Demedicalizing Depression: An Interview with Milutin Kostić

Milutin Kostić is a practicing Serbian psychiatrist trained in the tradition of biological psychiatry who has become a new figure in the critical psychiatry movement. Affiliated with the Institute of Mental Health in Belgrade, Serbia, he is currently a Fulbright scholar working alongside Lisa Cosgrove in Boston to challenge established norms in psychiatry and psychology.

Kostić utilizes his extensive training and traditional research methods to question the fundamental assumptions of his field. For example, Kostić critiques the flawed premises of genetics research in depression, arguing that it overlooks the heterogeneity of human experience. He uses analogies to illustrate how psychiatry often pathologizes normal human emotions, drawing parallels to how medical conditions are misunderstood when the context is ignored, like trying to treat the lungs alone in a society overrun by air pollution.

We will also discuss his latest study, which emphasizes the benefits of de-medicalizing experiences of depression rather than quickly resorting to diagnoses and subsequent treatments with medication or psychotherapy. His research also sheds light on the effects of biological narratives on patient perspectives, the complexities of drug dependency, and the profound impact of psychiatric diagnoses on individual identity.

The transcript below has been edited for length and clarity. Listen to the audio of the interview here.

 

Karter: To get us started, can you tell our listeners about your story? How did you train in psychiatry and traditional biological psychiatry, and how did you eventually come to see yourself more as a critical psychiatrist?

Kostić: I trained in medical school, where the focus was entirely on the biological aspects of medicine. The humanistic, social, and philosophical dimensions were on the margins, almost exceptional. We were taught to think in a straightforward cause-and-effect manner: this causes that, and this is treated by that, with very little emphasis on critical thinking. For instance, I find it fascinating that during my six years of medical school, I never heard about randomized controlled trials until my doctoral studies. We were simply told, “This is good, use this.” But how did they know? I had to pursue a doctoral degree to learn the methodology behind such assertions.

Medical school was all about the major exams: anatomy, physiology, pathology, histology, etc. The focus was always on what’s happening in the body. Naturally, when I started psychiatry, it felt like an extension of this focus: understanding what’s wrong with the brain, the emotions, the thoughts. During my psychiatry residency, I simultaneously pursued my doctoral studies, focusing on imaging and genetics in depression, trying to identify subgroups through polymorphisms to better understand these conditions. This defined my first seven years of psychiatry training and even continued after I became a specialist.

During my doctoral studies, it was hard to switch off. You’re in the zone, focused on your thesis and the goal of obtaining your degree. This intense focus often suppresses critical thinking. My first international conference was a turning point. It was in Barcelona, where I attended various sessions and browsed through books on psychiatry. One of the books I bought was “The Loss of Sadness” by Wakefield and Horowitz, which critiques the DSM diagnosis.

After finishing my doctoral thesis, I experienced a sense of loss and confusion. I had completed my residency and started a family, so I thought I should continue my work in genetics. I even began forming a genetic biobank at my institute and establishing connections with other genetic research institutes. However, my heart wasn’t in it. I was trying to push myself, but I felt empty.

Over time, I recognized that reading about genetics and psychiatry bored and irritated me, despite being the focus of my doctoral thesis. On the other hand, reading about the social and political aspects of psychiatry excited me and made my blood boil. This transformation was gradual, taking about a year. Slowly, I made a complete switch, relearning many things. I started several studies aligned with my new perspective, which felt more personally fulfilling because they were more truthful and made more sense to me. The more time I spent in biological psychiatry, the more it felt like a house of cards with no solid foundation.

 

Karter: Thank you. I do want to get to your recent studies. But just to dig into the genetics of depression a little bit further, from your perspective, having been deeply involved in that field, do you think the main problem with looking for genetic polymorphisms underlying depression is due to the heterogeneity of depression—like the construct is too broad and includes too many people with too many different symptoms—or do you think there are more fundamental issues with even looking for underlying genetic causes of depression?

