ADHD Diagnoses, Examining the Psyche, Withdrawal and PSSD Risks, ECT Harms and More: Robert Whitaker Answers Reader Questions

Welcome to the Mad in America podcast. This is our first episode of 2026 and I’m delighted to be joined by Robert Whitaker. Bob is with us today to answer questions sent in by Mad in America readers. Thank you to all of you who took the time to provide such thought provoking and important questions.

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

James Moore: Bob, welcome. Good to see you again. Thanks for joining me on the Mad in America podcast.

Robert Whitaker: Thank you, James, for this opportunity to interact with Mad in America readers. It’s something I look forward to every year. You’ve sent me some of the questions already, and they’re really great so I think we’re going to have a really nice discussion here.

Moore: Let’s kick off. The first question is from Kristen. Kristen asks, I’m wondering what you actually think of the ADHD diagnosis? I was put on antidepressants at 13, went through severe withdrawal at age 21, and was misdiagnosed and medicated for bipolar mania for years. Now in my 30s, I finally put together that I had ADHD the entire time. No medication works, so I just do without.

Whitaker: Thanks for this question. First, the ADHD diagnosis is in fact a construct. By that, we mean that there was no identification of a pathology or an abnormality in the brain that distinguishes someone that we say has ADHD from a non-ADHD person. Basically, what you see in terms of the diagnosis is they’re just saying that if we give people a survey on how fidgety they are, that somehow theoretically measures their attention. Then we take those who score at the highest on that scale, and we say, oh, that’s the group with ADHD.

The second thing that is important to understand is that the method for diagnosing is very imprecise. If you look at the questions, it’s like, how many times a week is a person like this? How distractible are they, that sort of thing? It’s a really fungible scale; it’s not precise. Really, what ADHD is, is psychiatry grouping certain people who say they have difficulty paying attention or staying focused. The person’s own understanding of themselves goes into the diagnosis. There is no sharp line separating those with ADHD from those without ADHD.

If, for Kristen, this sense of having this difficulty is helpful to her, great. That’s okay. Especially since she’s not finding that the solution is a drug treatment. When we look at people who get this diagnosis and then go down the medicated route, you really don’t see good long-term outcomes. You see a lot of adverse events related to the use of stimulants.

Here at MIA, we always want to be respectful of individuals who find something helpful to them. It sounds like Kristen has found that the diagnosis, in some ways, is helpful to explain her life. But I think it is also helpful for society at large to understand that it is a construct. There’s no genetic thing that shows that it’s separate from non-ADHD. There’s no known pathology. There’s no known specific response to stimulants, and that is just this way of sort of identifying people who say they lack focus or get distracted easily.

Moore: I was wondering, obviously, ADHD always used to be something that was talked about in relation to kids, particularly young kids at school, who lacked attention. But in recent years, there’s been an explosion, it seems, in diagnoses of adult ADHD. Is there really any difference between the diagnoses used for a kid with attention problems and an adult with attention problems? Or are they just broadly the same kind of construct?

Whitaker: As you say, James, initially it was seen as a diagnosis for youth in school. Really, kids who weren’t doing so well in school and who didn’t thrive in the school environment.

But you have to look at the larger story, it’s how psychiatric diagnoses and drug treatments have been marketed all the way back to 1980, when the American Psychiatric Association published the third edition of its Diagnostic and Statistical Manual. This is when they said, we’re going to adopt a disease model, and we’re going to say that these problems reside in the head of the individual. We have these drug treatments that are specific to them. That was a story that led to the great expansion of the psychiatric enterprise and more people getting diagnosed with depression, anxiety, bipolar, ADHD, that sort of thing.

But this is a commercial story. It’s a commercial story that basically helped sell drugs to youth who were struggling a little bit. Then what happened with the ADHD diagnosis is that the makers of stimulants for ADHD drugs said, oh, that market is getting saturated. How about we move into the adult market? They began promoting this idea to prescribers and to the public at large that adult ADHD was real, too.

