On December 29, 1987 Prozac was approved by the FDA. I was 12 years old at the time and one of the first children to be put on this medication. Despite an initial feeling of relief, the results were short lived and came with nasty side effects that led me to discontinue it.
I would suffer for another 20 years before finally figuring out the root causes of my severe depression and often suicidal ideation. A combination of two little known conditions: copper toxicity and undermethylation, both of which have a profound affect on thinking, feeling, and behavior. I was able to treat these conditions with nutrient and dietary therapy, which saved my life. To learn more about both of these conditions and the other chemistries I work with in my clinic, please listen to Episode 2 How Nutrient Deficiencies and Overloads Impact the Brain and Body. I also have many free articles here on my website that provide a deep-dive into how they impact us in so many ways.
This is a very important and personal episode for me because depression and mental illness continue to rise despite all the drugs available today to treat them. Drugs that don’t and never did have the necessary safety studies to ascertain their validity. In fact, a historical review of the scientific literature reveals how antidepressants and other psychotropic drugs, over the long term, increase the risk that a person will become chronically depressed and functionally impaired, which correlates with what we are seeing worldwide.
In this episode, we discuss:
- The history of psychiatric drugs
- The skyrocketing number of people disabled by mental illness
- How industry-funded randomized clinical trials are always biased in favor of the drug
- Who benefits from the distribution and use of psychiatric drugs
- How psychotropic drugs (including SSRIs, stimulants such as Ritalin, and benzodiazepines) affect the brain
Listen to the podcast here:
Within the below transcript, the bolded text is Samantha Gilbert and the regular text is Bob Whitaker.
What are the Hidden Harms of Antidepressants?
Welcome to my conversation with Bob Whitaker about the hidden harms of psychotropic drugs. Bob is the author of five books, three of which tell of the history of psychiatry. In 2010, his Anatomy of an Epidemic, Magic Bullets, Psychiatric Drugs and The Astonishing Rise of Mental Illness won the US Investigative Reporters and Editors book award for best investigative journalism. Prior to writing books, he worked as a science reporter at The Albany Times Union newspaper in New York for a number of years. He is the founder of Mad in America, a website that features research news and blogs by an international group of writers interested in rethinking psychiatry.
Welcome to the show, Bob. I’m really excited for this important conversation.
Well, thanks for having me. It’s a real pleasure and honor to be here. Looking forward to it.
Yes, likewise. As an investigative journalist, you’ve uncovered a wide range of material about the rise in mental illness in America. Before we dive in, what drew you to researching and writing about mental illness in psychiatry?
Well, this goes back to 1998 when I was doing a series for the Boston Globe on abuses of psychiatric patients and research settings. I wasn’t particularly interested in psychiatry at that time. I had just stumbled upon some instances of research where it was clear that the people volunteering for these trials were being lied to, and they were being treated in a way that was hazardous to their health. And during that initial reporting on that series for the Boston Globe, I started understanding and coming to see that the conventional story that had been told to us, a story of progress at that time, was that schizophrenia was due to too much dopamine. And that the drugs blocked dopamine like insulin for diabetes. They restored the normal chemical imbalance. They restored the normal chemistry levels.
Well, that’s a story of great progress. Think about that. That’s a story that they’ve identified the molecules that cause depression or the molecules that cause madness, and they can fix it. And the metaphor at the time is these drugs are like insulin for diabetes. But what I found, and this goes back to 1998, is that story wasn’t true. When you actually looked into the research literature, you didn’t find that they had found that depression was due to low serotonin or schizophrenia was due to too much dopamine. And I said, “Well, how does that happen? How is it okay to lie to people in this domain of our lives?”
At that same time, and remember the conventional narrative is a narrative of progress, better drugs, identifying the pathology, I found that schizophrenia outcomes in the United States had declined since the 1970s. And they were now worse here and in other developed countries than they were in countries like India and Nigeria. So all of that was a perfect setup for a journalist. We had one story that was believed by the public, and when you went into the scientific literature you found a different story. So that really was what motivated me.
Remember a journalist’s obligation is to be a faithful recorder of “the truth”, or whatever is in the scientific literature, to the public. So that’s what drew me to it. I felt that there was clear evidence that the story being told by conventional psychiatry, the American Psychiatric Association, academic psychiatrists and academic medical schools wasn’t true. And once you open that door you find that story of the difference between the scientific literature and what’s being told is persistent. It prevails wherever you look. And the other thing you find is that worsening outcomes, all sorts of long term literature that’s pretty scary. So that’s what drew me to it. So it’s very simple. It’s a classic journalistic exercise.
I’m so grateful that you chose to go down this path, because it seems like that’s not really the norm anymore. I don’t know if you have an opinion on that. That’s probably another show. But just the fact that back in the 90’s you saw what was happening, I’m sure horrified by what you uncovered, and chose to make a better choice than other people might. So thank you for that.
I also realized how important this was to society, because our society has organized itself around a false story. And we were raising our kids around a false story. Children were getting pathologized. They were getting diagnosed. And all of a sudden, our whole philosophy of being had changed around this false story. One of the reasons I stuck with it is I can hardly think of a more important story. Think about the role that story plays in our lives, that chemical imbalance story plays in our lives. It’s changed so many lives, including how we think about our children and how we raise our children. Yes, there was this classic sense of a false story being told, but the second part of it was that false story had changed us as a society. And that’s why I stuck with it.
I really appreciate you sharing that Bob. I couldn’t agree more. And it’s the same thing with food and the food supply. All the marketing around food, especially to children, these processed foods that have zero nutrients in them. And then we wonder why our children are suffering and in pain.