Kostić: There are a variety of problems, each one complex enough to discuss for hours. My main issue is that the starting premise is wrong. When your premise is flawed, no matter how excellent your studies are, you’ll end up with gibberish. We’re comparing apples and oranges here, and this is often called the heterogeneity of depression. However, I prefer not to use that term because it implies that depression is just a set of different types of the same disorder. Instead, I think it’s more accurate to talk about the heterogeneity of human experience. Words carry weight. When we say “depression,” we typically mean “major depressive disorder,” and when we say “disorder,” it implies something is wrong with the brain.

Medical philosophers and psychiatry philosophers often engage in complex debates, arguing that a condition doesn’t have to be a medical disorder to be significant. But this is Ivory Tower academics. In practice, when a psychiatrist, perceived as a figure of authority, tells a patient they have a disorder, it often leads the patient to believe something is fundamentally wrong with their brain, serotonin levels, or genetics. While there might be some truth to this in certain cases, it’s like saying there might be a problem with anything else—it’s uncertain, and we really have no clear idea.

The problem starts with the premise. We’re just lumping together people with symptoms and asking, “Why are they coughing?” It’s like taking everyone who coughs and putting them in an MRI to figure out why. But some people cough because of asthma, others because of cancer, a bacterial infection, or a tic. Some cough because the air is polluted. In that case, there’s nothing wrong with their lungs—the problem is the air.

We keep seeing a rise in diagnoses, especially with conditions like anxiety, depression, and adult ADHD, which exist on a continuum of normality. How focused should I be? How sad or anxious should I be? There’s a push for mental health awareness, but no one is asking what’s in the air. Why are more and more people coughing? It’s like everything is blamed on the brain. This is the biological basis of medicine, and it’s fundamentally problematic.

When you group together people who are sad for different reasons and try to find a genetic cause, you end up with nothing. It’s useless. There was a huge study in genetics and neuroimaging with a million controls. The abstract sounded fantastic, but when you read the fine print, you see the flaws. They asked participants one vague question: “Have you ever been to a psychiatrist or psychologist for nerves or something in your lifetime?” This was the depression group, even though the question could mean anything. Those who said no were in the control group. They compared apples and oranges. Even with such a large sample, they found meager positive results, explaining only up to 3% of the variance. I think even those 3% are just artifacts, false positives.

But even if they found that 3%, it’s nothing. Yet it makes an amazing headline in a top journal. You see how this clinical aspect is flawed—needing a million sample size, using the best genetics and the best statistics—and it’s still worthless. It’s hard to tell people that all of this is worthless. It’s worth less than a Cosmopolitan magazine you buy on the street, but it has so much power in the discourse that it’s ridiculous.

 

Karter: This is a great jumping-off point because not only is this way of thinking about depression scientifically worthless, but it’s actually potentially harmful when people start to understand their experiences through this lens. I want to pick up on that because both of your recent studies address this issue. Let’s start with the medical students’ perception study. Can you tell us a little bit about that study, why you conceived it, and how it played out?

Kostić: Sure. We created a vignette with patients showing symptoms of depression but also included some social circumstances. For example, one vignette had a patient with depression whose mother and daughter had also seen a psychiatrist. We wanted to see how these added details would influence the students’ views on treatment.

From this study, the most important result, in my opinion, came from a basic question we asked: “How effective do you think antidepressants are?” We analyzed the responses by year of study, from first to sixth-year medical students.

When we asked first-year students about the effectiveness of antidepressants, they rated it just above no effect, essentially saying the effect was modest. This aligns with the most positive meta-analyses, like the Cipriani study, which also describes the effect as modest. So, the first-year students basically got it right.

However, by the second year, the perceived effectiveness started to rise. By the fourth year, their perception had increased significantly, rating antidepressants between moderate and high effectiveness. This change highlights how education can shape and sometimes distort perceptions over time.

