American Thought Leaders - What Americans Aren’t Told About Psychiatric Medications | Robert Whitaker

Episode Date: December 17, 2025

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.

Can you just show me where you found that, say, 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? 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. In this episode, I sit down with medicine and science journalist Robert Whitaker, author of Anatomy of an Epidemic and Mad in America. That's the biggest irony of this whole story, the drugs actually induce an abnormality hypothesized to cause the problem in the first place. Whitaker challenges the idea that mental illness is caused by a chemical imbalance in the brain

and argues that some psychiatric drugs cause long-term harm. I was a believer in the narrative. I was a reporter who called up scientists and quoted what they said. And I began down a different path of challenging that narrative. I began to find evidence that that be lied, that narrative of progress. He calls for a shift toward alternative interventions and a more holistic approach to mental health. What happened to you after you published Mad in America? This is American Thought Leaders, and I'm Yanya Kellick.

Robert Whitaker, such a pleasure to have you on American Thought Leaders. Well, thanks for inviting me. It's a pleasure to be here. What would you say is the biggest, myth around mental health or psychiatry today? I think the myth that has become, is most well known was the story that the drugs fix chemical imbalances in the brain. So for example, depression was due to too little serotonin and drugs that upsertanernergic activity in the brain, therefore normalized 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 begins to be pitched in the United States in the late 1980s, early 1990s, a drug called Prozac that comes to market in 1988. And it is presented to the public

as an incredibly novel drug, a breakthrough medication because it fixes a seroton 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, they 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 activity. Maybe depression is due to too little serotonin.

That's 1965. Well, they then had to investigate do people with depression actually have too little serotonin before they go on the drugs. Now, as early as the 1970s, the first sort of, they had to find methods for making that investigation. But even by the early 1970s or late 1970s, people are saying, you know, we aren't really finding this. In 1984, I believe it was, the NIH did a big study on this question, and they said, We're not finding any lesion in the serotonogic system that it's 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,

it was no longer valid. They said, we've investigated many ways, and we just haven't found that serotonin is abnormally low in people with depression. 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 GPs that are prescribing psychiatric medication. 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 seroton theory. And then, for example, there was a there's a famous. This guy writes a book called, his name is Steven Stahl. He 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 monomine. It's just not real. So he says that in 2002. You can find Kenneth Kendler in 2004, who was an editor of psychological medicine, a big research in this field and he said this, we have hunted for big, simple, neurochemical for mental disorders and have not found them.

But the public, that's not what the public was told. But the public was told, and you can follow now the public pronouncements of the American Psychiatric Association, 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.

be true. However, that story, American Psychiatric Association and the pharmaceutical companies understood was a great way to promote treatment, the selling of drugs, and also elevate the prestigious 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've made this great medical advance, which fits into a larger narrative in the Western society. But yeah, 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 acted on the brain, investigated, and basically fell flat early on, 70s, 80s, 90s, and was discarded by the late 1990s within 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 that fix the chemical imbalance and then you're 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 you can chart those sentiments you can see that they were telling this on their website they even put a press release in 2005, 2006, saying, 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 is sort

of a way to sell drugs, basically, it got started in the United States and then it 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. Before I ask you about what these drugs actually do do, or what we know they do do, why don't you tell me a little bit about yourself and your background and how you got into this space? Sure. So my background was as a newspaper reporter. And starting in like 1988, I began covering medicine and science for a newspaper called the Albany Times Union in

in Albany, New York. And then I actually left, in 1994, I left daily journalism, and two things happened. First, I became director of publications at Harvard Medical School. And now this was at a time, people were talking about evidence-based medicine. We have to adopt evidence-based medicine.