I love how you said this has been organized around a false story. And it is absolutely a false story. And that’s why this episode is so important to me and having you on the show to talk about these important topics is so critical. I want people to see the truth. I want people to understand how our society, and our world as a whole, has changed as a result of basically big pharma and all this data that we’re going to get into in a minute.
Bob if we could set the stage a bit. The so-called psychopharmacological revolution started in 1955 with psychiatry discovering drugs for all kinds of mental disorders. Then in 1988 second generation psychiatric drugs such as Prozac, which I was put on when I was 12 years old, were introduced. Today we have many different classes of psychiatric medications. I’d love it if you would walk us through a bit of this history.
Are Antidepressants More Harmful Than Helpful?
1955 is seen as the date of the start of the psychopharmacological revolution. That’s what it’s called within the field. That was when the first drug Thorazine, the chemical name is chlorpromazine, was brought into a silent medicine. Now, the important thing to understand is that there was no research into the pathology of schizophrenia that led to the introduction of that drug. Basically, what happened is the drug was discovered because of research into anesthetics. The idea was you were looking for a drug that could help you during surgery where people would be numbed, but that you wouldn’t need to put them all the way out. So in other words, there’s some danger with the old anesthetics. This was going to be seen as a new way to do certain surgeries. They noticed that these drugs numbed people’s feelings, this group of chemicals called phenothiazines. And chlorpromazine is a phenothiazine. They numbed people’s emotions, they made them care less about the world and be less engaged with the world. So they said, “We need drugs that quiet people in asylums.” It’s a tranquilizer. It sedates people. It wasn’t introduced as an antipsychotic. It was introduced as a “major tranquilizer”, something to quiet people and make them move around less.
Then the antidepressants that we remember as the first generation antidepressants were also discovered by research into other drugs that could serve as magic bullets for infectious diseases, bacterial disorders, that sort of thing. Well, let’s say the first anti-anxiety agents came because they found that these were drugs that, in animals at least, no longer cared about things. They no longer mounted emotional reactions. And they said, “Okay, that’s a good way to do something for anxiety.” Antidepressants came from drugs for tuberculosis. When they gave them to the tuberculosis patients, it seemed like people became a bit more roused. They said, “Oh, we can use this for depression.” The point here is, the whole psychopharmacological revolution began by drugs that were being researched for other purposes. Their side effects, sedation, quieting people, rousing people, were seen as we can now use these with psychiatric patients.
When they were first introduced they weren’t called antipsychotics. They weren’t called antidepressants. They were called major tranquilizers. The benzodiazepines were called minor tranquilizers. Drugs or antidepressants were called stimulant rousers or something like that, because that was describing that change. So what happened? What happened was psychiatry wanted the same sort of antidotes to diseases that the infectious disease doctors had. And what did infectious disease doctors have in the 50’s? Antibiotics, which were quite a great advance. So at this opening they said, “Let’s start calling our drugs antipsychotics, antidepressants, antianxiety agents.” That is a story that starts telling of drugs that are a specific antidote to some known disease. Antipsychotic, there was something causing psychosis, this was just like an antibiotic. And in essence, what happened is that the naming set in a delusion that these drugs were in fact attacking or counteracting something biologically wrong, which wasn’t quite yet known. That’s where the chemical imbalance theory arose. They said, “Okay, if antipsychotics knock down dopamine, maybe psychosis is due to too much dopamine. If antidepressants increase serotonergic activity, maybe depression is due to little serotonin.” Those theories arise in 1965. And you have to understand psychiatry wanted a white coat. They wanted to have the same prestige in society that infectious disease doctors had.
Antidepressants came from drugs for tuberculosis. When they gave them to the tuberculosis patients, it seemed like people became a bit more roused. They said, “Oh, we can use this for depression.”
The next big moment is 1980. The American Psychiatric Association publishes the third edition of its Diagnostic and Statistical Manual. Before, many of these things were thought to be psychological or frightening in nature, responses to the environment. If you have that previous understanding that these things can be due to depression, anxiety due to your interaction with an environment that maybe you need to change the environment, right? It’s not a physical disease. In 1980, psychiatry said, “No, we’re going to reconceptualize these things as diseases of the brain. If you have depression, there’s something wrong inside your brain with your, there’s a pathology going on.” They said, “We haven’t really discovered the pathology, but we think it’s these chemical imbalances.”
Yes, we think.
But they didn’t say “we think”. They told us we know that there was a little bit of a problem. And actually it wasn’t even we think, it’s we’re guessing that it may be so. Once psychiatry had this new disease model, the drug company said this is fantastic. Because now every time someone’s having an emotional upset we can say it’s a disease, and we can get approval for a disease. And this meant 12 year olds who are going through their moods can now all of a sudden become a market. And they understood that they were going to greatly expand the market.
They brought new drugs to market that were no better than the older drugs, because they were now giving money to academic psychiatrists to test the drugs, to tout the drugs. We heard that, “Oh, Prozac is a breakthrough drug that will make you better than well.” Well, if you actually look at the data of the Prozac trials, they weren’t as good as the old drug. That’s number one, the old tricyclic, in terms of effectiveness. And I forget the number of trials that failed. It was like five didn’t even beat placebo. And that placebo group is not a real placebo group. They withdraw people from the drugs. Germany, for example, said this drug, fluoxetine or Prozac, is totally unsuitable for depression. Even the FDA reviewer said, “There’s going to be all sorts of problems. People are going psychotic, but we will approve it anyway.”
Of course, this doesn’t surprise me.
Prozac was on the covers of magazines, like Newsweek, saying, “Better than well”, “Breakthrough”, “They’ve discovered how the brain works”, “The problem is their powers are so great”, “They can make a shy person an extrovert now.” But if you look at the data, it was not a very effective drug. And people were going manic on it, which means you get put into the bipolar category. And there was no data to use this in kids at the time. There really isn’t still. The data is that it doesn’t work in kids.