Now, all of a sudden, adults were given an explanation for some of their difficulties in life. Maybe they didn’t like their job, or they said they couldn’t stay focused on one thing. But it’s taking the same construct and peddling it to adults. In a way, what you see is it’s a construct that tells people this is why you’re struggling with life. Whereas maybe in the past we said, well, life is difficult, and maybe I’m in situations that make it difficult to thrive in. It’s really a change in conception and thinking, but it definitely has a commercial influence.

If you want to understand the ADHD diagnosis, you have to see how it was first promoted to youth, first to boys, then to girls, and then to adults. Through that marketing lens, it can all make sense.

Moore: Understood, thanks, Bob. Moving on to the next question, which is from Larry. Larry says, generally speaking, our understanding of the psyche is woefully inadequate. This must be one reason why psychiatry remains a false profession. How far are you willing to go in your research or on the Mad in America website to begin a discussion along these lines?

Whitaker: Well, I think it’s a discussion that we’ve been having ever since we started Mad in America in January of 2012. We’ve had bloggers talk about phenomenological conceptions of the psyche. We’ve had many people writing about how the mind responds to the environment, that sort of thing.

In essence, with the disease model we’re criticizing, that’s a very reductionist model of the psyche, that we’re sort of puppets of our neurotransmitters. A main theme of Mad in America from the beginning is how that construct, that belief system, that model is not science-based, but it’s also not based in what we know from philosophy, what we know from religion, and what we know from literature about the essence of the psyche and how human beings move throughout the world.

I think actually this has been a fundamental aspect of Mad in America from the beginning, of saying what a mystery the psyche is.

I hope that makes sense. Great question. I think it’s central to what we do. But we are approaching this humbly, with humility, because the mind is such a complex, mysterious place.

Moore: I agree. To me, reading Mad in America doesn’t feel like reading a medical journal. It’s much richer than that. Almost every week, there are articles that consider philosophy, religion, social studies, how we relate to each other as humans, community, so it feels very different from the hard medical facts you might read if you visit some of the top medical journals.

Whitaker: That’s because, in essence, Mad in America’s understanding is that this part of our lives of suffering and difficulties doesn’t fit into a neat medical context. That’s the point. It really fits into a larger context of what it means to be human. What is the spectrum of experiences? We’re trying to have this very complex, broad exploration of this world we live in.

Moore: Okay, moving on. Dan asks, why is it that doctors aren’t taught or educated about the side effects and withdrawal risks regarding antidepressants? Also, what is the longest period that you know of that someone has waited before reinstating their drug successfully?

Whitaker: Okay, I’m not sure I understand the second part of that question.

The first part, why aren’t doctors taught about withdrawal problems and how to get people off antidepressants? That whole discussion undercuts the conventional narrative that has been promoted to us by the psychiatric guild and by pharmaceutical companies that these are safe and effective drugs. When people go through their medical training, a conventional understanding is that these are safe and effective drugs and that they help people. There’s even an understanding that if they’re safe and effective, that you’re not going to talk about changes in the brain that lead to withdrawal symptoms, okay? It just doesn’t enter that conventional narrative.

If you start focusing on the difficulty coming off and persistent withdrawal symptoms and why that is happening, meaning because the drug has changed your brain, you get a totally different conception about the risks of using these drugs in the first place. Medical training is really formed by that commercial influence and that commercial story. It’s pitched as a story of medicine and science, but you really have to take a step back and look at the financial influences behind that story, and we all know that the market for psychiatric drugs is a big one. They have a story that is necessary to sell those drugs to the public. The withdrawal information doesn’t fit within that positive story.

Moore: SSRIs were seen as such an advance over barbiturates and tricyclic antidepressants that the story that went with them was that in every way, they were a much better way to treat people with depression.

Whitaker: They were an antidote. They were fixing a chemical imbalance in the brain, so they were specific to a problem that was causing depression. Once you have that out there, are you really going to start telling people, wait a minute, these drugs induce a chemical imbalance, and that’s why you have trouble coming off. They are perturbing normal functioning. It doesn’t fit with the story that was told when Prozac was launched in 1988.

