorder or disease, whatever you want to call it, then compliance should be associated with a better outcome. So they measured medication use in the second study, and here’s what they found. In the developing countries, they used the drugs acutely, short-term, but not chronically. 

So only a very low percentage were maintained on the drugs. In the U.S. and the other developed countries, of course, that was the standard of care. So suddenly now, I was confronted with studies by the World Health Organization, which I think we all agree is a prominent health organization in the world, that found much better outcomes in poor countries where they didn’t use the drugs long-term. So this too belied what I knew to be true, right?

Now what happened is, after that Boston Globe series, I got a contract to write a book, which became Mad in America. It was really meant to investigate this question: Why would living in a developed country lead to poor outcomes for people diagnosed with schizophrenia, because we had this model of progress? 

So the very first thing I did was start calling up people, including some of the people I had called for the Boston Globe series, who had told me that the drugs fixed the chemical imbalance in the brain. I said, can you just show me where you found that too much dopamine is the cause of schizophrenia? Or can you show me where you actually found that too little serotonin is the cause of depression? 

And I swear to God, here’s what they said. Oh, we didn’t actually find that; that’s a metaphor for explaining why they should take the drugs like insulin for diabetes. And I said, well, I understand that like insulin for diabetes is a metaphor, but surely you actually found these chemical imbalances, and I just want to read the research where you did. The first person said no, we didn’t really find it; the second person said no, we didn’t really find it. 

Then I went to the makers of Risperdal, which is a second-generation atypical antipsychotic, and Risperdal was being marketed as fixing not only a dopamine imbalance in the brain but also a serotonin imbalance in the brain. I actually managed at that time to get to the actual researchers. And you know what they said? Oh yes, that’s just such nonsense. You know, we’re just sort of embarrassed that we say this. 

So as I began to write a report on Mad in America, which would trace the treatment of the seriously mentally ill in the United States from colonial times until today, I started with this sense that we have a modern narrative of progress that isn’t science-based. And so that’s how I got into this because I had one belief system. I had reported on that belief system. 

I had been rewarded for that belief system because that Boston Globe series was a finalist for the Pulitzer Prize in public service. And yet now after that, I’m suddenly doubting whether one element of that, the relapse studies, were really as abusive as they might have been, because maybe there was a good reason to see if people could come off.

So for your listeners, it’s important to know. I was a believer in the narrative. I was a reporter who called up scientists and quoted what they said, calling up the leading figures in any particular field of medicine. I was rewarded for that. And I began down a different path of challenging that narrative or questioning that narrative when I began to find evidence that belied that narrative of progress.

Mr. Jekielek:

It seems to be very rare in the field right now to question this narrative. I’m aware of, you know, a handful of people that do it very publicly. It’s sort of shocking. Why do you think that is? 

Mr. Whitaker:

Well, there are two different reasons. So let’s say you’re a psychiatrist, and you begin challenging the narrative that governs your field, and that the field itself has built its reputation around. Now, what’s going to happen? Are they going to listen to you? Or are they going to kill the messenger? Are they going to oust you from the tribe? Now, in the United States, the leading schizophrenia doctor at the NIMH, the head of schizophrenia studies in the 1970s, was a man named Loren Mosher, okay? 

And he ran a study, a very famous study in the 70s called the Soteria House, where they took, and it was a randomized study, where they took newly diagnosed psychotic schizophrenia patients, and they were either treated conventionally in the hospital with drugs, or they were taken to a house, which was called the Soteria House, an ordinary house staffed by ordinary people. 

And the idea here was that by being with people, their psychosis would abate, and they could learn to be with others. The way medications were used in that house was they didn’t put them on antipsychotics right away because they wanted them to be emotionally engaged with each other and with the staff. Now, if people weren’t getting better after some time, they did use dosages, and then they would see who could come off. So it was a selective use model.

Now, what happened? That model, the Soteria arm, had equally good short-term outcomes, and the abatement of psychotic symptoms was just as good over six weeks there as in the hospital, and they had better two-year outcomes. So Loren Mosher now says, in terms of medication use, 40 percent never used the drugs, 40 percent used them temporarily, and only 20 percent long-term, okay? He says we need to rethink the use of these drugs, okay? Because clearly many people can do better without them and that a selective use model, in fact, would lead to better aggregate outcomes. 

So what happened? They ran this experiment for 10 years; they did a second house to show that it could be replicated. What happened to Loren Mosher? He was fired from his position and pushed out. And why was he fired? He was fired because that story was so threatening to the story that the American Psychiatric Association guild wanted to tell, which was that its drugs were very effective because that’s what’s becoming their product, not talk therapy, but drugs. His research and a couple of other studies of this type really undercut that story. 

Now, they had two chances there, American Psychiatric Association: either listen to the science and respond, which threatened the guild’s image, or oust that person. Well, they chose to oust that person. And I can tell you other such stories in terms of what happens to people, professionals. who once upon a time were seen as leading scientists, good scientists, and said, wait a minute, this science doesn’t support the story that we’re telling. Well, guild interests are very strong. The financial interests are very strong. In psychiatry, we have those guild interests merging with the interests of the pharmaceutical companies. 

So you can really come under attack as a professional, no matter what your reputation was before, if you begin to break with your tribe. And I use tribe deliberately. It becomes a tribe, a medical tribe. So that’s an explanation for why professionals are hesitant to break with their tribe. It’s not good for their career. 

Mr. Jekielek:

Before you give me the other reason, what happened to you after you published Mad in America? 

Mr. Whitaker:

Okay, so this is the second part. So I know I’m a reporter, right? It’s really interesting if you’re a reporter. When you cover—like, so I had a sort of normal start, I didn’t just start covering science, right, and medicine, I started covering business and politics. And when you’re covering business and politics, you’re sort of trained to say, you know, don’t trust everything they say, okay? Because they’re selling a story through you to the public. And try to use documents to sort of like really see if what’s happening with the business or the politicians. But don’t just go call people up and trust what they’re saying, okay? 