And one of the thoughts about evidence-based medicine is doctors can be deluded about their 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. So that was very prominent in the early 1990s. And then the second thing that happened was this. I co-founded a publishing company in 1994 called Center Watch that looked at the business

of clinical trials and the business was dramatic, clinical testing of their drugs. And the point of looking at it from a business is the spending on clinical trials was dramatically increasing in the late 1880s, 1980s and 1990s. 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 you 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 that by having such a financial uh environment for the

testing of drugs. It was corrupting the testing of drugs and it was corrupting what the public was told about the actual results from those trials. There was adverse effects were being hidden, the efficacy was being exaggerated, that sort of thing. And 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 not notable for an exaggerated sense of efficacy and safety was they were promoted to the public. And the way I knew that is I use freedom of information

requests to get what the FDA 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 that the FDA investigators were saying you're going to see, but that wasn't part of the message

given to the public. So I then went to the Boston Globe, who I'd written for before, and said, I'll do a series of 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 that. 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 were maintained on the drug half the people 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 I called people up, they said, oh yeah, antipsychotics fix a dopamine imbalance on the brain like insulin from diabetes. So we said, well, why 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.

As I was doing, so that narrative that I was a believer in is a narrative of progress, right? 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. And they said they had declined since the 1970s, not improved, and were now known.

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 is these dark ages, right? So how can it be that with these modern drugs that fix chemical imbalances are we no better than when they put people in showers and did all sorts of sort of harsh somatic treatments? Okay, that was number one. The second was I then stumbled upon studies done by the World Health Organization, cross-cultural studies, that compared outcomes in three developing countries, India, Columbia, Nigeria, to longer-term outcomes in the U.S. and five other developed countries.

Now, everybody was diagnosed with schizophrenia by Western doctors and studies. And what they found after the first study was that the outcomes in the developing countries were much, much better than in the developed country. 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'm saying, what? We're so proud of our medicine. Why would you do better if you're in India or Nigeria than in the US 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 was after the first such study, they hypothesized 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 better outcomes. 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 few low percentage were maintained in the drugs. 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 say 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 and it was really meant to investigate this question. Why would living in a developed country lead to poor outcomes for people diagnosed with schizophrenia? Okay? Because we had this model of progress. So the very first thing I did is I started calling up people, including some of the people who I'd called up for the Boston series, Globe series, who had told me that the drugs fix the chemical imbalance in the brain. I said, can you just show me where you found that, say, 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. and first person says no we didn't really find it second person no we didn't really find it and then i went to the makers of risperol which is a second generation atypical and risperol was being marketed as fixing not only a dopamine imbalance in the brain but as a serotonin imbalance in the brain and i actually managed at that time to get to the actual researchers and you know what they said

yeah that's just such nonsense uh you know we're just it's just i'm sort of embarrassed that we say this so as i began to write report on Matt in America, which would trace the treatment of the seriously mentally ill in the United States from colonial times until today. I started with the 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 finalists 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 I was a believer in the narrative I was a reporter who called up scientists and quoted what they said called 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 didn't that be lied that narrative of progress. It seems to be very rare in the field right now to question this right 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? Well, there's 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 for the tribe? Now, in the United States, the leading schizophrenia doc, at the NIMH, the head of schizophrenia studies, was a man, in the 1970s, was a man named Warren Mosher, okay? And he ran a study, a very famous study in the 70s, called the Sataria 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 Satira House, an ordinary house, staffed by ordinary people. And the idea of what was here was that with being with people, their psychosis would abate, and they could learn to be with people. And the way medications were used in that house was they didn't put them on anti-psychotics right away

because they wanted them to be emotionally engaged with each other and with the staff. And now if people weren't getting better after 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 satiria arm, had an 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 Lauren Mosher now says, and in terms of medication, you used 40% never used the drugs, 40% used them temporarily, only 20% 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? And they ran this experiment for 10 years.

They did a second house to show that it could be replicated. What happened to Lauren Mosher? He was fired from his position, and he was pushed out and made, and why was he fired? He was fired because that story was so threatening to the story that the American Psychiatric Association as a Guild wanted to tell, which was that its drugs were very effective, because that's what becoming their product, not talk therapy, drugs. and his research and a couple other studies, that's type, really undercut that story. Now, they had two chances there, American Psychiatric Association, either listen to the science and respond, which threatens sort of the gild 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, we're seen as leading scientists, good scientists, and said, Wait a minute. This science doesn't support the story that we're telling. Well, gild interests are very strong. The financial interests are very strong. In psychiatry, we have those guild interests merging with 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. Before you give me the other reason, what happened to you after you published Mad in America? 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 I didn't just start covering science, right, in medicine. I started becoming 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 giving different walking orders. And you're 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 the beauty of science and they want to maintain the integrity and they're open-minded people okay because theoretically science is a story of 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 now you as a reporter saying but wait a minute that's not based in science they're not really uh 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 it's it's they don't have enough knowledge about the actual literature or even how to read it and it just