Moore: As to the second part of Dan’s question, I think what he’s asking here is when someone has come off their antidepressant, they may have tapered, they may have come off quite suddenly, some people then are forced to go back on. They are forced to reinstate because they think it might be their only way of addressing the withdrawal symptoms. I think Dan’s interested in whether you know of people who have waited quite a long time before reinstatement, and whether that was successful or not?

Stuart Shipko is someone we’ve interviewed a couple of times, and he’s written for Mad in America quite a few times. I think his view is that the longer you wait to reinstate, the less likely you are to get relief from your symptoms because your body is attempting to readjust to its pre-drug state.

Whitaker: In a way, I’m hesitant to answer this. There’s nothing in the psychiatric literature that answers this question. This shows the absence of information regarding the whole experience once you’ve been on these drugs and tried to come off.

I think there is some sense that, and I certainly heard this from people, that the longer they’ve been off and still have some persistent difficulties and try to reinstate, often after reinstatement, they’re not getting any sort of even an immediate boost. But I don’t really know anything about the longest that anyone has been able to reinstate and have a benefit.

You know this better than I do, James, honestly, about the whole withdrawal issue. But it does point to the fact that we have this whole area of experience now, that people have been on antidepressants for a long time and other psychiatric drugs, but particularly antidepressants and SSRIs, and we see all these accounts of how difficult it is for many people, and how symptoms may persist, and about different strategies for trying to get off. But it’s all bubbling up from the grassroots. It’s bubbling up from people sharing lived-experience stories.

The amount of information trying to categorize these problems, attempts to really understand them, is so minimal. It’s a black hole, and Dan’s question goes really into that black hole.

Moore: I completely understand and sympathize with those people out there who are desperately seeking some relief from their dreadful symptoms. But as you say, it’s a complete lottery, and we know that because for some people, they can switch these drugs on and off, stop them suddenly, and have almost no problems at all. They don’t even notice. Yet other people take them for a short time, maybe just weeks, and then try to stop, only to suffer dreadful symptoms for weeks, months, years, whatever it may be. It really is a lottery, isn’t it?

Whitaker: It’s a lottery in terms of response to the drug in the first place. There’ll be a spectrum of responses, some good, some just nothing. Then, as you say, in terms of people’s experiences withdrawing, some people can get off these quite easily and fast. Others, no. It is a lottery, and maybe that would be really helpful as we probe or write about this, you need to put it out right front and center, it is a lottery. It’s not one experience fits all, far from it.

Moore: On to the next question. Disa asks, how do we come up with a plan to demand that Marty Makary at the FDA address the scandal that is ECT?

Whitaker: This is really an important question and a good question. It’s remarkable because the evidence that ECT causes brain damage is overwhelming, and it goes all the way back to the 1940s. They understood ECT did something similar to a closed head injury. A closed head injury is a concussion, so you don’t see a gash or a break in the skull.

We understand that professional football players often end up with closed head injuries, concussions, etc., that have horrible long-term effects, behavior control, suicidal impulses, that sort of thing. Here we have a so-called therapy that we know in fact causes memory loss among other problems. That’s a sign you’re damaging the brain. That’s the only way to put it. It is a brain-damaging therapy. That’s number one.

Second, it’s not effective for curing depression over a long period of time. What happens with ECT? You suffer this blow to the brain, right? There is some sense that if you have a  closed head injury, the body floods you with a sort of hormonal response that’s meant to repair injuries. But does that last? As far as I know, if you look beyond 30 days, there’s really no evidence that ECT provides relief from depression, which is usually what it’s given for. Next thing you know, it’s not like you’re given one ECT, and pretty sure this is the same in the UK, you’re given a series of ECTs.  Sometimes it’ll be six, sometimes it’ll be 12, sometimes it’ll be more than that. How do we get Makary or the FDA to respond to this?