Then you get moved to the medical desk or the science desk. And all of a sudden, you’re sort of given different walking orders. And your walking orders are this: these people are really brilliant, these people in white coats, biologists and all. And they’re people of integrity. They love science, and they love the beauty of science, and they want to maintain the integrity, and they’re open-minded people, okay? 

Theoretically, science is a story of the evolution of one idea replacing the other, okay? Your job is to interpret what they say so it’s understandable for a lay public. You’re no longer expected to question what you’re being told because they’re elevated. They’re now, you know, people in white coats; they have an elevated status, a prestigious status. This is who we believe in our society: the scientists, the medical experts, okay? 

Now, you’re a reporter, and you’re going to begin undercutting them? Newspapers don’t want to; they’re really loath to do that because the editors don’t know the research, the actual research literature. They know the conventional narrative. They know this is the narrative they sell to the public. 

And now you as a reporter are saying, but wait a minute, that’s not based in science. They’re not really—or that not only based in science, that their own science contradicts it. They’re just really not in a position to be open-minded to that because they don’t have enough knowledge about the actual literature or even how to read it. And it goes against an even much larger narrative, which is that we trust scientists and we trust medical doctors, especially if you go back 25 years ago. 

So what happened to me, I think it’s the real key to understand, is in that first book, Mad in America, it goes from colonial times until today, sort of talking about the abuses up to the time when antipsychotics arrived in asylum medicine, which was in 1955. You can talk about the dark old days, okay? Because that’s sort of part of the official history. 

But then the idea is we had the psychopharmacological revolution, this great advance in care. Now, what I did in this going forward was show that there wasn’t a great advance in care, as documented in their own research literature, as documented in NIMH-funded studies. 

What I followed was NIMH-funded research. And as you follow that research across time, and I’ll talk about this tomorrow, you find a very different narrative. You find a narrative where right away, there was worry that maybe antipsychotics were increasing the chronicity of schizophrenia. By 1980, there was even a thought—no, there was evidence and a conclusion—that it seems that the drugs, what antipsychotics do, is block dopamine receptors. In response to that, your brain goes through this compensatory response, trying to maintain a homeostatic equilibrium. And it does that by increasing the density of its dopamine receptors. 

Your brain now is more biologically vulnerable to psychosis than it was in the first place. And the researchers concluded this has two problems. When you try to come off the drugs, it’s not that the natural disorder returns, of course the disorder does, but rather you’re going to have this withdrawal effect. And if you stay on the drug because of this, you’re likely to become sort of chronically psychotic. 

Mr. Jekielek:

You’re basically telling me this is causing brain damage, aren’t you? 

Mr. Whitaker:

Well, yes, the antipsychotics cause brain change. Two things, if you want to talk about antipsychotics, then I’ll finish up my story. Antipsychotics are known to cause abnormalities in neurotransmission, okay? So like antidepressants. And there’s a 1996 paper by Steven Hyman, who was the director of the NIMH at that time, that sums all this up. So you have something, a drug that perturbs the normal activity of neurotransmitters in the brain, okay? It either blocks receptors or it blocks the reuptake of that molecule from the synaptic gap.

Now your brain, being this extraordinary neuroplastic organ, what does it do? It goes through some compensatory adaptations to try to maintain this normal functioning. And as Steven Hyman said, at the end of this compensatory process, your brain is operating in a manner that is both qualitatively and quantitatively different from normal. So rather than being normalizing drugs, which are abnormalizing drugs, that was seen as a problem regarding why these drugs could make you more biologically vulnerable to psychosis.

By the way, the antidepressants, if you look in the research literature, they say it’s this compensatory process that may be the reason you end up with a greater chronicity of depression once you go on that drug. But there’s a second element: Since you talk about brain damage with antipsychotics, in the 1990s, of course, what do we get in medicine? We get MRI technology, right? So now with MRI technology, we can measure brain volumes.

Now, a very famous researcher, who was editor-in-chief of the American Journal of Psychiatry, so this isn’t some critic, named Nancy Andreasen. She came up with a theory that schizophrenia is a neurodegenerative disease characterized by brain volume loss, okay? So she begins a big study of, I think, 500 patients, young patients diagnosed with schizophrenia. And she finds that, especially during the first year, there is a shrinkage of brain tissue, a pretty notable, like 6 to 7 percent in volume.

And then she reports, but she’s saying at this time, that’s the disease, okay? Then she reports, as this brain shrinkage happens, you get a worsening of the negative symptoms, you get a worsening of cognitive function, and you get most functional impairment. So she’s saying this is our problem. The drugs don’t stop that brain shrinkage. 

However, there have been researchers giving antipsychotics, both the first generation and second generation antipsychotics, to macaque monkeys, and they suffered the same brain shrinkage. Now, monkeys don’t have schizophrenia. So then the question became, is it the drug or the disease that causes the brain shrinkage? 

So Nancy Andreasen and researchers went back and said, yes, it’s the drug. And now there have been something like 26 other studies saying it’s the drugs, antipsychotics, older drugs and newer drugs. So you probably haven’t heard of that. The public’s not told of this, but in the research literature, there’s a line of research that you can trace that shows that the drugs shrink brain tissue, particularly in the first year, and that shrinkage, not surprisingly, is associated with a worsening of symptoms, functional impairments, etc.

Now, you ask what happened to me. So I had a good reputation as a journalist. That series for The Boston Globe was a finalist for the Pulitzer Prize. I won some other awards. The book came out and it got a mixed reaction. There were some actually nice reviews by non-psychiatrists, but then there were some really brutal attacks. 

My favorite one was by a psychiatrist named Latorre. He said he used to be a good journalist, but now it seems like he’s writing like he’s a Scientologist, which is a way of saying that you can’t trust a thing he’s saying. So there was a real attack on my character as a journalist, you know what I mean? And my agent at that time, because at that time I just wanted to make a living writing books, she said to me, Bob, don’t write about psychiatry anymore. It’s too controversial. It was definitely some pretty brutal attacks. 