It goes against even a much larger narrative, which is that scientists we trust, medical doctors, we trust, okay? Especially if you go back 25 years ago. So what happened to me? I think it's real key to understand is in that first book, Matt in America, you know, it does go from colonial times until today. Now, sort of talking about the abuses up to the time of when antipsychotics arrive in asylum medicine, which is in 19, You can talk about the dark old days, okay? Because that's sort of part of the official history. But then the idea is that we had the psychopharmacological revolutionist, great advance in care.

Now what I did in this going forward was showing 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 in, as you follow that research across time, across time, and I'll talk about this tomorrow, you find a very different narrative. You find a narrative where right away antipsychotics that was worried that maybe antipsychotics are increasing the chronicity of schizophrenia. By 1980, there's even a thought that, they're not a thought. There's evidence and a conclusion that it seems that the drugs, what antipsychotics

do, they have a blocked 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 with psychosis than it was in the first place. And the researcher said, 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, but rather you're going to have this withdrawal effects. And if you stay in the drug because of this thing, you're likely to become sort of chronically psychotic.

You're basically telling me this is causing brain damage, aren't you? Well, yes, the antipsychotics cause brain change. The two things, if you want to talk about the 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 Stephen Hyman. It was director of the NIH at this time that sums all up this explanation.

So you have something, a drug that that perturbs normal activity of neurotransmitters in the brain, okay? It either blocks receptors or blocks the re-uptake 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 trying to maintain this normal functioning. And as Stephen Hyman said, at the end of this compensatory process, your brain is operating in a manner that is both qualitatively and quantitatively. different than normal. So rather than being normalizing drugs that are abnormalizing drugs, that was seen as a problem why these drugs could make you

more biologically vulnerable 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 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, very famous researcher. She was editor-in-chief of American Journal of Psychiatry, so this isn't some critic. They're 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 six, seven 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 had been researchers giving antipsychotics, both the first-generation, second-generation antipsychotics, two 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 Andreas and researchers went back and said, yeah, it's the drug, and now there's 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 surprising, is associated with a worsening of symptoms, functional impairments, etc. So, but now you ask what happened to me. So, I had a good representation, a good reputation as a journalist. That series for the Basso Globe was a finalist for the

Pulitzer Prize. I won some other awards. The book came out and it got a mixed reaction. There was some actually nice reviews by non-psychiatrists, but then there were some really brutal attacks. My favorite one was by a psychiatrist named Eufollatory. 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 this time i just wanted to make a living writing book she said to me bob don't write about psychiatry anymore it's too it's too controversial uh 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 here? Bob, it's just 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 all 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 sort of science books of that year, 2002. And most important of all is 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, but 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, then I wrote two other books, sort of rejuvenated my reputation as a reliable narrator of science. And then I returned with anatomy of an epidemic. And anatomy of an epidemic is a frontal assault on that narrative, okay, because it's looking at how these drugs alter long-term outcomes and the first review that appeared about five minutes after midnight of the publication date likened me to a South African dictator who by virtue of denying that denying 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 after

I got my radio interviews canceled, no more newspaper reviews. It was a very effective way to shut down that book initially. So I first came across the 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. 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've reached out to you this is yeah this is what

there's been the most rewarding thing of my professional life or just one of those rewarding things in my whole life i have received so many calls 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 psychiatrised, 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 resistance or whatever, and I was seriously ill. And then I saw when I read your book a different pass for myself.