Where I’ve seen critiques of ECT be successful, and they were successful in California in the 1970s, for example, you had psychiatric survivor groups really making a campaign against ECT. It’s somehow making known to the larger public that this is a brain-damaging therapy. Memory loss is just not a minor thing; it’s central to who we are as human beings. It’s central to how we humans go about our lives. We treasure our memories. We’re harming a central core of what it means to be human. We need to make that clear. Then, if we move into the evidence-based place, right, whether it’s effective, we need to make it clear that it’s really not effective over the long term, past 30 days.

Now, John Read, of course, has been campaigning like this. We need to make this research known and part of a core element in our public consciousness. Then we need to do a big petition on, say, www.change.org, and get 50,000 signatures and send it to the FDA. I think that’s the best process. The petition should include a number of people who’ve had ECT and can speak to the harm it has done to their lives. Again, though, you have the guild that’s telling a different story about how this is, in fact, such a wonderfully effective treatment for those who don’t respond to drugs. That’s the battle we have to do.

Moore: It strikes me that personal testimony is incredibly important here, isn’t it? In the responses from psychiatry that I’ve seen to the critique of ECT, they seem to be saying the people who have suffered damage are the outliers. They seem to be trying to convince us that only a very small number of people have negative outcomes, and the other people go on to lead successful lives after the procedure, but when these things are studied, that doesn’t seem so clear.

Whitaker: First of all, you see persistent memory problems when you’re actually studying it. You don’t see just outliers. You see it as a principal part of what happens, especially after a series of these things, okay? It is not a rare adverse event. It is a common impact of having it done.

James, what you’re speaking about, here’s the problem. To be honest with you, the guild, in essence, is a propaganda machine. It’s always defending what it does, regardless of what the evidence actually shows.

Moore: This next question is related to the ECT discussion as well, and it’s from Mary. Mary says, can you comment on the split between psychiatry and neurology? This is strange considering how psychiatry is so focused on the brain. What about traumatic brain injury or chronic traumatic encephalopathy? Supposed psychiatric issues might actually be from a brain injury of some kind. Where is MIA on all of this?

So again, this speaks to brain injury and whether we cause that by either the use of medications or the use of electroshock.

Whitaker: Well, there are brain injuries that lead to psychiatric symptoms, like traumatic brain injury, that sort of thing. You can have a loss of emotional control. There are infectious illnesses that lead to psychiatric symptoms. Syphilis is well known. If it’s not treated, end-stage syphilis had psychotic symptoms involved. Parkinson’s disease, for example, often leads to psychotic symptoms. Inflammation of the brain clearly can lead to psychiatric issues. Things we call psychiatric issues, whether it’s depression, anxiety, lack of impulse control, that sort of thing.

The first thing you should be doing is physical workups to see if these other physical causes are present, and that used to be the case. It used to be understood you’d give a physical workup to see is there a physical problem, a neurological problem, causing what we see as psychiatric difficulties.

Then, what happens in 1980 is the American Psychiatric Association adopted this disease model, and now, it’s going to say that those psychiatric symptoms are their own disease, okay? That’s what we treat, and we’re not going to look for these neurological things because we see these symptoms themselves as elements of discrete diseases.

This leads to a horrible outcome where people with a neurological problem go undiagnosed if they first show up at the psychiatrist’s office. Now, what happens is they’re getting treated for these psychiatric symptoms with psychiatric drugs, which basically just add to their neurological difficulties, the functioning of their brain. This is part of the real reason the disease model has failed because it has eliminated all of these biological pathways to psychiatric symptoms, and there clearly are biological pathways.

Then there are other pathways. There are social pathways. There are psychological problems. There are traumatic pathways as well, and okay, but now, that distinction has been blurred, okay, much to the detriment of our society.

Bottom line is psychiatry has crowded in on neurology and tried to grab these patients for themselves, and that has been done much to the detriment of the population because it blurs this necessary understanding of a distinction between the two.