Heartbreaking. I’m so glad you walked us through that. I wanted to start there, because I want our readers to understand the history and how these things come to market. Because it’s hush hush. Big Pharma owns the media and owns a lot, right. So we don’t hear about these things. They land on the cover of major magazines. They’re pumped into commercials that we see when we’re at the gym working out. They’re everywhere here in America. I think this is really key to start here. So thank you for that.
Bob, in your book Anatomy of an Epidemic, you investigated why the number of adults and children disabled by mental illness has skyrocketed over the past 50 years. And you talked about that a little bit. Would you mind sharing with us more of what you found in that regard with your book?
Can Antipsychotics Cause Long Term Damage?
What I was interested in when I set out to do this book was how do these medications affect people long term? Because the clinical trials only look at six weeks, right? And they only look at how well the drug knocks down the target symptom a little better than placebo. And oftentimes, it’s just so tiny. Even in those clinical trials run by drug companies that are designed to make the drug look good. The difference in reduction of symptoms is so small, even in the antipsychotic trials. So I was interested in a new question since we had this explosion of people using these drugs and staying on the drugs long term. And I knew that generally it’s not like the burden of mental disorders is going down in our society, which is usually what happens. If you get new great drugs for a disease that make people better than well, the burden of that disease is going to go down in society, right? And instead, I knew that things were getting worse. More kids ending up in hospitals, more kids getting diagnosed with bipolar.
So what I did is look at this very key question. How do medications shape people’s lives over the long term? Now, you would think that would be something that the profession would be looking at, but they had sort of ignored that. There were some studies. And the studies didn’t give them the results they wanted, so they didn’t tell that to the public. So as a way to look at the rising burden of mental illness, I said let’s just look at the number of people on disability. So I went back to the introduction of Prozac, because as you said that was the start of the second generation. That was the first of the new SSRI (selective serotonin reuptake inhibitor) antidepressants. Then we got new antipsychotics, and all these new drugs are said to be better than the first. In 1988, there were 1.2 million adults receiving a federal disability payment due to a mental disorder, meaning depression, psychosis or psychiatric disorder. 1.2 million. And that’s when we get Prozac. And that’s when we get this extraordinary rise in the use of antidepressants. And we actually get a rise in the use of antipsychotics too. Well, what happened? As the use of these drugs went up, the number of people on disability went up, and they went up in lockstep.
By the time I was writing Anatomy of an Epidemic, when I was doing the research in 2008, the number of people on disability had jumped from 1.2 million to 4 million. That’s a three fold increase. And the number of kids on disability under 18 had risen from 16,700 to something like 600,000. So now we have a marker of more and more people becoming disabled by depression, by bipolar, by ADHD. And it goes up in lockstep with the use of these drugs. So something seems amiss there. And then I went through the pieces of a puzzle to put together a story about how there is an evidence-based narrative of how these drugs affect long term outcomes. And I did it for schizophrenia, I did it for depression. With bipolar, I looked at where the bipolar patients were coming from because bipolar used to be a rare disorder.
So now we have a marker of more and more people becoming disabled by depression, by bipolar, by ADHD. And it goes up in lockstep with the use of these drugs.
Here’s the key part of this intellectual exercise. You have to start with understanding what is the natural course of the disorder. Meaning what is the capacity to recover in nature from depression. What is the capacity for a kid who doesn’t like school to get into a different environment where they’re engaged? And then with schizophrenia what were recovery rates for first episode patients entering asylums prior to the arrival of the drugs? Depression was understood to be an episodic disorder, to be of two types. One part was just to be a normal reaction to life. And this can happen due to setbacks in life, you get divorced, you lose a job. That was understood to be totally episodic. You’re going to get better. And if you did a survey, the public would say I will just ride it out, it’ll get better. That was the natural course of depression, except for one group. They said this is a group that had clinical depression. They were remaining depressed longer than it seemed they should in response to whatever the setback in life was, or there wasn’t even a setback in life. And that was basically your group that ended up in the hospital, okay? Now, even in that group, 85% would be discharged within a year. And if you go back to the first episode group, 50% would never have another episode, another 30% would have an episode maybe every three to four years. Only about 15% became chronically ill,15 to 20%. That is that small group of people that had clinical depression. So what you see is generally people get better. Depression is something that they can get better from. They make changes in their life.
With this reconception of depression as a disease, you now have a chronic condition. You have to take a drug because you have this chronic condition. Now what happens is we put together this narrative in the scientific literature. So the first thing is, you sort out what is the natural course of the disorder. Now, in order for your drug to be helpful it has to beat that. The Hippocratic oath is don’t make your patients worse. What Hippocrates was saying is there’s a natural capacity to recover in nature from so many things. And in order to not make patients worse, you have to beat that natural capacity to recover. Let’s say 40% of people on antidepressants do well. That’s not what happens, but let’s say they do well. Now those 40% are going to say, “Wow, I’ve been really helped by this drug.” But in the old days, it was 85%. So you’ve lowered that recovery. I’m just trying to say this is how you have to conceive of a drug’s effect. Some people may do well on them, but you want to look at outcomes in the aggregate.