And I will say something personally as well. Sometimes your friends even began looking at you with a little bit of like, did you go off the deep end here, Bob? Is this a conspiracy? Because they don’t know, right? And so they think that maybe you went off the deep end, you have some anti-drug bias, and all you’ve done is follow the research literature. So it was tough. But I will say two things happened.

There were some nice reviews. It was sort of cited eventually as one of the best science books of that year, 2002. And most important of all was people with lived experience, people who’ve had these diagnoses said, thank God someone finally told our story. You actually listened to us. So that was quite rewarding. Anyway, I would say I was basically banned from writing about psychiatry at that point from major media because I was seen as biased. 

And then when I wrote Anatomy, I wrote two other books that sort of rejuvenated my reputation as a reliable narrator of science. And then I returned with Anatomy of an Epidemic. Anatomy of an Epidemic is a frontal assault on that narrative, okay, because it’s looking at how these drugs alter long-term outcomes. The first review that appeared about five minutes after midnight on the publication date likened me to a south African dictator who, by virtue of denying that AIDS was caused by a virus, had caused hundreds of thousands of people to die, and my book was as dangerous as that south African dictator. So I was likened to an AIDS denier. Five minutes later, I got my radio interviews canceled, no more newspaper reviews. It was a very effective way to shut down that book initially.

Mr. Jekielek:

So I first came across Anatomy of an Epidemic in Laura Delano’s book, where she, of course, was in the system for years on all sorts of cocktails of psychiatric medications. And she came across the book. It was kind of an emotional, seminal moment in the book because she realizes that everything she believed might not be entirely true. I’m guessing you’ve gotten a few people who have reached out to you.

Mr. Whitaker:

Yes, this is what has been the most rewarding thing of my professional life or just one of the most rewarding things in my whole life. I have received so many calls and emails that say, like, I read your book and my life changed because I saw myself not as someone chronically ill, which is the story, but as someone who got psychiatrized and diagnosed because we also greatly expanded the use of diagnoses. 

And then the next thing you know, I went down this rabbit hole of drugs. I got worse and worse, and I was told I was treatment resistant or whatever, and I was seriously ill. And then I saw when I read your book, a different past for myself, that in fact, I was a relatively abnormal person. I was having a difficult time, or even if I was having an extremely difficult time, I could have had every chance to have that as an episode, and my life would have been totally different. And like many people like Laura, then, with that new understanding of their past, could envision a different narrative going forward. 

Of course, what Laura envisioned was a narrative off medication and just sort of resuming a real life and not a life as a mental patient. And I’ve heard that story over and over again. And the reason it’s convincing is because what they can do is see in the narrative of science that I tell with all these citations, and they can go to those sources, and they can see that science was, in fact, not telling of chemical imbalances, not telling of discrete diseases, like bipolar is necessarily very different from schizophrenia, and of drugs that can cause two things: a chronification of symptoms, greater functional impairment, and a movement from a less severe diagnosis to a more severe diagnosis. 

You see people getting initially a diagnosis of anxiety or depression and the next thing you know they got a bipolar diagnosis. Same thing with ADHD [Attention deficit hyperactivity disorder]; you can move from ADHD to bipolar. So they suddenly had a tale of science that allowed them to understand their past differently and, equally important, an optimistic vision for what could be their future.

Mr. Jekielek:

So the thesis of the anatomy of an epidemic or an element of the thesis is simply that it’s the increased medications that are now interacting with each other that often will result in these symptoms that look like mental illness. Or at least that’s what I got out of it, okay? But why don’t you tell me what?

Mr. Whitaker:

Yes, it’s not necessarily that. Of course, people end up on polypharmacy, and that’s a mess because the drugs are interacting with each other. The major thesis of this is this: the way the book was conceptualized. We have this story that we’re making great progress in diagnosing and treating mental disorders, right? And we have drugs that fix chemical imbalances. Now, normally in medicine, if you have a disease where you get better at diagnosing it and you have effective treatments for it, you’ll see the burden that disease takes on society diminish, right? 

But instead, we get 1987; Prozac comes to market, first- to second-generation drugs. And rather than diminishing the burden of mental disorders, as measured by people going on government disability, it has skyrocketed. It increased from like 1.2 million adults in 1987 to around 4 million adults in 2007, which was when I began doing that. So that doesn’t make sense, right? 

So I raised the question: what does science tell us? What does the history of research tell us about the long-term impact of these drugs, these different classes of drugs—antipsychotics, antidepressants, benzodiazepines, stimulants? Because the evidence base that is cited to us doesn’t talk about long-term; it talks about short-term efficacy and that these relapse studies conducted in a subset of people show that you’re at a greater risk of relapse when you come off, at least for a period of time. 

But that doesn’t tell you how people are functioning. It doesn’t tell you what the natural course or the natural capacity to recover is. So I wanted to find out: what does science tell us about the long-term impact of these drugs? And so that’s what I looked at. And what you can find over and over again is a very different narrative than what’s told to the public. And that is a narrative that the drugs don’t fix chemical imbalances, but they, in fact, induce the very changes in the brain hypothesized to cause the problems. 

So, for example, low serotonin is always hypothesized to cause depression. Now you go on an antidepressant, which ups serotonergic activity and acts as an accelerator. So what does your brain do? It dials down its own serotonergic machinery and puts the brake on it to try to maintain an equilibrium. Got too much? So, accelerator, brake. 

But this deficiency in serotonergic transmission, this abnormally low level, that’s the very thing that was hypothesized to cause depression in the first place. So that’s the biggest irony of this whole story. The drugs actually induce an abnormality hypothesized to cause the problem in the first place. So the theme is this: A, what do the drugs really do to the brain?