that in fact that 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 it's, what they can do is see the, 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 was necessarily very different from schizophrenia. And of drugs that can cause two things, a chronification of symptoms, gradal 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 next thing you know, they got a bipolar diagnosis. Same thing with ADHD, 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. I mean, 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 that's what I got out of it. but why don't you tell me what yeah it's not that necessarily that of course people end up on paula pharmacy and that's a mess because the drugs are interacting with each other the the major thesis of this is this the way to get 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 balances now normally in medicine if you have a 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 of the second generation drugs. And rather than diminishing the burden of mental disorders, as measured by people going on government disability, it had skyrocketed. It increased from like 1.2 million adults in 1987 to a around four 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 history of research tell us about the long-term impact of these drugs, these different classes of drugs, antipsychotics, antidepressants, benzodiazepines, because the evidence-based 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 about the natural course or the natural capacity to recover. 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, 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, acts as an accelerator. So what does your brain do? It dials down its own serotonergic machinery, puts the brake on it to try to like maintain an equilibrium. You got too much, so accelerator break, okay?

This deficiency in serotonousy transmission is abnormally low, 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, it's A, what did 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, you find a narrative of science.

This is really key. Yeah, we only say, oh, we only listen to RCTs, but this is a narrative of the 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, in the aggregate. In the aggregate. And how does that compare, how does the on medication, aggregate outcomes compared to, like, aggregate unmedicated outcomes or the natural capacity to recover, and you see greater chronicity.

You see greater risk of disability and, you know, and less able 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 unmedicated, the medicated kids were more likely to be functionally impaired later on. That was an in-I-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 start using often multiple drugs. And you see this great increase in disability to 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 than before. More cycling, more functional impairments, more unemployment, more disability. So even the experts there are saying, what's going on? We're having this worsening outcomes with bipolar. So the theme of anatomy of an epidemic is this writ large. We have our society has organized its thinking, its behavior, it's 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, a guild interest, pharmaceutical interest, 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, increased 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 who told this, 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, does tell it poor long-term outcomes. And 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 Joe. Harrow was a psychologist. Job 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, one public, are treated with drugs, okay? Treated with antipsychotics and they're discharged. And they're just going to be, the researchers,

heroin Joe Burns, just going to follow them up at two years, two and a half years, four and a half years, seven and a half years, ten years, 15 years, and 20 years. And at each assessment they're going to see, are they using that 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 amounted this study, NIMH funded, best one in modern times, their hypothesis was we'll find better outcomes in those of medication compliant because that was the belief, right? So what they found, though, is there were 64 schizophrenia patients and 81 with milder psychotic disorders that

stayed in the study for 15 years. What they found among the 64 schizophrenia patients, there was about 25 who stopped taking their drug by year two, okay? Any drugs, any, any, any, and any, any, antipsychonics and they 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 are on drugs did not such that the recovery rate meaning no symptoms and working or in school half time a decent social life was eight times higher for the group off medication 40% versus 5% and there was 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 forget which journal they managed to find to get 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 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 there's the in this american psychiatric association next book there was like one line for a while it 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 in 2008 meeting, I was there. Here's Martin Hill. 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 paper? No newspaper. No, it's, you know, it's what you would call a statistically significant outcomes. Oh my God, the differences were so dramatic. And they, you know, it's, you know, it's a, it's what you would call a statistically significant outcomes.

Oh, my God. The differences were so dramatic. And they even published numerous times explaining what they thought there was the biological mechanism. They looked at their data from different ways, everything they could. They ended up getting about five, six papers published. But none of this was ever promoted to practicing doctors to the public. Now, they both died recently. And even in their obits, like, Ira was famous enough that there was a small. but the New York Times, they still have never reported that there's this eightfold higher recovery rate, or that here's the most thing amazing at all. The schizophrenia patients off medication long-term had better aggregate outcomes than those with milder disorders who stayed on the drugs long-term. Which suggests strongly it's the medications that are... What is the what is the variable that seems like it is? I'll tell you a small funny story a little bit. it. 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 him together in one chart. He had one chart for the schizophrenia on global assessment function and one chart of 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 those with with milder disorders on it. And he actually got quite mad at me at that time. He said, who are you? What are you against the drug?