So let’s continue with the story of antidepressants. They really got introduced and more widely used in the 70’s. You start seeing clinicians saying, “Okay, maybe my patients are getting better faster. But now they’re relapsing more quickly than they used to. The episodes are coming closer together.” So the very first study of this in the 70’s was done in the Netherlands. They said, “Yes, if you use antidepressants, or ECT (electroconvulsive therapy), at the time, you increase the frequency of the episodes.” And there are other people that said, “Yes, it seems that the drugs are causing a quantification of the disorder.” There were epidemiological studies done in the 80’s. And then the NIMH (National Institute of Mental Health) holds a big conference on this. And they say, “Yes, it runs a chronic course now. People are remaining symptomatic, maybe a little bit less than that when at baseline, but they are remaining symptomatic, sort of dysphoric.” So what did they do? They didn’t say that the drugs were causing this. They said, “Oh, we’re at last discovering the real course of depression. It runs a chronic course.” But, that’s to save their drugs. They were studying the course of medicated depression.
In 1999, the third edition of The American Psychiatric Association even says we used to think it was episodic. Now we know it’s chronic. And what they said was, in fact, only 15% of first episode patients now have a single episode of depression. And what happens now is the rest tend to have relapses, or they never remit on the drugs or relapses. So the other 85% are now running a more chronic course. So what I was trying to do was put all these pieces of puzzle together, right? What was the natural course? What did epidemiological studies show about the course of the medicated era? What did they recognize as the medicated course? And were there studies done to look at long term outcomes? And now there have been a number that have been done, but they don’t tell the public about it because the outcomes are so poor.
The biggest study was called the STAR*D (Sequenced Treatment Alternatives to Relieve Depression) study. It was 4,041 patients, done by the NIMH, the largest antidepressant trial ever conducted. And they said, “The results from this are going to guide our care.” And of that 4,041 patients, at the end of one year, 108 were well. That’s a stay well rate of 3%. All the other patients either never remitted (they were given four different tries to remit), remitted and then relapsed, or dropped out. And the study protocol said a drop out was a failure. So at the end only 108 were still in the trial, and they paid people to stay in the trial, and were still well. The public was initially told that the remission rate was 67%, and we now know that the antidepressant helps people. That was all a fabrication. The way that study was done is first you were seen to remit. And then if you were remitted, you were doing this one year follow up. In fact, I think only 26% of researchers got to look at the data ever remitted. And then the stay well rate ended up at 3%. So what I’m trying to say here is you put these pieces of literature together, these facts together, and you get a conclusion. Antidepressants increase the chronicity of the disorder. They worsen long term outcomes. The first edition was published in 2010.
There have now been a number of other long term studies, and some are retrospective, that was triggered by Anatomy of an Epidemic. And guess what they’ve all found? Every single new study at an international level is finding that medicated depression runs a more chronic course. So that’s what I did in Anatomy of an Epidemic. I did it for schizophrenia. I did it for ADHD. And what you find across the board is an increased chronicity. You will see an increased risk of becoming functionally impaired, i.e. disabled. And you see this risk with depressants and stimulants. A number of people have a manic reaction in response to an antidepressant like Prozac. Once they have a manic episode, and stimulants are the same thing, they’re now seen as bipolar. And once they’re seen as bipolar they’re put on polypharmacy, and they’re really screwed. And so you can see a method for creating mental patients, lifelong mental patients, with this form of care.
And with the SSRIs arriving in 1987 or 1988, and then we get others, bipolar goes through the roof. The increase in bipolar in adults more than doubled in the first nine years. And there was a 40 fold increase among kids being diagnosed with bipolar. So what you also see, the other bottom line, when you look at the literature is you have a mechanism for creating disabled patients. So you take someone with a mild problem and give them an antidepressant. There’s a risk they’ll have a manic episode. And once that happens, they get diagnosed with bipolar. And once you’re diagnosed with bipolar, you’re seen as having a lifelong, severe illness.
Wow. I really appreciate you walking us through that, Bob. And that’s what I see clinically in the people that I serve. And it’s heartbreaking to see that these drugs are created by design. The bias in the studies, the lying to the public and doctors lying to doctors. Do you feel like this is by design so that big pharma can generate more money?
Well, certainly it worked from a capitalistic point of view for big pharma. Because in 1987, when Prozac came into the market, we spent as a country $800 million on psychiatric drugs. When I was researching Anatomy of an Epidemic, which was in 2008, the market had grown to $40 billion. So that’s a 50 fold increase in market size. And so from any sort of capitalistic perspective that’s extremely profitable. That’s a success story. That’s a capitalistic success story. You’ve created a market. The drug companies love the chemical imbalance story because you really make money from drugs that are taken long term, not just acute. Just think about it. Do you want a client for 30 years or do you want one for three months? You want your client for 30 years. So this whole model was good for drug companies and they moved in. Now, where they’re really to blame is, so often the drugs weren’t effective over the short term. So they spun those results. And they paid academic psychiatrists to say they’re really great. And they hid adverse events.
The drug companies love the chemical imbalance story because you really make money from drugs that are taken long term, not just acute. Just think about it. Do you want a client for 30 years or do you want one for three months? You want your client for 30 years.
So the drug companies were responsible for two things: producing short term clinical trial results that exaggerated safety and efficacy, and hid harms. And then, of course, they promoted the chemical imbalance story to make it chronic. So, clearly, pharma companies deserve a lot of blame. But who do we really expect to tell us the truth? Academic doctors and academic psychiatrists. American psychiatry in the 1980’s threw their hat in the ring saying we’re going to see these as diseases of the brain. And their authority over our lives grew as this whole psychiatrization of the public happened. They became sort of the philosophers of our age. It worked to their advantage, because now they were seen as doctors in white coats. The media came along because of academic psychiatrists saying this is what we’d found. But what you find is that in the 1980’s and 1990’s, the pharmaceutical company bought academic psychiatry. So virtually every academic psychiatrist was being paid to be a consultant, an advisor, to do the trials and to do continuing education. So now we have individual psychiatrists that are invested in the story, because they’re getting money. They’re also being promoted as the experts in the world, but they’re also the ones writing the textbooks. Money is also flowing to the medical schools. Money is flowing to the journals. So there was a huge money flow that went to the academic psychiatrists, to the journals, to the medical schools, and psychiatry itself. They were invested in telling this story of diseases of the brain, and we have great therapies. They had their own guild interests. So all those interests were aligned.