Let’s follow that. And then let’s see, what does science tell us about how that affects the course of the disorder over time? And what you find is a narrative of science. This is really key. Yes, we only say, oh, we only listen to RCTs. But this is a narrative of science that’s coherent over time, from the moment that drugs are introduced till today. 

And what you find over and over again in research of many types—cross-cultural studies, MRI studies, some randomized studies, naturalistic studies, every type of study you can think of, we keep getting this final first conclusion that these drugs are increasing the chronicity of the disorder. Now, that doesn’t mean nobody does well. Some people do well, but you have to say…

Mr. Jekielek:

And the aggregate.

Mr. Whitaker:

And the aggregate. And how does that compare? How do the on-medication aggregate outcomes compare to, like, aggregate unmedicated outcomes or the natural capacity to recover? And you see greater chronicity; you see a greater risk of disability, and you know, and less ability to, like, you see greater unemployment, that sort of thing. That’s one thing you find, okay? And you find it with antipsychotics, you find it with antidepressants, stimulants. There was one trial that did show that the medicated kids were more likely to be functionally impaired later on. That was an in-eye image study. 

And then with bipolar, you find two things. It used to be a rare disorder. Even that used to be seen as an episodic disorder, by and large. And then we start—two things happen. We start expanding the boundaries for who we’re going to call bipolar, and we often start using multiple drugs. And you see this great increase in disability with bipolar, and you get the experts in manic depressive illness, which now is known as bipolar illness, saying, well, you know, our outcomes for bipolar illness have dramatically worsened compared to before. More cycling, more functional impairments, more unemployment, more disability. So even the experts there are saying, like, what’s going on? We’re having this worsening outcome for bipolar. 

So the theme of Anatomy of an Epidemic is this, writ large. Our society has organized its thinking, its behavior, how we raise children, how we think of psychiatric difficulties around the narrative of progress, of medical progress, of chemical imbalances and stuff, right? Of known diseases being given effective treatments. But that is a false narrative. And you can see why it was promoted. It promoted guild interests, pharmaceutical interests, that sort of thing. 

What you really see as a narrative of science is this other narrative of drugs that don’t fix chemical imbalances that actually cause chemical imbalances, increase the chronicity of disorders, increase functional impairment, and you see rising disability rates wherever you see this paradigm of care adopted in this increase in the use of psychiatric drugs. 

So it’s a story; it’s a book about how we, as a population, in essence, were betrayed by our leaders—our medical leaders in American psychiatry—who told us about this narrative of progress of chemical imbalances when their own research didn’t show it. And they also never promote research that actually does tell of the chronicity and tells of poor long-term outcomes. 

I’ll give you a very concrete example. The best longitudinal study we have of schizophrenia outcomes in modern times, in the drug era, was done by Martin Harrow and Thomas Jobe. Harrow is a psychologist; Jobe was a psychiatrist from Illinois. They recruited 200 patients into their study in the late 1970s. It’s a naturalistic study. 

Everybody in the two hospitals, one private and one public, is treated with drugs, okay, treated with antipsychotics, and they’re discharged. And they’re just going to be the researchers, heroin drug users, just going to follow them up at two years, two-and-a-half years, four-and-a-half years, seven-and-a-half years, 10 years, 15 years, and 20 years. 

And at each assessment, they’re going to see, are they using those antipsychotics? Are they symptomatic? Have they been in the hospital? How are they socially functioning? How’s their cognitive functioning? How’s their anxiety levels? And are they psychotic? Now, when they did this study, when they mounted this study, NIMH funded the best one in modern times, their hypothesis was we’ll find better outcomes in those that are medication compliant because that was the belief, right? 

So what they found, though, is that there were 64 schizophrenia patients and 81 with mild or psychotic disorders that stayed in the study for 15 years. What they found is among the 64 schizophrenia patients, there were about 25 who stopped taking their drugs by year two, okay? Any drugs, any antipsychotics. And that group was doing a little better in the aggregate at year two than the group taking drugs.

And then what happened between year two and four-and-a-half, their outcomes diverged. The group off medication got dramatically better, while those who were on drugs did not, such that the recovery rate, meaning no symptoms and working or in school, half-time and decent social life, was eight times higher for the group off medication, 40 percent vs. 5 percent. And there were other methods that showed that the spectrum of outcomes was just so much superior for the non-medicated group, working, that sort of thing. 

What happened when they tried to publish that? The editors wouldn’t publish it. They finally got it published in one journal. I forget which journal they managed to finally get it. It was in a UK journal, a Journal of Mental Health and Disease or something like that. American journals wouldn’t publish it. NIMH funded the best study we’ve ever had. They wouldn’t publish it. Why not? Because it’s so threatening to their narrative. 

And in the textbooks, you know what they say about the textbooks? In this American Psychiatric Association textbook, there was like one line for a while that said it showed that not everybody needed to be on the drugs long-term. They didn’t report the eightfold higher recovery rate. So that’s an example of what is kept from the public. Here was, you funded it, we funded it, the taxpayers funded it. It’s the best long-term study that’s been done in modern times. 

You know what they concluded in front of the American Psychiatric Association at the 2008 meeting? I was there. There’s Martin Harrow. I conclude that patients diagnosed with schizophrenia off antipsychotic medication long-term have significantly better global outcomes. That was his bottom line. Have you read about that in any newspaper? No. 

Mr. Jekielek:

It’s what you would call a statistically significant outcome.

Mr. Whitaker:

Oh my God. The differences were so dramatic. And they even published numerous times explaining what they thought was the biological mechanism. They looked at their data in different ways, everything they could. They ended up getting about five or six papers published. But none of this was ever promoted to practicing doctors or to the public. 

Now, they both died recently. And even in their obituaries, like Ira was famous enough that there was a small obituary in the New York Times. They still have never reported that there’s this eightfold higher recovery rate. Or that, here’s the most amazing thing of all, the schizophrenia patients off medication long-term had better aggregate outcomes than those with milder disorders who stayed on the drugs long-term.I’ll tell you a small, funny story, a little bit. 

