Why We Can’t Stop Arguing About S.S.R.I.s

What’s missing in the national conversation on mental health medication.

By David Wallace-WellsRachael Bedard and Anthony Rostain

Produced by Jillian Weinberger

Robert F. Kennedy, Jr. and the MAHA movement are hoping to curtail the use of S.S.R.I.s — a class of drugs commonly prescribed for anxiety, depression and a host of other psychiatric issues. How should patients think about starting and staying on S.S.R.I.s today? In this episode, the Opinion writer David Wallace-Wells and the contributor Dr. Rachael Bedard talk with the psychiatrist and professor Dr. Anthony Rostain about what we know — and don’t know — about S.S.R.I.s and how doctors and patients should navigate the uncertainty.

Why We Can’t Stop Arguing About S.S.R.I.s

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The transcript has been lightly edited for length and clarity.

​David Wallace-Wells: I’m David Wallace-Wells. I’m a writer for New York Times Opinion and a columnist for The Times Magazine.

Rachael Bedard: And I’m Rachael Bedard. I’m a primary care physician and a contributing writer at New York Times Opinion.

Wallace-Wells: One in six Americans is on antidepressants. And a lot of Americans think that number is too high, that we’re prescribing too many S.S.R.I.s, that we’re giving them to children too young and that we don’t really know how to get people off those drugs, even when they want to. The nation’s top health official, Robert F. Kennedy Jr., is kind of leading the charge.

Archival clip: Health and Human Services commissioner R.F.K. Jr. is starting a new initiative targeting the overuse of psychiatric drugs, especially in children. The new plan urges doctors to prioritize holistic care, like exercise and nutrition, instead.

Archival clip: Health and Human Services commissioner R.F.K. Jr. is starting a new initiative targeting the overuse of psychiatric drugs, especially in children. The new plan urges doctors to prioritize holistic care, like exercise and nutrition, instead.

But R.F.K. and MAHA are not alone. People have been debating these drugs and their effect on our society for decades. We’re in a new moment now, where people are arguing about it more — and Rachael and I have been talking a lot this summer about these issues. But that conversation is often at the highest level and ignores a lot of the clinical experience — what this looks like on the ground between patients, kids, their parents and their doctors.

Bedard: As a primary care doctor, I currently work in a homeless clinic. I previously worked on Rikers Island, in the New York City jail system. I’ve always worked in populations where there were very high incidents of comorbid mental health issues. And as a primary care doctor, I’ve prescribed antidepressants and medicines for anxiety to patients hundreds of times, probably thousands of times, and have thought about these questions a lot myself, around how I’m selecting patients who are good candidates for medicine — and when I’m choosing to medicate them, frankly, because I can’t get them access to other services I wish I could get them access to, like talk therapy.

So to hash this all out, we’ve invited Dr. Anthony Rostain to join us today. Dr. Rostain is the chair of psychiatry and professor of psychiatry and pediatrics at Cooper Medical School of Rowan University. Thank you so much for being here.

Anthony Rostain: I’m so happy to be here. Thanks.

Wallace-Wells: So let’s start with some history. Where did S.S.R.I.s come from? Why did they seem like a very big deal? And how did they become so successful, in the sense of so many Americans coming to use them so prolifically?

Rostain: Well, first of all, the S.S.R.I.s ushered, from my point of view, a new era in psychopharmacology.

Wallace-Wells: And when was that?

Rostain: It was introduced by — the F.D.A. approved it in 1987. I happened to have been at Penn when it was being tested, so — as I was a resident — and I saw that patients who were taking it were getting better, and that they weren’t having side effects that some of the other antidepressants had. At the time, the primary antidepressant in use were in classes called tricyclic antidepressants, which are still used occasionally. And they had a lot of side effects and potentially harmful side effects: arrhythmias; people could accidentally or on purpose create situations where they would die from an overdose.

So the fact that this medication came along, there was really, really a tremendous relief at the ability to prescribe something that’s safer and better tolerated. How they evolved is a whole story in and of itself, of how science, medicine and society evolved; because initially, they were approved primarily for depression, and little by little, the use was extended to anxiety, to obsessive-compulsive disorder, to social anxiety and to PTSD.

Suddenly, we saw many uses that we could use the same medication for. And we’ve all wondered, in the clinical field and in the general policy field, at what point are we doing this safely? And I think it’s healthy, actually, to be having this conversation right now.