From the very beginning of medical studies, we’re driven to trust medicine and the drugs we prescribe. We’re taught that what we do is inherently good. I think this was the most interesting part of our findings because it shows that we need a complete overhaul—not just in psychiatry, but at the root. We need to address the culture, the media, and the education system to help people understand that things aren’t always as they’re presented. We need to start in medical schools.

For instance, as you mentioned, I’m here on a Fulbright scholarship. In my proposal to the American Embassy, they asked about my future plans. One of the things I wrote was that I want to introduce a topic in medical schools about overtreatment and overdiagnosis. Unfortunately, by the time students get to internal medicine, psychiatry, or neurology, the focus is mostly on what you should and can do. There’s almost no emphasis on what you shouldn’t do. It’s just assumed that you have to do something. This mindset has contributed to the current state of psychiatry.

 

Karter: When you spoke about your own training at the outset of the interview, you mentioned that the way issues are framed as part of the medical school curriculum leads one to naturally assume that we’re working on correcting some underlying pathology with tools we think might help. This framing makes the issue seem concrete, but it can be really misleading. It’s interesting that your study shows students actually get less accurate reads of the research the more they learn.

Kostić: Yes, but they’re not. They’re not reading research, and that’s a big problem. Research should inform evidence-based medicine. Instead, we’re getting our information from textbooks that simplify the message.

It’s going to be so hard to counter that because the alternative is much more complicated. It’s much easier for a doctor to think, “This patient has these symptoms, so I’ll prescribe this medication.” It’s simple, and patients like it too. They feel reassured, thinking, “This doctor knows what he’s doing. He’s in control.” It’s nice for both the patient and the doctor, but it’s not necessarily good.

 

Karter: This is a great bridge to the next study, the watchful waiting and depathologization study. Getting indoctrinated into this way of thinking about depression has consequences, as you said, for patients. They come in and, because they screened positive—maybe with their GP using a PHQ-9 or something like that, which has its own issues—they potentially meet the criteria for a depression diagnosis. They hear they have a disorder and that treatments are available. This significantly impacts how patients think about and understand their experiences. Your study looks at an alternative approach, using a model you’d typically see in treatment design studies. Can you walk us through how you conceived this study, how it ran, and what you found?

Kostić: Initially, the study was conceived as a longitudinal study of patients with depression to see what happens when you don’t treat it. There aren’t many studies on this. But it quickly became clear that you can’t just not treat someone who comes to you for help. So, we changed our approach and decided to first tell them, “Maybe you don’t have a disorder.” Many people think that to validate their suffering, they need to be diagnosed with a disorder. But I don’t think a single one of my patients isn’t suffering. The fact that I don’t believe many of them have a disorder has nothing to do with their suffering.

Quite the opposite, I think that to really help them, we need to understand them as social beings. In cognitive behavioral therapy (CBT), which is used in psychiatric settings and is considered evidence-based for some conditions, there’s the concept of learned helplessness. This can be true and useful for some people. Some get stuck in these helpless models of thinking, but then we turn around and tell a patient they have a depressive disorder, which can actually cause hopelessness. So, we’re treating hopelessness on one hand but causing it on the other.

Our approach was to tell the patient, “There’s a chance you don’t have a disorder. We don’t know, and we’re not trying to diagnose you. Maybe there is depression, maybe some people have a brain disorder. What I know is that I don’t know who has a brain disorder, and I know no one else knows because I know what the science says—we don’t know. There’s a chance you don’t have a brain disorder, and there’s a chance things will get better.” This is the basis of depathologization.

But then again, they came because they’re suffering. They didn’t come because they were bored. They came to me because something was wrong. Let’s give them some advice. It doesn’t have to be psychotherapy. You don’t have to be a psychotherapist to give advice. Often, the best psychotherapists are a parent, a spouse, or a friend. If you can get support from them, it’s the best psychotherapy in the world. Sometimes, you do need professional therapy, but it doesn’t have to be complex. It can just be empathy. It can be someone hearing you. It can be someone alleviating your fear that you have a disorder, which I’ve seen happen a lot in my practice.