So I went to that 2008 meeting, and I listened to Martin Harrow. And afterwards, he had published a chart with those different outcomes, but he had never put them together in one chart. He had one chart for schizophrenia on global assessment of function and one chart for the milder disorders. And I said, have you ever noticed that if you put these charts together, because it’s the same scale, your schizophrenia patients off medication are doing better than those with milder disorders? 

And he actually got quite mad at me at that time. I said, who are you? Are you against the drug? Do you have some bias here? And I said, no, I’m just asking you about your own data. Well, he was, and then he sort of relented. He said, off the record, you know, I had trouble getting this published. And I had to sort of lighten my own explanation. But what he did then is he went back to his own data, he and Thomas Jobe. They said, Whitaker is right. And he actually cited me in one of their final papers. 

And then one other thing that happened is after I published Anatomy and Epidemic, I did get some people saying we need more research on long-term outcomes. And I helped found a nonprofit called the Foundation for Excellence in Mental Health Care with the idea they would get money to fund long-term outcomes. Now, once that was started, I withdrew from it because I didn’t want it to be seen as tainted. And they actually provided funding to Martin Harrow and Thomas Jobe to do further research on their long-term outcomes. 

I mention that because I did that because I believe in science. I believe in data. And I believe that we did need more research into this sort of thing. And they have funded other types of research. But that tells you about the betrayal. The public deserves to hear whatever the results are, rather than the self-selected stuff and all this long-term stuff kept hidden from the public. And we can talk about the biggest antidepressant trial ever conducted because they did exactly that with the STAR*D [Sequenced Treatment Alternatives to Relieve Depression] trial. 

Mr. Jekielek:

You started telling me about this earlier. What do these drugs actually do? 

Mr. Whitaker:

Well, what they do, and this is what we’ll talk about, is the mechanism of antidepressants and antipsychotics. First of all, we’ll talk about what the mechanism of action is—the singular mechanism of action that is seen as characteristic—but the drugs actually have much broader effects than what is said to be the singular mechanism of action. So let’s talk about how neurons, first of all, communicate in the brain. 

You have a presynaptic neuron, right, that releases a molecule which we call a chemical messenger, a neurotransmitter. Serotonin is one; dopamine is one. They cross that very tiny gap between neurons and bind with receptors on the surface of the neuron, the cell that receives that message. And if it’s a molecule like serotonin or dopamine, they are known as excitatory molecules, neurotransmitters, which cause a second neuron to fire, okay? That’s how neurons communicate in the brain. You also have chemicals that can be released that prevent this neuron from firing or lower the firing of it. So what does serotonin do? Serotonin is released in that tiny gap, right? 

Now, in order for this messaging system to remain crisp, you have to remove that serotonin from the gap, right? And serotonin is removed from that gap in two ways. It is either taken back up into the presynaptic neuron and stored for later reuse, or an enzyme comes along and metabolizes it, and that serotonin metabolite is called off as waste, okay? What the first generation of antidepressants did is they blocked that normal reuptake of what are known as monoamines; serotonin is a monoamine. Or the monoamine oxidase inhibitors, they block the enzyme that metabolizes the monoamine. So both of them prevented the normal removal of serotonin. Serotonin stays longer in that gap. That’s theoretical.

Mr. Jekielek:

Hence the name SSRI [Selective Serotonin Reuptake Inhibitors]. 

Mr. Whitaker:

Yes, and it’s going to cause this neuron to fire more rapidly. Dopamine, what the antipsychotics do is that molecule sits in the receptors on the postsynaptic neuron, but it’s like pouring glue into the lock. It’s not actually activating that receptor. It’s just blocking it. So now dopamine is released. You’ve got so many of the receptors blocked, you’re thwarting, you’re inhibiting the normal passage of neurotransmitters, of messages along the dopaminergic pathways. 

So dopaminergic pathways help with motor movement and the basal ganglia. So that’s why sometimes you get slowed movement or even Parkinsonian symptoms. The limbic system is also reliant on the dopaminergic tract. That’s why you get this emotion. When you block it, you get this emotional numbing. The frontal lobes are responsible for, they require a dopaminergic tract and you get sort of a diminishment in frontal lobe activity as well. 

So that’s what the drugs do. They interrupt or they perturb normal neurotransmitter activity in the brain. And now they have other side effects we don’t know about. I mean, other actions, but that’s the, because they’ll bind with other receptors too, but that’s seen as the mechanism of action that is therapeutic.

Mr. Jekielek:

But they’re not, it sounds like they are correcting some kind of, maybe this is the problem, it sounds like there’s some sort of chemical correction happening, right?

Mr. Whitaker:

With chemical change happening, the question is, are those systems malfunctioning or abnormal before you go on the drug? So a depressed patient, for whatever reason, are their serotonergic tracts operating at a low level? They don’t find that to be so. Same with, so that’s the problem. The dopamine story is a bit more complex, but still, as Steven Hyman said, we’re just not finding a lesion in the dopamine system that is the cause of schizophrenia. 

Mr. Jekielek:

Okay, so you gave me the gold standard study in antipsychotics. What about in antidepressants? What do those studies say?

Mr. Whitaker:

The history writ larger, the larger narrative is up until the antidepressants, depression was understood to be an episodic disorder. The experts in mood disorders in the 1970s at the NIMH and elsewhere said, one of the things about depression is it almost always clears up on its own with time. And so no matter what we do, we can expect a good outcome. And basically, the thought is when they’re introducing antidepressants, maybe they can shorten the time for recovery. 

But then what happens, you start seeing that once people are medicated,you see some clinicians saying, you know, maybe my patients are getting better faster, my depressed patients, but now they’re relapsing more frequently. Now, epidemiological studies that follow the course of medicated patients are finding that actually at the end of one year, maybe only 15 percent are well when they used to say 85 percent were well. 