The only problem was that science didn’t support it. What that did is corrupted academic psychiatry. They stopped telling us about the long term outcomes. The STAR*D study is a great example. They just made up that 67%. They did all sorts of variations with the protocol, numerical manipulations to make the outcomes look better. And then with the 3%, they hid that data. It took outsiders two years to really figure out what the long term outcomes were. So the problem is the market for these drugs causes money to flow in many different ways throughout the organizations that provide the narrative to the public. It went to organizations like NAMI (National Alliance on Mental Illness), the patient advocacy organizations. They all got money. In fact, in some instances, a drug company set up patient advocacy organizations, and gave them money to say this is what the patients are saying, too. So that’s what happened. You have to look at this as a capitalistic story that created a huge market. And they probably wish that the drugs worked to improve long term outcomes, but they didn’t. And so they basically all got invested in a fake story.
That’s what happened to us. The worst is the kids. If you look at medicating kids with antidepressants, those trials were negative even in the short term. You saw kids going psychotic, manic, and having sexual dysfunction. Those trials of antidepressants in youth are a story of harm done, even over the short term. And we have an NIMH study, called the TADS (Treatment for Adolescents with Depression) study, where again they pretended that there was no excess risk of suicide in the Prozac group. But in fact, something like 18 of 19 who became suicidal were on Prozac. But they hid that. I can tell you how they hid that.
Are Antidepressants Harmful in Children?
Bob, in my practice I see a lot of children, very young children, put on these medications. It seems like they’re okay in the beginning, but again, long term, that’s the scary aspect of this. I am curious what you found out about that?
I’ll talk about the TAD study. And then we can also talk about the ADHD study. Before antidepressants and SSRIs came on the market, depression was seen as a disorder of the mature personality. Kids were known to be emotional. They went up and down, especially during the teen years. But what happened is in the early 90’s the adult market was getting saturated. I think we had three or four SSRIs on the market by this time, Paxil and others had come on the market. So they said we need to expand our market and they looked at kids. Kids were an untapped market because in the past we weren’t using antidepressants much. Very few kids were given antidepressants before Prozac arrived in the market.
So the first thing they do is they have an academic psychiatrist say, “Oh, kids can suffer from the disease of depression too.” They had to reconceive childhood, all that emotional stuff. And now they’re going to say if you’re depressed as a kid you have a disease. First of all, they had to reconceptualize that. So they do studies. The initial studies were all negative. And then we find that when they look at those studies, there’s an increased risk of suicide for those kids, right? And then we get a blackbox warning on the SSRIs for kids. You’re doubling the risk of suicidal action. The NIMH then mounted something called the TAD study. This gets the NIMH to really look at this question. It had an odd design. It had Prozac, cognitive behavior therapy, Prozac plus CBT (cognitive behavioral therapy), and then placebo alone. It was a three month study. And here’s the way it went. You were first in active treatment for six weeks. And then there was another twelve weeks you went into a follow up period. So maybe it actually was four months, I can’t quite remember exactly the link. But there was an initial treatment stage, maybe that was six weeks, and then you would go into a follow up part. Now here’s the key. What they did with the placebo patients after that initial treatment station is put them on Prozac. Now, I randomized the placebo. During my weeks on placebo, I’m not suicidal. I go on the drug and I become suicidal. They chalked up that suicide to the placebo group, even though it occurred once I was put on antidepressants. So in truth, the graphic in the suicide report that showed that the placebo patients were seen as becoming suicidal; it happened after they were put on antidepressants.
Oh my gosh.
Now this is really key. So the official NIMH conclusion was Prozac doesn’t cause any increased risk of suicide. That was in the abstract from the NIMH. I know parents whose kids were put on Prozac because of that study, and then the kids committed suicide. And what you see with Prozac suicides, they are often these very violent suicides. They hang themselves. It’s not a normal way you see things going. When I wrote this article saying here’s the real suicide data from TADS, mothers were crying on the phone to me saying I told my kid to take Prozac because the article said it didn’t cause excess suicide.
Gosh, that’s heartbreaking.
So that’s the TAD study. They lied in a way that caused children to die. Prozac got approved for marketing, but the way they designed the study was so biased against placebo. Kids did some self-evaluation of their depressive symptoms. They didn’t improve on Prozac compared to placebo. Parents didn’t see improvement, only the doctors did. It was their measuring.
If you really look at this, Dr. David Healy has done an extensive review of antidepressant trials and kids. He says they’re all negative. So we have kids being medicated with a class of drugs that increase the risk of suicide, cause sexual dysfunction in many of them and don’t even improve the depressive symptoms. Now, what do you say about a medical discipline and pharmaceutical operations that treat our population this way? It’s outrageous.
It’s heartbreaking. It is absolutely outrageous.
As you say, kid’s brains are developing. They need their emotions to get through it. A number of kids who are put on antidepressants as teenagers, then go through puberty on antidepressants and then maybe go to college. They want to become sexually active, but something like 25% develop what’s called PSSD which is Post SSRI Sexual Dysfunction. In other words, they don’t regain their sexual interests. Think about that.
Yes, that’s huge. ADHD is such a big one.