Moore: Thank you, Bob. Okay, moving on. The next one is from Trinn, and this came through Facebook. Trin says, is there any new research being done about what actually gets damaged in the body, brain, and nerves when a person has injury from taking or withdrawing from psychiatric medications?

Whitaker: This is a great question, and it leads to an answer that says we need precisely that. We need research focused on in what way do the drugs cause harm to the brain, cause malfunctioning of the brain, and changes to the nervous system and the regulation of the nervous system that may persist even after drug withdrawal.

We’re getting clear signs that, in fact, you are causing a dysregulation of the nervous system, some sort of neuronal and nerve injury that persists in some people even after they withdraw from the medications. It seems to be particularly pronounced with the SSRIs, even more than with the antipsychotics, although we know that antipsychotics can cause tardive dyskinesia, which persists afterwards, which is a sign of a dysregulation of the dopamine system.

But why don’t we have that? Because there is no financial drive for looking at the harms of these drugs. Drug companies aren’t interested in it. The American psychiatric guild is not interested because that would be criticizing their own products, right? So, where is the money going to come from?

What about the NIMH? The NIMH is promoting mental health access. It’s promoting mental health treatments. It’s not motivated to fund things finding harms from mental health treatment. We lack in society those forces that would help us investigate and do research on prescribed drug-caused injury. It’s something we need desperately.  It’s clear there is, with the persistent withdrawal symptoms, a neuronal injury that’s happening, a nervous system injury that’s happening, and unfortunately, while there is this bubbling up from grassroots saying this is what appears to be happening, we don’t have a mechanism in our society for investigating drugs through that lens of what harm they’re doing. This really would be like a neurological injury lens. That’s what we need, but we don’t have it.

Moore: It’s so desperately needed because if you are someone that’s experienced withdrawal and tries to look up any official guidance about what might be going on, typically you’ll see something that says something like you might experience flu-like symptoms. Yet, when you talk to people who have experienced it, they’re having stomach problems, paresthesias, sleeping problems, balance problems, gait problems, the whole gamut. I have never personally had the flu that’s caused that wide range of symptoms.

The flu-like symptoms thing goes nowhere near explaining how widespread the effects of withdrawal and post-withdrawal can be. The poor people who go to their doctor with these things end up falling into groups with chronic fatigue type problems and fibromyalgia, and other kinds of non-specified functional problems, where the doctor’s trying to say, this is just you, this has nothing to do with the drug. So you’re right, we absolutely do need more research on this.

Whitaker: What you just described is a story of an iatrogenic injury. It’s an injury to the nerve system. The nerve system is no longer able to regulate itself or perform its normal functioning. That shows how profound this injury is. It’s an injury to a bodily system that is so critical to our ability to function in society. It should be front and center of any investigation that needs to be done today.

Moore: This next one’s from Greet, and again is related really nicely to how widespread nervous system injury is in drug withdrawal. Greet says, how common is it to get post-SSRI sexual dysfunction (PSSD), and heal from it? It’s a horrible existence without emotions, love, good cognition, and sexuality.

Whitaker: I sought to write a magazine article on PSSD in 2011, and so I interviewed people with it. As this person says, it’s a horrible thing because it’s not just sexual dysfunction. It’s like an inability to mount an emotional response to the world itself, like to the beauty of a rainbow, to art, to really become emotionally engaged with another human being. It’s not just that you have some impairment of sexual functioning. It’s your impairment of the ability to engage emotionally with the world, which is very, very profound.

Now, when I did this in 2011, it was basically almost not on the radar, and the magazine finally wouldn’t publish it. I looked at how the magazine was funded, and they had all these pharmaceutical ads.

At that time, it seemed like maybe 25% of people actually had some sort of PSSD after they came off. Then there were varying times of recovery from that. Some people did seem to get it back after a year or six months after a year. Some people resolved after a couple of years, and some people it seemed not to resolve at all.

Now, the other element that I remember is that it was particularly prevalent in kids who were put on SSRIs during the formative development of their puberty. They had an extra risk of developing this. But it could also happen to people who went on antidepressants as adults. Particularly with the SSRI antidepressants.