So there’s an NIMH panel, I think it’s 1985, to try to assess this conundrum about why it is running a chronic course. And what they say is, oh, we’re finally discovering the true course. Those older epidemiological studies were flawed. But what you’re seeing is this is the course during the antidepressant era. 

By 1998, the American Psychiatric Association was saying this is real, it’s a chronic disease. Only one-third of people respond to, or only one-third of people basically remit on antidepressants, remit meaning the depression goes. Of those that don’t remit, that’s the precursor to a sort of chronic course. And even though those who do remit, half don’t stay well. So that’s where they get the 15 percent and 85 percent. 

But you also see in the literature this, where people are starting to ask, well, what is the natural course of depression in real-world patients? So they do such a study early on in the 90s, and they find that for people who don’t take antidepressants, the disability rate is like six times higher for those who take antidepressants. That’s an NIMH study. 

But now here’s the big study, okay? The big study is known as the STAR*D study, and it is going to be mounted in the late 1990s. And the idea is this: those trials that get drugs approved by the FDA, they’re not conducted in real-world patients. They’re conducted in a very select group of patients that aren’t suicidal, that don’t have comorbidities. We want to know how effective antidepressants are in real-world patients and clinical practice. 

And they say, as they mount this study, and I’ll tell you how it’s designed, this is going to be the study that guides our use of antidepressants and guides our thinking about their merits, how they’re used, and we’re going to disseminate this information as quickly as possible. This is the study that will be the evidence base for the prescribing of antidepressants. That’s in the written literature, okay? Now, they want it to mimic ordinary clinical care, so it’s not placebo-controlled.

But what happens is anybody with a HAM-D [Hamilton Rating Scale for Depression] score of 14 or higher is eligible. That’s like a moderate level of depression, okay? But it’s outpatient. It’s not hospitalized depression, okay, which scores are in the 20s and stuff. They’ll get treated with an antidepressant for 12 weeks, and we’ll see if they remit at the end of those 12 weeks. And if they do, we’ll enter them into a follow-up trial to see if we can keep them well for a year. 

But if they don’t remit on the first drug, we’ll give them a second drug chance, another 12 weeks, and maybe it’ll be a combination of drugs or a combination plus psychotherapy. And people will get four tries to remit, okay? And anybody who remits will then be put into the follow-up trial to see how long we can keep them well. That’s the design. 

The news that is promoted is so good. What you heard published at the end of this was that 70 percent of all patients after four tries remitted; they got well. They were cured. Okay. And that became the statistic that was cited in the media and was still cited 15 years later about the proof of the efficacy of antidepressants. Okay. Now, did I mention the long-term outcomes? No, I didn’t because they hid the long-term outcomes. 

But here’s the real story of the STAR*D trial: 70 percent never remitted. What happened was that the outcomes were so poor, the investigators started using protocol violations to manipulate the data. They switched from a HAM-D scale to something called a QIDS [Quick Inventory of Depressive Symptomatology], even though the protocol said, do not use the QIDS scale. It’s not a validated scale for measuring outcomes. That led to more people being seen as remitted.

They also did a thing where they had people who weren’t eligible for the trial. In other words, they weren’t depressed enough, or either they lacked the baseline score or they didn’t reach that 14. They said, we’ll include them anyway, including people who were in remission at the start of the trial by their baseline score. But these people who weren’t eligible will now count them among the remitters. And then what we’ll do, we’ll say of the dropouts who hadn’t remitted, if they had just stayed in the trial, like all those who stayed throughout for—how many more remissions would we have had? And we’ll calculate a theoretical rate. 

So that’s how they got the 70 percent. They violated the protocol in all these ways because the protocol, by the way, said dropouts are going to be counted as treatment failures. Anyway, a very enterprising psychologist named Ed Piggott and some colleagues got the protocol, and then they used their Freedom of Information request to get access to the actual case report data. 

And what they found is that if the protocol had been followed, only 35 percent would have ever been said to be remitted, not the 70 percent. Now remember, the 70 percent was quoted in the New York Times and over and over again in the Wall Street Journal as evidence of why these drugs work. You just have to keep trying and trying again. So those results were inflated twofold. 

And by the way, this really helps push the selling of antidepressants worldwide, this study. How about long-term outcomes? How many people, what they said was, we’re going to study how many people remit and stay well and in clinical care for one year because we want to keep them in clinical care. So let me ask you, of the 4,041, this is the largest and longest antidepressant trial ever conducted, of the 4,041 patients who entered that trial, how many remitted, stayed well, and remained in the trial to its end? That’s the success group. That’s the stay-well, the documented stay-well.

Mr. Jekielek:

And what was the length of the study? 

Mr. Whitaker:

One year.

Mr. Jekielek:

Oh, so that’s not long term.

Mr. Whitaker:

Well, so you remit, say, after one of those first ones, after the 12 weeks, then you have a one-year follow-up. 

Mr. Jekielek:

I see. Okay, so the long term is actually one year, we’re not looking, okay, I don’t know, it’s obviously bad. 

Mr. Whitaker:

But just what would you expect, just thinking of a 4,041 and these drugs are effective? 

Mr. Jekielek:

If they were effective, I would hope it would be three-quarters or something like that, at the very least. 

Mr. Whitaker:

At the very least, right? Of the 4,041, there were only 108 who reached that end, who remitted, stayed well, and remained in the trial. And of that 108, there were some who, in fact, weren’t depressed enough to be eligible for the trial in the first place. In other words, almost nobody. That’s the worst result I’ve ever seen from an antidepressant trial, from an antidepressant study, ever. 

Do you know what’s interesting? If you read their final study, there is a graphic that tells that, okay? But they don’t explain the graphic. You can’t understand the graphic, okay? I looked at it and I couldn’t make any sense of it. But Ed Piggott, he finally deciphered it and he went to one of the key, the original investigators, a guy named Maurizio Fava. 