I’ve seen people who look really depressed and anxious, and when I tell them, “Maybe it is, maybe it isn’t. Let’s wait and see. Think about what you can change in your life, what the problems are,” they come back after a week and say, “I’m still unhappy about these things, but it’s so much more manageable now. I don’t think there’s something wrong with me; I just have to figure out how to deal with these things. I don’t need to come here anymore; I just have to work on my whole life.” This is a powerful thing.

The second aspect was to give them advice. The third thing was that we didn’t impose anything. We said, “You might have depression, or you might not. We can give you advice, but you don’t have to take it. You have options. If you want medication, you can have it. If you want to wait and see, that’s fine too. Drugs have risks and adverse effects, so we can wait and see.”

Some patients said, “Doctor, you’re great, but I came here for antidepressants. I didn’t come here to chat.” That’s valid. If I refused them the medication, it would only increase their anxiety. This aspect needs to be addressed in the public sphere because they’re already so entrenched in the message that medication is the answer. We respected their wishes.

Shared decision-making is extremely important. We didn’t do a randomized controlled trial (RCT) because I think it would be impossible. I’m considering ways to do it because it would be the best approach. But it’s extremely hard to do an RCT for a psychological intervention like watchful waiting. People think watchful waiting means doing nothing, but that’s not the case. This type of watchful waiting is impossible in today’s world.

Maybe it was possible 50 or 100 years ago when someone might come in and say, “I feel sad,” and you could say, “Let’s watch.” Now, they come in saying, “Doctor, I have depression.” Seventy percent of the patients come in saying, “I have depression.” We have to first depathologize.

I love evidence-based medicine. I think it’s extremely important to implement it as much as possible, as often as possible. But some people misunderstand its aspects and limitations, thinking it always gives us true answers. That’s not the case. In internal medicine, you can measure efficacy theoretically. In psychiatry, with all the cultural impacts, I’m not even sure we can do that validly.

I remember two patients who came to me on antidepressants. I didn’t prescribe them. I do prescribe sometimes, but very rarely and usually only when patients ask. These two had been prescribed by other physicians. One said, “Doctor, I’m having problems with impotence.” I said, “Yeah, it’s probably because of the antidepressant. We can start tapering it off.” He replied, “No, please don’t take it away. I feel awesome. I don’t want to go back to how I felt before. I just wanted to know if this is because of that, and if so, I’m fine with it.”

The second patient came in with the same issue, saying, “Doctor, I have a problem with impotence.” I said, “It’s probably because of this medication.” He responded, “Please, we must stop the medication. I can’t live with this.” Both were right for themselves; both had their own truth. There is no objective truth in these cases. This is the problem with evidence-based medicine. When we analyze benefits, they are true for the individual. Saying someone should or shouldn’t take a drug leads us into a paternalistic model where we claim to know what’s best.

It’s good for a person if they believe it’s good after analyzing the risks and benefits. That’s why we didn’t need a randomized controlled trial (RCT) for watchful waiting. Just presenting the option can work. In our sample, two-thirds of the patients were better after three months without drugs using our model. That’s a pretty good number.

 

Karter: Following up on presenting the risks and benefits of antidepressants to patients, you mentioned sexual dysfunction as one of the potential harms people aren’t always aware of. Another issue that’s gotten more attention in recent years is withdrawal effects from long-term use. I saw that you published on suicidality emerging from rapid Venlafaxine discontinuation. Could you tell our listeners a little bit about how you discuss withdrawal or discontinuation effects with patients when they’re considering starting an antidepressant?

Kostić: In clinical settings, it’s often unclear why a patient is getting worse. The automatic assumption is that the depression is returning. That’s what I was taught in residency, and it’s what residents are still often taught. This is also what many patients think because they’ve been told there’s something wrong with their brain, and if they stop taking the drug, things will get worse.