Wallace-Wells: So you mentioned there, in talking about that history, the contrast with the previous class of drugs, primarily in terms of the safety — that you could feel comfortable giving this to more patients, because the risk of some serious side effects was much, much lower. Back in time — we imagine we’re still in the late ’80s, early ’90s — how did the contrast look in terms of efficacy? Was there also a marked benefit that hadn’t been seen in the previous class?

Rostain: There was a sense that these were as efficacious and better tolerated, forgetting about the serious side effects. I think the overall early studies showed that yes, you could have a really good impact on moderate to severe depression with these S.S.R.I.s.

Bedard: I’m wondering if we can talk a little bit about mechanism, and how the theory of mechanism has changed over time from one that was quite simple — the idea that the S.S.R.I. meant that you had more serotonin, a happy transmitter, soaking your brain — to where we are now, where there’s more nuance to how we think they work.

Rostain: Yes. So it’s true. I trained at a time when everybody had hypotheses. If you had schizophrenia, you had too much dopamine. If you had depression, you had too little serotonin. It isn’t that simple, and the brain is obviously more interesting, and we understand it better than just a chemical imbalance.

So what we think, No. 1, we know that all S.S.R.I.s do the same thing: They slow down the recycling of the serotonin molecule, which is a neurotransmitter — a very important neurotransmitter. But what it really is doing over time is reshaping the circuits in the brain that affect our mood, that affect our ability to handle stress, that allow us to make less reactive kinds of decisions. And over time, what we’ve really come to look at is neuroplasticity — which is the term we use now.

When we’re stuck in a depressed state, or when we’re anxious all the time, we can’t learn, OK? Our brains are locked into a pattern, and neuroplasticity is actually the mechanism by which we learn. So clinicians talk — we talk to our patients about the idea that if we give you this medication, not only will you feel less depressed or less anxious, but you’ll be able to learn some new tricks. And that’s the idea — that this helps your learning and adaptation.

Bedard: And that’s really interesting, because the notion of depression as a chemical imbalance was sort of culturally accepted for a long time, and was the way that people conceived of this. And frankly, it was the way that I think lots of doctors spoke to their patients about it: There’s a chemical imbalance, and we can give you this medicine that will resolve that. I don’t know that people think of depression as something where their brain needs to be rewired — and that idea can be pretty scary for people, I think.

Rostain: Of course. That’s what people want to know. Is this going to change my brain? And if so, is that going to be a good thing? So what we’re trying to get at with depression — we sort of have this model in our minds now, that the circuits in the brain that modulate your mood seem to not be allowing you to feel positively, and you’re so stuck in this circuit of negative emotions.

Actually, the brain has two different circuits: one for positive emotions, one for negative emotions. So one way I explain it to patients is to say, the positive emotional circuits are underpowered right now, and the negative ones are running the show. This might quiet the negative and allow the positive ones to be more present. Is it a permanent rewiring? No, because if we stop the medication, you go back to base line. But hopefully, when you do come off the medication — say your depressive episode is over — you will have learned how to feel better, and you will be able to push back against the negative more effectively.

Wallace-Wells: I think we’re going to talk, in a minute, about going off the meds, but just to stick on this point for a second — and to raise an ignorant reflexive response — how strange is it that we developed this tool of drugs with one theory of depression, have evolved past that theory of depression, observed the drugs still basically working and are continuing to prescribe them? How unusual is that? How unnerving should that be? Do you understand it when patients express alarm about this?

Rostain: Let me say, to be quite honest, we still don’t know what depression is.

Bedard: Or exactly how these drugs work.

Rostain: Or exactly how these drugs work. And that doesn’t stop us from using them, because people are coming to our office saying, “I’m in pain. I need help.” I mean, the same, by the way, is true for pain medications and pain syndromes.

I mean, these are really interesting. The brain is a fascinating organ, and unfortunately, we have to simplify this, because we don’t have any better way of explaining it at the moment, with new nonpharmacologic interventions, like transcranial magnetic stimulation. We can begin to think about, oh, maybe we can change your brain in positive ways without you having to be on medication.

Wallace-Wells: So this is where some of my own, I guess I would call it a kind of naturalistic fallacy, comes in. I have some tendency to think if we understand the precise mechanism — that insulin regulates blood sugar in the blood — I trust that it’s appropriate to intervene when that’s necessary. But if we’re much more confused about the system, I have a little bit of a pause about the idea of taking meds like this, and certainly prescribing them en masse as we’ve........

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