And then if you look at the stimulants, we did a study in the 1990’s, called the MTA (Multimodal Treatment of Attention Deficit Hyperactivity Disorder) study. First it compared drugs to behavioral therapy over fourteen months. And the study showed a little bit better diminishment of ADHD symptoms at fourteen months and a little better reading scores. So they said all these drugs work long-term. That study continued and at the end of three years, being on medication was a marker of deterioration, not of benefits. At the end of six years, they had higher delinquency rates, they were shorter because the stimulus suppressed growth and greater signs of functional impairment. So which of those three results are parents told? Fourteen months? Three years? Six years? You know the answer. So this is part of the betrayal of the public. It’s so profound is the only way to say it.
So we have kids being medicated with a class of drugs that increase the risk of suicide, cause sexual dysfunction in many of them and don’t even improve the depressive symptoms. Now, what do you say about a medical discipline and pharmaceutical operations that treat our population this way? It’s outrageous.
It is so profound. In the work that I do in the area of mental health, which includes OCD, ADHD, and eating disorders. That’s another big one. I work with a lot of young ladies that struggle in that area, men too, but mostly the younger female population. It’s truly heartbreaking. And autism is another area that I work extensively in with families. And that’s another show. But I’m really so appreciative of you walking us through what the data shows, has shown, and continues to show.
There was another recent study that came out about SSRIs, and people are talking a lot about that as well. And just the whole concept of a serotonin deficiency. And that leads me into my next question that I’m curious about, the chemical imbalance hypothesis. You’ve talked a lot about that already. What’s interesting about that is that the normal functioning of neurotransmitters is perturbed, and it leaves the brain functioning in an abnormal manner. And long term the repercussions are tremendous. Can we talk a little bit about each one, and how they act on the brain? You talked a lot about SSRIs and serotonin, but do you mind getting into more of the mechanism of action for us?
What Do SSRIs Do to Your Brain?
Sure. And let’s start with the antidepressants, because that low serotonin theory is so well known. So how do neurons communicate in the brain? You have a presynaptic neuron that releases a neurotransmitter, a chemical messenger, into a tiny gap between neurons called the synaptic cleft. Serotonin is a chemical messenger. And then that chemical messenger binds with receptors on the receiving neuron, which we call the postsynaptic neuron. And that’s how messages get passed along neurotransmitter pathways. Serotonin is an excitatory messenger that causes that second neuron to fire. And that’s the basic mechanism. Now in order for that messaging system to be crisp, what happens is there’s a pulse and serotonin is released into that gap. It binds with receptors, this happens so fast, and now the serotonin has to be removed from the synaptic cleft. That’s the way you get a pulse in and out. Now it’s removed in two ways. Most of it goes back up into the presynaptic neuron on the synaptic channels and it gets stored there for release. Then there’s a small amount that is carted off as waste once an enzyme comes along and metabolizes it.
So what they found is the drugs we know as SSRIs, and even the first generation, basically worked in this way. That’s basically what happens is they blocked the normal reuptake of serotonin. If you have the drug Prozac, it prevents that serotonin from going back up into that presynaptic neuron. Serotonin stays in that gap longer than normal. So you say you’re upping serotonergic levels. Which right away you can see you’re perturbing normal function. You’re blocking this normal process of taking things back up. In 1965, they came to understand the mechanism of action of the drugs that have blocked this normal reuptake. So they hypothesize that people with depression have too little serotonin, and that’s why the drugs are effective. So now they have to do studies in patients before they go on the drug to see that they have too little serotonin. As early as 1984, the NIMH was concluding they were not finding that people with depression have anything wrong with their serotonergic system. There were some more studies, all different ways of studying serotonergic function. In 1999, the APA (American Psychiatric Association) published the third edition of its textbook of psychiatry. In that manual they said the low serotonin theory of depression has not panned out. We just did not find it to be so. But yet the public wasn’t told that. The public continued to be told that it was due to low serotonin.
Now, that’s half the story. The other half of the story is what happens to your brain when you block this normal function. The brain is having all these feedback loops and is so neuroadaptive, it changes its own architecture. The drug is upping serotonergic activity. Your brain is trying to maintain what we call a homeostatic equilibrium, and diminishes its own serotonergic activity. It does so in two ways. The presynaptic neurons start putting out less serotonin than normal. And the postsynaptic neurons actually decrease the density of the receptors for that molecule. In 1996 Stephen Hyman, who was director of the NIMH, wrote a paper saying the paradigm for understanding psychotropic drug action. He says these drugs perturb normal activity. The brain, in response to this, goes through this compensatory adaptation. It’s trying to maintain its normal functioning, its homeostatic equilibrium. And at the end of this process, the brain is now operating in a manner that is both qualitatively and quantitatively different from normal. That’s the head of the NIMH, who was a neuroscientist. That’s not me speaking.
Here’s the irony of this. The drugs, antidepressants, induce the very abnormality hypothesized to cause depression in the first place. Because once you go on the drug you end up with a serotonergic system outside of the drug that is desensitized to serotonin, that has a low serotonergic activity. Now, you can apply that to every psychiatric drug. By the way, when research is now away from the public eye, and talk about why depression runs such a chronic course, they’re pointing to this. They say these drugs cause this compensatory adaptation, SSRIs. And over the long-term, that may induce dysphoria, a permanent sort of chronic low level depression. And if you’re on these drugs long enough, it may not be reversible. So science was showing that these drugs, antidepressants, rather than fix a known chemical imbalance, or if there was nothing known to be wrong, were creating a brain that now operates in an abnormal manner. And that abnormality may become permanent. And if so, it may cause chronic dysphoria and other symptoms. And one of the symptoms it may cause in some people is persistent sexual dysfunction. I see that a lot.