Are you have something of bias here? And I said, no, I'm just asking you about your own data. Well, he was, and then he sort of relent. And he said, off the record, he said, 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 Job and they said, Whitaker's right. right and he actually cited me in one of their final papers and then one other thing that happened

is after i published an out of an epidemic i did get some people saying we need more research on long-term outcomes and i helped found a non-profit called a 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 to be seen as tainted and they actually provided funding to martin harrow and thomas jill to do further research on their long-term out outcomes. I mentioned 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 Starr-D trial. You started telling me about this earlier. What do these drugs actually do? Well, what they do, and this is what, we'll talk about the mechanism of antidepressants and antipsychotics. First of all, we'll talk about what is the mechanism of action,

the singular mechanism of action that's seen as characteristic, but the drugs actually have much broader effects than what it said is to be the singular mechanism of action. So let's take 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, cross that very tiny gap between neurons and they 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're known as excitatory molecules, neurotransmitters that causes 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 or lower the firing of it so what does serotonin do so you you serotonin is released in that tiny gap right now in order for this messaging system remain crisp you have to remove that serotonin from the gap right and serotonin is removed from that gap in two ways it either is taken back up into the pre-synaptic neuron and stored for later reuse or an enzyme comes along and metabolizes it and that serotonin

metabolites that cart off his waste okay what the first generation of antidepressants did is they block that normal re-uptake of what are known as monoamines neurot serotonin is monoamine or the monomine oxidase inhibitors they block the enzyme that you know metabolize metabolizes the monoamine so both of them prevented the normal removal of serotonin serotonin serotonous stays longer that gap that's theoretically and hence the name yeah yeah yeah yeah it's gonna cause this neuron to fire more than dopamine what the antipsychotics do is that molecule sits in the receptors on the post synaptic 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 block you're thwarting you're inhibiting the normal passage of neurotransmit of messages along the dopaminergic pathways. So dopaminergic pathways help with motor movement in the basal ganglates and that's why sometimes you get slowed movement or even Parkinsonian symptoms. The limbic system is also reliant on the dopamine energy 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 dopamine energy track 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 activating the brain. And now they have other side effects we don't know about, I mean, other actions, because they'll bind with other receptors too, but that's seen as the mechanism of action that is therapeutic. 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? If the chemical change happening, the question is, are those systems malfunctioning are abnormal before you go on the drug? So a depressed patient, for whatever reason, are there serotonergic tracks 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 Stephen Hyman said, we're just not finding a lesion in the dopamine system as the cause of schizophrenia. Okay, so you gave me the gold standard study in antipsychotics. What about an antidepressants? What is that, what do those studies say? 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 NIH 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 their course of medicated patients are finding that actually at the end of one year, maybe only 15% are well when they used to say 85% were well. So there's an NIMH panel, I think it's 1985, to try to assess this conundrum about why is it 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

anti-idepressant era. By 1998, the American Psychiatric Association is saying, this is the 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 depressions goes. Of those that don't remit, that's the precursor to a sort of a chronic course. And even though those who do remit, half don't stay well. So that's where they get the 15 and 85%. 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 people who don't take antidepressants, the disability rate is like six times higher for those who take antidepressants. That's an in-a-M-H 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 at 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 are 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 Hamdi 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 antidepressants 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 and see how long we can keep them well. And the news that is promoted is so good. What you hear published at the end of this was that 70% 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 Stardee trial.

70% never remitted. What happened was that the outcomes were so poor, the investigators started using protocol violations to manipulate the data. So they switched from a Ham D scale to something called the quids, even though the protocol said, do not use the quid scale. It's not a validated scale for measuring outcomes. That led to more people being seen.

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. 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 hadn't remitted, if they had just stayed in the trial, like those who stayed throughout four, how many more remissions would we have had and will calculate a theoretical rate? So that's how they got the 70%. 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, they 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% would have ever said to be remitted, not to 70%. Now remember, the 70% was quoted in the New York Times and over and over again, the Wall Street Journal, as evidence that why these drugs work, you just have to keep trying and trying again. Okay, so those results were inflated twofold. Okay. 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 4,040, 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 in the trial to its end? That's the success group. That's the stay well. Documented stay well. And what was the length of the study? Oh, so that's not a long term. Well, so you remit, say, after one of those first ones, after the 12 weeks, then you have a one-year follow-up.