One patient came to me with a story that stood out. She had never had suicidal ideations before. Then, the pharmacy ran out of her medication, and she missed it for two or three days. Suddenly, for the first time in her life, she had suicidal thoughts, which went away when she resumed the drug. Six months later, she had no problems, gained some weight, and her doctor decided to adjust her medication.

What I found interesting is that her previous psychiatrist knew about the risks but not enough. She told the patient, who was on 225 milligrams of Venlafaxine, to take three days of 150 milligrams, three days of 75 milligrams, one day without any, and then start the new medication the next day. This was too rapid. People often don’t realize it can take months, sometimes even years, to safely taper off these medications. This is all new data that many clinicians and patients aren’t fully aware of yet.

Right when she started tapering off her antidepressant, her depression seemed to return, and she had a suicide attempt, which she thankfully survived. Now we’re going much, much slower with the tapering. There was polypharmacy involved, but Venlafaxine was the only change during this period. One of my co-authors, Martin Plöderl, suggested calling it a Challenge-Dechallenge-Rechallenge paradigm.

What’s also interesting, and a bit historical but important, is that the first time I heard about withdrawal in SSRIs was in 2019. This was when Davies and Read’s systematic review came out, showing that around 50% of patients experience withdrawal effects, and a quarter have severe withdrawal effects. This was almost 30 years after Fluoxetine hit the market. Why? Because the drug manufacturers have no monetary incentive to study this.

In ’94, Professor Giovanni Fava published on the possibility of chronicity of depression using antidepressants, but researching this area requires money and people. It often relies on a small number of enthusiastic individuals searching for the truth, like those at Mad in America, while the other side is a machinery of thousands of people and billions of dollars. This is one reason why it took so long for major attention to come to this topic. Thankfully, in the last five years, more is known about it.

I find it fascinating how willfully blind we physicians and psychiatrists can be. I now make it a prerogative to always discuss the possibility of starting without antidepressants with my patients. I think doing less is often better than doing something unnecessary. But I present the options to my patients and respect their decisions. When they want to try medication, I say, “Okay, but know this: it may cause addiction or withdrawal. If we get into that, keep it in mind so we don’t use it for too long if it’s not necessary. If you decide to stop and negative feelings return, it might be withdrawal rather than depression coming back.”

This all takes time, which is a problem when you have 30 patients waiting. It’s much easier and quicker to say, “Here’s the drug; take it three times a day.” But that approach is worse. We have to make things more complicated, and this is never easy.

 

Karter: I’ve heard it expressed—perhaps a rather cynical position—from some psychiatrists, especially on Twitter and elsewhere, that providing fully informed consent about the limited efficacy of antidepressants and the potential for harm could reduce the placebo effect and, therefore, the healing potential for the patient. I would like to hear your response to that perspective.

Kostić: As you said, it’s a cynical view, and it aligns with the practice of undervaluing harms and overvaluing benefits. When we think about shared decision-making, we consider whether a drug is good, bad, or how it will heal. If I tell a patient they have a disorder, of course, they’ll think they need a drug. But this initial premise is potentially very wrong.

If you keep the patient in the dark to preserve the placebo effect, you’re treating them based on a potentially false premise. If you tell the patient they might not have a disorder, the healing potential or placebo effect becomes less crucial because you’re not pathologizing them unnecessarily. This is a moral issue. Do I have the right to tell my patient that their carcinoma is malignant when it might be benign? No. I have to tell them the possibilities. We don’t tell patients they will die if they might not; we present the odds.

We’ve decided to treat symptoms as disorders, but you may not have a disorder. Maybe you’re just sad or afraid because life is complicated.

I understand the challenges in extreme cases, like psychosis or dementia, where shared decision-making can be difficult. These are often discussed on platforms like Mad in America, and while I don’t always agree, I respect the need for these conversations. We must remember the dangers of too quickly deciding that someone can’t make decisions for themselves. However, there are cases where patients struggle with decision-making, and we should focus more on compliance. In these specific cases or diagnoses, I have some understanding of the concept.