How common is it? It’s at last being acknowledged as something that can happen even within the field. They’re, of course, downplaying it. There was a recent New York Times article on this, which I think, I forget what they said, was sort of a semi-rare occurrence like maybe 2%, 5%. That was basically it.

Well, the true prevalence is much higher. We don’t want to admit it. The powers that be want to underplay it. First thing is, we don’t know the prevalence. My sense is that it is indeed higher for those who are put on antidepressants and SSRIs in puberty. Now, what is the recovery rate? We don’t know. It hasn’t been well studied. We also don’t know the mechanism of the injury, right?

How long does it take sometimes to heal from injuries of this type? Often, you can heal from these injuries. It seems very variable. For some people, it can happen in months, for some people, a year or more, some people, a couple of years. Then there are some people who, honestly, it seems like they never get back their sexual function and emotional response. Hopefully that’s a very small percentage. One wishes it were zero. But the mere fact that we don’t know is telling us that it’s like a canary in the coal mine question. We should be investigating this.

Moore: What strikes me is if you do go on forums for PSSD, when new people arrive to try and find out a bit more about what’s going on with them, they’ll have found this forum on Facebook or Reddit, and they’ll say one that they had no idea that antidepressants could affect your sexuality in any way at all, and secondly that if they have gone to their doctor or psychiatrist to say they’ve got sexual difficulties, they are inevitably told that it’s a function of their depression.

Whitaker: This goes back to the original report of adverse effects with the SSRIs. There was actually a lot of sexual dysfunction apparent, but what they did was they attributed it all to the disorder and not to the drug. When they first came out, it was like, oh, maybe one percent have sexual dysfunctions that is drug-related. Really, it’s the disorder, not the drug. It just goes back to how we have a narrative fashioned by protectors of the drugs, and this is a long-standing thing; they assign it to the disease. I’m not saying depression is a disease, but in their mind, it is the disease and not the drug.

Again, this is part of the extraordinary betrayal, James. As you know, we’ve had a number of personal stories on Mad in America that tell of people’s struggles with PSSD. They’re heartbreaking. They’re utterly heartbreaking because they tell of people who feel like they’ve lost their ability to engage in life. If we go back to the initial non-industry funded trials of the SSRIs, you know what they said was the incidence of sexual dysfunction on the drugs? Anywhere from 50 to 90 percent, depending on how you define it.

Now, the irony is, one of the things that showed up here was that men took longer to ejaculate. This is obviously a sign that you’re disrupting things, but they said, oh great, now we can market SSRIs for premature ejaculation. We can take this adverse event and put it to use for those who have difficulty making love.

Again, it’s like this betrayal of the public’s right to know about the risks and benefits, and it goes back to the marketing and selling of these drugs, which came out through collaboration between the pharmaceutical companies and the psychiatric guilds. They have betrayed the public because they have not been willing to address these harms; instead, they have hidden them.

Moore: Thanks, Bob. Just to reiterate that if people out there do want to read about what we do or don’t know about PSSD, then if you go to Mad in America and search for PSSD, as Bob said, you’ll find personal stories and you’ll find research news articles, so it might be worth having a look there if people are interested.

Whitaker: Right, and those stories will talk about surveys of prevalence, as well, so you can get an update on that.

Moore: On to our last question, and this one, Bob, if you’ll indulge me, is actually from me, and it’s kind of based upon the changes that I’ve seen in Mad in America over the years that I’ve been involved.

I joined Mad in America in 2017, that’s when the podcast kicked off, and in the intervening years, it’s been obvious that the way that people produce and consume news is changing.

So what I wanted to ask is how Mad in America competes in a world of shorter attention spans and sensationalized clickbait competition? Refuting misinformation needs time and space; it doesn’t really easily fit into a social media landscape. Psychiatry can use catchy slogans, as it did with the chemical imbalance myth, but countering that requires evidence. How can critics respond to propaganda with scientific and intellectual rigor, while having to compete in a market that’s flooded with AI-generated slop and fact-free sound bites?