I see. And then we're going to... Okay, so the long term is actually one year. We're not looking. Okay. I don't know. It's obviously bad. But just what would you expect just thinking of 4,041 and these drugs are affecting? If they were effective, I would hope, it would be three quarters or something like that, at the very least. At the very least, right? Of the 4,041, there were only 108 who reached that end, who remitted, stayed well and in the trial. And of that 108 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 an out-impressant study ever but they didn't 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 I couldn't make any sense of it but Ed Pickett he finally deciphered it and he went to one of the key the original investigators guy your name Maricio Fala and he says am I reading this right that by the end you had only 108 patients that

We're in the trial and well. And Ritz, your father said, yeah, yeah, 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. It's shocking. This is the big, 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, work. Stay in and you'll find one that works. That's what they said. And you can go look up New York Times and you'll see even as late as a year ago, they're still quoting a 70% efficacious rate. Truth was, 35% whoever 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 that, 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 Pigott and people about how they reanalyze the case report data. They've told of the protocol of violations, but the American General Psychiatry won't retract 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 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 that does that make sense of course such a betrayal of the public is it's such a betrayal of the duty of a medical profession to be honest about the merits of its therapies and i will say an anatomy of an epidemic i i write about that what were the influences why did they hide this stuff up? And there is some cognitive distance 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 distance going on, but there's also people making a lot of money from pharmaceutical companies by helping build these markets up. Has anyone remotely tried to do sort of a cost-benefit analysis of use or non-use?

I don't know even, I'd have to think seriously how one would do such a, such an analysis. But of, of the, well, just, you know, the introduction of these drugs and they're playing this 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. Yeah, yeah. Right.

Yeah. Well, I'll tell you of one very precise, very good study that does tell up 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? The disability, 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. health over time as we have embraced this disease model of care. There is a sort of a really good example of possibilities, say, with antipsychotics that exist

in the research literature today. And there's a group in northern Finland that beginning in the late 1980s, early 1990s, that rethought schizophrenia in psychotic disorders. They broke with the west of Western 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 develop 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 a family, and they make sure that the person who is, is, who is seen as having the psychosis, bearing the burden of making known this disruption spaces,

can begin to be comfortable with people again and not afraid of people. But here's how they use antipsychotics that they did for more than 20 years. When people first came in, they did not put them on antipsychotics. And the reason they did in is because they felt that the person needed to have their emotions in order to be able to engage in this dialogical process. And they had a measure called a grip on life. And as long as a person's grip on, 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, listen, I think you could benefit from a low dose of antipsychotic

and, you know, a certain percentage would take them. 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 Mosch's satirium model. And here were the results. At the end of five years, and 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% used them at a time, and then 20% were on them long-term.

And their outcomes became by far the best in the Western world. At the end of five years, 80% of their patients were recovered. and working or back in school or at least looking for a job, okay? We don't get anything like that with our psychotic patients, okay? Any participate in terms of work participation, social functioning? It just sounds like we can adopt this system. Well, yes, you know, I wrote about it in anatomy of an epidemic, and then it did become exported.

And 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. And I think the results are going to be very good. However, so the therapeutic part was adopted and really it has expanded throughout the Western world. Japan's got involved with it. But as it got exported, it got exported into environments where they said, we'll adopt this except for one fact.

We're not going to not use antipsychotics right away. So we'll do all the dialogical practices and we'll organize this sort of thing. and we'll study our outcomes, but we still have to use the antipsychotics because in the US, for example, to not give antipsychotic to someone a psychotic exposes you to medical negligence,

if anything goes wrong. So I think we're gonna be here, it has been exported, but it's been exported without the medication arm. And if you were had, Yaku Seiko was sitting here before you, he's one of the people who helped develop it and with the real research, on it he would say the selective use of antipsychotics was so critical to the good outcomes we had

but yeah well i mean it just it sounds like not putting people on medication whenever possible is a critical part of Thank you. Thank you. Thank you. Thank you. Thank you. Thank you. Thank you.

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