And he says, am I reading this right? That by the end you had only 108 patients that were in the trial and well? And Maurizio Fava said, yes, that’s true. It’s always good to have another set of eyes on it. Now that’s what that says. So they actually confirmed that. 

Have you ever seen that reported in a newspaper? It’s shocking. This was the most expensive, the longest and largest antidepressant trial ever conducted. It’s supposed to guide future care. The public was told, look at these drugs, stay in and you’ll find one that works. That’s what they said. And you can go look up the New York Times and you’ll see even as late as a year ago, they’re still quoting a 70 percent efficacious rate. The truth was, 35 percent who ever got well, even for a moment, and virtually no one who was well and still in the study at the end. 

Now, if the public had been told the honest results, what would have happened after 2005? Would we have embraced antidepressants in the same way? If that became the news, listen, almost no one’s staying well. But they didn’t tell us this. They hid that. They still haven’t retracted that study, even though it’s fraudulent.

It’s been published in the BMJ, this whole sort of, by Ed Piggott and people, about how they reanalyzed the case report data. They’ve told of the protocol violations. But the American Journal of Psychiatry won’t retract the study. And they have yet to get anyone interested in writing about it among the major newspapers, although apparently the Wall Street Journal may be preparing an article finally. But there you go. That’s the problem.

Mr. Jekielek:

Part of the challenge with this information is that it’s been such a long time that, I mean, the way you tell it, right, for decades, we’ve just been lied to as a society in a very extreme way. It’s just hard to believe it, that it could be like that, right? Does that make sense?

Mr. Whitaker:

Of course. It’s such a betrayal of the public. It’s such a betrayal of the duty of the medical profession to be honest about the merits of its therapies. And I will say in Anatomy of an Epidemic, I write about that. What were the influences? Why did they hide this stuff up? And there is some cognitive dissonance going on, you know, that you want to believe in the drugs and you find a way to discount this information. Oh, these aren’t randomized clinical trials, so we’re not going to pay attention to them, that sort of thing. So there is some honest cognitive dissonance going on, but there are also people making a lot of money from pharmaceutical companies by helping build these markets up.

Mr. Jekielek:

Has anyone remotely tried to do sort of a cost-benefit analysis of the use or non-use? I don’t know, even I’d have to think seriously about how one would do such an analysis. Of psychiatric drugs? Well, just, you know, the introduction of these drugs, and they’re playing such a central role in psychiatric treatment versus a scenario where that just simply isn’t the case. And we’re using, I don’t know, talk therapy, this other example of bringing people into, you know, groups, very sort of sporadic use of drugs for very short periods of time. These are the things that I heard over the course of this interview kind of worked.

Mr. Whitaker:

Well, I’ll tell you of one very precise, very good study that does tell of the possibilities. What we do know is we’re spending more and more money on psychiatric disorders. That’s all we hear about these days, right? If you start talking about disability payments, that’s obviously a huge cost. So what you actually see is soaring expenditures related to mental health over time as we have embraced this disease model of care. There is a sort of really good example of possibilities, say, with antipsychotics that exists in the research literature today. 

And there’s a group in northern Finland that, beginning in the late 1980s and early 1990s, rethought schizophrenia and psychotic disorders. They broke with the Western model of medicine. They said, we’re not going to conceive of psychosis as happening in the individual brain of the individual, but as in the in-between spaces of people. They become afraid of people, that sort of thing. 

And they developed something called open dialogue therapy, which is sort of, it’s a little bit complicated, but it’s where they have group meetings with more than one psychiatrist and with the family, and they make sure that the person who is seen as having the psychosis, bearing the burden of making known this disruption in spaces, can begin to be comfortable with people again and not afraid of people. 

But here’s how they use antipsychotics, which they did for more than 20 years. When people first came in, they did not put them on antipsychotics. And the reason they did this is because they felt that the person needed to have the emotions in order to be able to engage in this dialogical process. And they had a measure called a grip on life. As long as a person’s grip on life was improving, in other words, they would shower, they would come to these meetings, that sort of thing, they would not use antipsychotics. 

But if they weren’t getting better after a couple of weeks, they would say, I think you could benefit from a low dose of antipsychotic, and a certain percentage would take that. And then after six months, of those who were exposed to antipsychotics, they’d see who could come off and who needed to stay on the drug. So it’s a selective use model, really very similar to Lauren Moshe’s Soteria model. And here were the results. 

At the end of five years, they studied every patient that came through their services. It’s part of Finland called Western Lapland. After five years, two-thirds of their patients had never been on antipsychotics. They recovered without it. Another 13 percent used them at a time, and then 20 percent were on them long-term. And their outcome became by far the best in the Western world. 

At the end of five years, 80 percent of their patients were recovered and working or back in school, or at least looking for a job. We don’t get anything like that with our psychotic patients, in terms of work participation and social functioning. 

Mr. Jekielek:

It just sounds like we can adopt this system.

Mr. Whitaker:

Well, yes. I wrote about it in Anatomy of an Epidemic, and then it did become exported. In fact, I think there’s going to be a report on its export to the UK very soon, maybe even next month, a trial. I think the results are going to be very good. However, the therapeutic part was adopted, and really, it has expanded throughout the Western world. Japan’s gotten involved with it. 

But as it got exported, it was introduced into environments where they said, we’ll adopt this except for one fact: we’re not going to stop using antipsychotics right away. So we’ll do all the dialogical practices, and we’ll organize this sort of thing. We’ll study our outcomes, but we still have to use the antipsychotics because in the U.S., for example, not giving antipsychotics to someone who’s psychotic exposes you to medical negligence if anything goes wrong. 

So I think we’re going to be here. It has been exported, but it’s been exported without the medication arm. If you had Yaku Seiko sitting here before you, he’s one of the people who helped develop it and was the real researcher on it. He would say the selective use of antipsychotics was so critical to the good outcomes we had. 

Mr. Jekielek:

Well, I mean, it just, it sounds like not putting people on medication whenever possible is a critical part of whatever treatment scenario. I mean, at least this is what’s coming through to me. As we finish up, I’m wondering if you could comment on that and maybe also offer a final thought. 