What you see with schizophrenia is basically the same story. Those drugs block dopamine receptors. In response, the brain increases its density receptors. It induces what’s called a dopamine supersensitivity. And as early as the 1980’s, researchers were hypothesizing that this drug induced dopamine supersensitivity caused people to become more biologically vulnerable to psychosis, more vulnerable to relapse, more vulnerable to severe illness and psychotic episodes. So again, buried in the research literature is the story of drugs that may have some short-term efficacy. But on the whole, they induce physical changes in the brain that are understood to worsen long-term.
So that’s the story and think about the betrayal there. You go to a doctor for many years, and you were told that you had a serotonin imbalance. You say, “Oh, that’s why I’m depressed, I have to take this drug for life.” And science was showing that they didn’t know anything was wrong. There’s nothing wrong with your serotonergic system. But, after you take the drug there will be. That’s an incredible betrayal. And by the way, I think the study you’re talking about was done by Joanna Moncrief and Mark Horowitz. They looked at this long history of the low serotonin theory of depression. They looked at the research to see if people with depression had low serotonin, and they said it was never there. So what they did is this comprehensive review that said there was never any evidence for it. So think of that. I knew this. It was there in the research literature. It was no surprise, but the public treated it as a big surprise. And by the way, if you’re a journalist writing that this isn’t true, when the expert says this is what’s being told to the public, your fellow scientific journalists think there is something wrong with you.
Yes, good point. I’m glad you said that.
Who are you to say that there’s no low serotonin? I said, “Well, I’m not saying it, it’s what’s in the literature.”
To your point, the betrayal is so astronomical. And we’re seeing this with many different classes of medications. Statins are another good example of a betrayal that started from a faulty study. Most people are aware of Ancel Keys and that whole issue. But I think it’s so important to always look at the long-term repercussions. And again, especially when they’re being given to children that are still growing. Keep in mind that when children enter puberty, there are going to be a lot of different types of changes.
In the work that I do, yes, there are biochemical imbalances that run in families. Nutrient deficiencies and overloads that can impact the brain. Things like copper overload and zinc deficiency are a huge concern in mental health. These are all areas that I work in. But we can correct these things without the use of drugs. And I always want to give that encouragement to the parents. If a drug is given, six months appears to be a decent time frame. Do you know of any specific research to support the shorter durations or that just hasn’t been done? I’m just curious what you thought about that too?
For antidepressants or an SSRI?
Yes, like six months, just to help someone initially if they really feel that they want to take something for a short period of time. While, for example if they were to be working with me, we get the nutrition on board, we look at some lab work for any of the nutrient deficiencies I mentioned and support them from there. I don’t know if there’s any study on that. I don’t think they’d probably be inclined to do that.
Should Antidepressants be Taken for a Short Time?
Here’s what happens in a lot of the clinical trials. I’m not talking about a trial that compares to what you’re talking about with nutritional change. People are seeing a diminishment of symptoms. The question is, is it any more than what the placebo group is experiencing? In the antidepressant trials the difference at the end of six weeks is so small, it’s not clinically meaningful. It’s like two points. And that’s coming in trials where the placebo group isn’t a true placebo group. It’s people who’ve been on antidepressants and they’re washed out. They’re taken off the drugs. So really, you’re seeing the people recuperating from that withdrawal thing. And by the way, there’s something called a running phase. If you’re taken off of your antidepressant and you do well, you’re washed out of the trial. It’s only if you’re not that you stay in the trial. So you see the confusion? There are people getting better with the drug. But, it’s really no better than with the placebo group. So why use the drug? Then there’s about 15% of people on antidepressants that do get a benefit, over six weeks, that you don’t see in the placebo group. If that’s true, it means there’s also people getting worse on the drug compared to the placebo group.
But here’s the thing. The NIMH did a study comparing drug to exercise to drug plus exercise. Now at the end of six weeks, the drug plus exercise was better than exercise alone. But at the end of nine months exercise alone was better to either drug alone or drug plus exercise. And drug plus exercise was no better than drug alone. It was as if the drug hampered the recovery rates. So what I’m trying to say to you is, these drugs can cause a change in behavior and feelings over the short term that some people find helpful. But there aren’t good studies showing that, at six months, it’s better than a natural recovery from depression. Particularly if you’re engaging in some sort of change in life like eating better foods, getting exercise and maybe you can socialize in a different way. I know somebody who asked all his patients to become volunteers, to do volunteer work. So I know of no study with depression that shows that six months drug treated patients are doing better than unmedicated patients. Particularly if they do something else to change their lives.
The best study, over a long term, was done by the NIMH on this. And they found that the disability rate long term was very negligible for those who didn’t take drugs, but it was like seven times higher for those who took medication. So I guess what’s complicated here is, so many people will talk about feeling better. That’s true. But they don’t know what they might have felt if they hadn’t done it. And when you do a comparison against that, the benefits sort of disappear. And by the way, there’s even evidence related to that with psychotic patients. Often in first episode stories they will use agents to help people sleep. So they will use sleep medications, or they can use benzodiazepines as needed to sort of diminish the anxiety. But if you do that, compared to antipsychotics, and combine this with intensive psychosocial care, there’s actually the same diminishment of symptoms at the end of six weeks in psychotic patients. The group that has done this the best, in northern Finland, really tries to keep people off antipsychotics in the beginning. And then they would use benzos to help people get sleep because they felt that way people could become emotionally engaged in a social situation. Which was so important to sort of regaining function. What’s really important is, we’re not saying do nothing. The question is, what do you do to help people?
I think that’s really key, because I want our readers to know that this is a conversation meant to inform and support. It’s not about judgment, or that you’re doing anything wrong if you’re on a specific medication, if you’re on an SSRI That’s not at all what we’re saying. I simply wanted to be able to have you come on and explain the data, explain the research and talk about what was actually seen.