 

Karter: I want to finish up our time here by spending a little time on what’s coming in the future for you. I wonder if you could share a bit about what you and Dr. Cosgrove are working on for your Fulbright. You mentioned earlier what you hope to achieve with that, but could you share a little more about where you see your work headed in the next few years?

Kostić: Well, one of my goals is to write a book. Using my shared decision-making approach with patients, I’ve gained a lot of practice explaining complex matters in understandable terms. I get wound up, as you can see, and talk a lot, but I try to keep it comprehensible so that more or less anyone can understand it. I want to use this skill—or talent, or whatever you want to call it—to write a book for the masses about the connection between identity and disorder.

When we tell a patient they have a disorder, it changes their identity and how they perceive themselves. I want to explore this using several examples: depression and anxiety, adult ADHD and autism, addiction, and gender dysphoria. Each of these carries different aspects of the interplay between identity and disorder.

With depression and anxiety, it’s a top-down process. The message comes from pharmaceutical companies, the media, and the medical establishment, telling patients they have a disorder, leading them to believe they have a faulty brain. With adult ADHD and autism, it’s fascinating because it’s more bottom-up, originating from social media and philosophical circles of neurodiversity. These concepts gain traction in the public sphere, putting pressure on the medical guilds to adapt. And, of course, the guilds and pharmaceutical companies are eager to comply because there’s monetary gain involved.

In addiction, we see the direct forming of identity. You stand up in front of a group and say, “I am Kostić, and I am a sugar addict,” and this becomes part of your identity to help you understand and fight the problem. I think this approach has its merits. I’m not saying it’s always bad; I’m trying to understand it from all angles.

The fourth topic is gender dysphoria, previously known as gender identity disorder. Along with dissociative identity disorder, it’s one of the few disorders where identity itself is in question. This raises entirely different questions and answers. This is a subject I’m deeply into, and I’m nearing the end of my work on it. I’m looking forward to possibly getting it published, but I felt compelled to write it and get it out there myself.

With Lisa, we’re working on several things. I mentioned Zuranolone, a new drug for postpartum depression. There are some obvious flaws in how it’s presented and marketed, and we want to tackle this issue. We’ve also finished a critique of prolonged grief disorder and the pathologization of grief.

As I mentioned, I’m delving into shared decision-making, not just about drug choices but about the disorder itself. One without the other is useless. I also plan to write about the physiology gap, a theoretical concept questioning the utility of biological research in psychiatry.

In traditional medicine, we know how physiologically normal lungs function and can compare that to pathological lungs. But in psychiatry, we compare people labeled as “depressed” to those without problems, which is illogical. To understand pathology, we should compare depression to sadness. But we don’t know the physiological basis of sadness, so any differences we find are claimed to be pathological markers of depression, which isn’t accurate. This oversight in reasoning is astonishing.

When I get back to Serbia, I plan to do a study with Lisa on our notions of drugs based on their designation as medicine. This is important because many drugs like psychedelics, marijuana, and MDMA, which were street drugs 20 years ago, are now becoming medicines. We have some ideas for questionnaires to understand people’s relationship to this change. I think this is massively important.

Personally, I’m for the legalization of all drugs. I believe it’s a moral position. Politically, examples show it shouldn’t have massive negative societal effects. But this doesn’t mean I think drugs are good. Every drug can be harmful. Alcohol is a legal drug, and it can be harmful. We recognize this with age limits, etc. It’s important for people to understand the risks and have a healthy fear of the drug.

I think the designation of a substance as medicine lowers this fear because there’s a bias where street drugs are seen as dangerous, but medicine is seen as good. If I take marijuana to get high, that’s my choice. But if I say I’m treating my anxiety with it, I might start using it every day, shifting from wanting it to needing it. This is a dangerous premise. This applies to MDMA and psychedelics too. I believe they should be legal, and people should have the right to decide for themselves. However, I would prefer them to be decriminalized rather than medicalized because the potential for misuse is greater with medicalization. This is another study I’m looking forward to.

 

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