Whitaker: Well, trying to respond to all the slop and the propaganda is like whack-a-mole, because it’s coming up every day, and it’s just constant. I’m going to go to the first part of your question, and that is how people consume information today, and in the era of AI. It certainly has changed, and it has changed where there’s this flood of information out there now, a flood of sound bites, and a flood on social media, and people coming to web magazines to read is actually becoming less and less. You can see a drop-off in people going to media websites, because they’re getting their information in bits and pieces through other forms. What do we do? We recognize that we have a challenge in this changing landscape for media.

We have to find how we can deliver an insightful and in-depth understanding, which means a narrative that helps us understand where diagnoses come from, what drugs do, what the outcomes are, and what the alternatives are. How can we give people a different narrative for understanding what has been in the past, what led us to this point, and what narrative can guide us in the future.

Again, in a certain sense, what we want to do is help people understand that the disease model that has governed our thinking is a failed model of care in every way, and then help them see the possibilities of a different narrative. We talked about a narrative that is not rooted in the disease conception of the brain. How do we do that?

Well, what we’re going to be doing is having more of our own content that has originated within MIA that can really help flesh out this narrative. So fewer blogs that just come in over the transom, but really more in-depth essays and science reports. Our science reports are going to move from this is what happened in this study and here’s how it was done, into how whatever is appearing in the research literature fits into broader, evolving themes.

That’s what you’re going to see in the coming year, James. We’re also going to see more MIA radio podcasts because they are a great forum for exploring these ideas, not just telling of what people know, but exploring all these things and learning from them and engaging an audience in the exploration. We may also increase the frequency of our personal stories. Then, more of these in-depth MIA reports of larger themes. We’re going to be spending more of our energy and more of our funding on original content that we are generating ourselves or that our freelancers are generating under our editorial control.

One of the reasons we want to do this is because we understand that readers, rather than coming to us every day for the daily update, will hopefully be visiting us once a week to see the themes that have been published here that can help them continue to have their own narrative understanding of the big picture. More in-depth features, more content that we are controlling.

That’s the idea. It is in response to a changing landscape for media websites. I think in order to continue to have a claim on the public, you really have to help them solidify a new narrative for what was wrong and also what is possible. It’s a new narrative both for themselves personally, themselves professionally, and for how society can think about these things.

Moore: Well, I look forward to those changes, Bob. My reflection on it is, I think what I enjoy about reading MIA articles or being involved with the podcast is that you get to understand the thought process of how someone came to a conclusion about a particular issue. That’s not what you get from AI. You can type in a Google search, and you can get a three-line answer to a question, but it tells you nothing about how that answer was arrived at. The way the answer was arrived at is a critical part of the understanding of why this issue might have changed or might not be what we think it is. I think that’s what MIA, through its personal stories, its science news, and the podcasts, can provide.

Whitaker: I love that idea that there’s a complexity to how we think about things and how we arrive at conclusions and how we experience the world. We want to honor that complexity and reflect that complexity and that process. That’s certainly our goal. It is a challenge in this time of two-second social media bursts. As you say, the fact that AI can regurgitate information so quickly, and people are starting to rely on that, well, people do need to understand that’s a regurgitation. It’s not original thinking. It’s not process thinking. Hopefully, people understand what AI is really about. It is about uncritically regurgitating data.

Moore: Thank you, Bob. I think people sent in some great questions, and I thank you so much for your generosity in giving us so much time to talk through them. I really do look forward to what sounds like a new chapter for Mad in America, one driven out of necessity, but even so, I look forward to seeing how Mad in America develops over 2026 and beyond.

Whitaker: Well, necessity hopefully is an opportunity for change and the mother of invention. Hopefully, we’re following that path. I just want to say it’s really a pleasure being here on this podcast and to have the chance to hear from our readers with all these great questions. The questions really were provocative, which is what we need, and I want to thank our listenership for providing us with these questions and this opportunity.