Mr. Whitaker:

Two final thoughts. I think we know enough about this failed paradigm of care that we need a real social societal discussion on how we should be responding to psychiatric difficulties or emotional difficulties, the different types you have. We need to know this information about these psychiatric medications and their effect on the long term and incorporate that into our thinking. I believe now that, yes, you should try environmental responses first like the house that we talked about.

You want to help restore sleep. You want to help restore diet, exercise, social functioning, that sort of thing. To sort of reconceptualize these things as, we know that human beings are responsive to their environment, right? And environment is composed of many things, food, exercise, friendship, meaning, all those things. And can we create environments for people who are struggling that provide these things and see how they do and delay the initial use of medication. 

I think if that doesn’t work, then I think the medications can have a place for a short period of time. Stabilization, maybe help someone sleep. Sometimes it may be good to have your emotions numbed if they’re so painful for a period of time. But then you should really try to limit long-term use. That’s what it’s telling us. 

And one of the reasons is there’s so often a capacity in us to recover, to re-stabilize. You’re not the same person you were when you were 20-years-old. I’m not the same person I was when I was age 20. So we have to realize people do change, their capacity changes. So I don’t want to be the person that says what I think it should be. 

What I think is our society should reconsider this with this information and with the understanding that environments matter because we human beings are very responsive to environments. And then going to our kids, I think we should really stop pathologizing our kids and start thinking about how we can build better environments so we don’t have 25 percent of our kids coming to college with a psychiatric disorder and on drugs. So that’s clearly a failure. 

The only other thing, you brought up something a little while ago. How can we understand this betrayal by, in essence, American psychiatry of its public duty? And I spent a year in a lab at Harvard University studying institutional corruption. And the idea with institutional corruption is that even good people can get involved in environments, institutional environments, that stray from their public duty, their civic duty, and then suddenly there becomes a different standard that they now accept. 

So it’s a look at like, what are the influences on an institution that can cause it to become corrupt? The whole institution becomes corrupt. And that’s how you actually have to see American psychiatry under this lens of institutional corruption. What were the influences that really arose in 1980 when they adopted a disease model that led to this betrayal in which they told us a false narrative while hiding all the information related to bad outcomes with the drugs and what they really did.

Mr. Jekielek:

Okay, so bottom line, what do you hope the institution of psychiatry will do?

Mr. Whitaker:

Well, first of all, the narrative is changing since I wrote Anatomy of an Epidemic in 2010 to where we are today. There’s increasing acknowledgement that this paradigm of care has failed. The World Health Organization has public documents saying we need a paradigm shift in care because it’s failed. 

The former United Nations Special Rapporteur for Health said the same thing. This disease model has failed. We have to change it. There is increasing acknowledgement within the psychiatric literature, some of this was prompted in response to me, that they don’t have information about, they don’t have evidence that these drugs improve long-term outcomes.

So now you’ll see, for example, Nassir Ghaemi writing a piece saying that we have no evidence that these drugs improve long-term outcomes. He accepts lithium. He thinks lithium does have a long-term benefit in terms of reducing mortality or other things that are seen as long-term benefits. So we should be using these drugs, listen to the psychiatrist, in as low a dosage as possible and for as short a time as possible. Now, he’s a very well-known psychiatrist. 

So now you’re starting to hear that narrative come from within psychiatry as if they’re discovering it. Great, because then they can own it. So I will say the narrative is changing, which opens up possibilities. And there is some real questioning even within psychiatry now of this narrative. 

And we even had Dost Ongur, who is the editor-in-chief of JAMA Psychiatry, which is a, you know, mainstream psychiatric journal. He wrote in the spring of this year, we have to admit that outcomes, long-term outcomes for serious major disorders, mental disorders, have worsened over the last decades. So now we’re suddenly validating basically the story and anatomy of an epidemic. He’s talking about schizophrenia, bipolar, OCD. They’ve worsened, he says. 

Now, he doesn’t want to blame it on the drugs. He’s blaming it on sort of social conditions, lack of social support. fine. But that is an admission that what we’re doing, things are getting worse. So that opens up the possibility of a paradigm shift.  So what do I wish for? The problem for psychiatry is what’s its product? What’s its product in the marketplace? 

Mr. Jekielek:

Well, I mean, we’ve been discussing it. You’re saying it’s drugs.

Mr. Whitaker:

Yes. They became prescribers of drugs, and then the psychologists and counselors do all these other things. The problem is that it puts them in a bind because it’s hard for them to say our drugs aren’t helpful if that’s what our product is. Be like General Motors saying our cars don’t run very well. Nevertheless, my hope would be that psychiatry could find a new role, sort of helping to administer and create and develop environments that are supportive, selective use models that have an evidence base for them, and can really promote sort of a holistic approach to these problems, environmental approaches, looking at food, exercise, all the things I’m talking about, meaning in life. That would be my hope. 

Is it going to happen? I don’t know. I mean, there is a lot of sort of momentum towards that change, but we’re also hearing momentum towards like, oh, no, the answer now is ketamine or the answer is psychedelics, which is still a drug based solution. And I guarantee if you look at the data on that, it’s not good for the long term. So I don’t know, it’s up in the air. It’s really up in the air. 

And I will say one final thing. I think there is a lot in our society today that is not very health promoting. You know, there’s how we raise our kids and the food we eat and that sort of thing. So social media, there’s a lot of reasons, I think, that people become sort of dysphoric, social isolation. But that’s my hope. Let’s see what happens. But the biggest thing is, has the narrative changed? It is changing. And that paradigm shifts can happen rather quickly once the larger narrative begins to change.

Mr. Jekielek:

Robert Whitaker, it’s such a pleasure to have had you on.

Mr. Whitaker:

Thanks very much. That was a really nice interview.

 

This interview has been partially edited for clarity and brevity.