Again, I love this term, that betrayal of the public. It’s a sad concept. But it’s important that we say it, because it really is a betrayal with repercussions for generations thereafter. So if we look back through the 60’s and the 70’s, at the children that were born to mothers that were maybe on some of these medications and the changes that occured. The epigenetic changes that can occur over the generations is something that I think about a lot. There aren’t any studies about that. I wish there were. But to your point there’s so much that goes into this. And my concern also is outside of the side effects, the negative side effects, from these drugs that are neurological and cognitive.
What about the other effects that occur such as dysregulation of the gut microbiome, joint issues and autoimmune induced issues? We know that SSRIs dysregulate the gut microbiome. They do have antibiotic-like effects. And there are a couple of studies on that, which I will link to in the show notes. But we know the gut microbiome has a huge impact on the brain, that whole gut brain connection. I talk about that a lot, especially in psychosis. So I just want our readers to know that there are options that don’t include something that is going to potentially harm you. Because the data is just not there that these are effective remedies.
We talked a little bit about stimulants. We know all the issues with Ritalin, and then the benzo class that impacts GABA (gamma-aminobutyric acid receptors). Those can be especially nasty. What did you uncover about those, Bob?
Well, the interesting thing about the benzodiazepines studies is they were understood to be addictive going back to the 1970’s. And they were also understood to lose their efficacy after about four weeks in terms of reducing anxiety. Basically, there’s the same story of benzodiazepines as with antidepressants and the other drugs. So GABA is actually an inhibitory function. Neurons can either be excited or they can be inhibited. You need a break from this activity. That’s how the brain is designed by evolution. What happens with benzodiazepines is the same thing. Benzodiazepines put the brake on even harder on neuronal activity. But what happens is your brain now starts reducing its own GABA receptors, its own production of GABA. So now you’re driving your brain into a state where its normal break on neuronal activity is disappearing, or it’s becoming diminished. And when you try to come off you no longer have your normal breaking neuronal activity.
That’s why people going through benzo withdrawal talk about all these weird sensations, skin things and stuff. It’s because you’ve removed the break, and you’ve dysregulated the firing of the neurons. And the problem is, with long term use of benzos, you see greater anxiety. There’s a greater risk of becoming agoraphobic, afraid to go out, diminishment of functioning and diminishment of ability to engage socially. The thing with benzodiazepines is, they were known in the 1970’s to be addictive and have an incredible withdrawal effect. So you shouldn’t prescribe them for more than three or four weeks max. I think benzos can be really great when you’re having horrible moments or something, right? A one time use. They’re very effective. But next thing you know, because of this story, they started keeping people on benzos long-term. And now we have all these people addicted to benzodiazepines. And when they try to come off, it’s just a horror show. Can we go back to one other little thing?
Yes, please do.
Natural Alternatives to Antidepressants
When we were saying earlier that we’re not talking about doing nothing. One of the important things about uncovering this research, is what you see over and over again, is actually an optimistic story. That people go into a difficult time with anxiety. They can make changes in diet, exercise and socialization. Maybe it’s a crappy job. Maybe it’s a lousy relationship. But you can make changes. And as you change your environment these emotional difficulties, these other psychiatric difficulties, diminish. Human beings have resilience. One of the problems is this brain disease story took away that understanding of our resilience, and the fact that we’re built to be adaptive and responsive to the environment.
The other thing we talked about is the gut. Serotonin is big in the gut, right? And by the way, I saw this information once where they looked at utilization of health resources in the five years before someone went on an SSRI and then in the five years after. What you see is utilization is going along at a certain level. They go on an SSRI, and it bumps up way higher to another level. That’s because there’s all these other problems, like the gut problems that show up. So for your audience, it is important to not be pessimistic about this. Because what it really is telling is this capacity for human beings to get better,
Yes, amen to that.
So that’s the optimistic part.
I’m so glad you said that, Bob, I really appreciate that. Because I do want to end here on a positive note. And again, in the work that I do, there’s so much that we can do in terms of nutrient therapy. Figuring out where the deficiencies are, where the overloads are, looking at the gut microbiome and addressing any infections there. That’s a big part of my work because the gut brain connection is so profound. I do appreciate that.
We’re so blessed to have you and your work. I’m sure you’ve been attacked for your work. So I’m sure this hasn’t been easy over the years. But clearly, you’re quite resilient yourself. You continue to speak and you have this amazing website that we will be linking to in the show notes, Mad in America, so that people can read more of the studies. Also your great work and your books. We’ll be linking to those as well. Thank you for coming on today, Bob, and I really appreciate having you.
Well, thank you for having me. It was really a nice interview. So thanks so much.
I’m so grateful to Bob for literally putting his career on the line to share the truth about psychiatric medications. Bob reminds us that when it comes to psychiatric care, patients need to be proactive and try to understand the research literature regarding the merits of psychiatric diagnoses and the risks and benefits of psychiatric drugs. Because the usual information provided to the public is out of sync with the information found in the research literature.
- Bob’s website Mad in America
- Bob’s books
- RxISK – maintains a searchable database of adverse effects of prescription drugs that have been reported to the FDA in the United States, Health Canada, and to RxISK.
- Research and Studies
- Eat for Life Episode 2: How Nutrient Deficiencies and Overloads Impact the Brain and Body
- A Review of the Antimicrobial Side of Antidepressants and Its Putative Implications on the Gut Microbiome
- The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) Trial: A Review
- The Treatment for Adolescents With Depression Study (TADS): long-term effectiveness and safety outcomes
- Multimodal Treatment of Attention Deficit Hyperactivity Disorder (MTA) Study
- The serotonin theory of depression: a systematic umbrella review of the evidence