Inspired by Terry Bisson’s “They’re Made Out of Meat” (1991), and more recently ’s “They Die Every Day” (2025)… and of course, Jacques Lacan.

“You’re back.”

“I’m back.”

“The report better be ready, it’s already late.”

“I want to flag something before we file it.”

“Flag what?”

“The wanting structure of this species. I don’t think we’ve captured it accurately in the previous reports.”

“The wanting structure is the part that everyone finds most straightforward. They desire things. They pursue them. They acquire them, experience pleasure and satisfaction, or fail to acquire them, and experience distress. What’s missing? What’s to capture?”

“That’s what I thought too. That’s what many of them think too. But it isn’t right.”

“Walk me through it.”

“Let’s start with what they want. They openly articulate what they want, quite confidently. But if you observe them over seasons, over years, over a lifetime, they don’t actually pursue what they say they want. They don’t even seem particularly keen on pursuing happiness. They pursue what others appear to want. Or what they think others want them to want. Or what they think others would want them to want.”

“Okay, that’s just social influence. They are social creatures. It’s mimetic contamination.”

“No. Listen. Underneath the influence, there isn’t anything else. Nothing autonomously generated. It’s not that their authentic, intrinsic desires get distorted by the social field. There is no authentic desire at all. Their desire is the desire of the other. All the way down.”

“...all the way down?”

“Yup, all the way down.”

“What about the infants?”

“It’s even worse for infants. They are emotionally fused with the primary caregiver. They want to be the sole object of her desire. And when they figure out there is a wider world out there, with rules and stuff, it just leaves them all messed up.”

“That… that doesn’t make any biological sense.”

“You tell me.”

“All right. Bracket that as an anomaly. What else?”

“They all want something unattainable, but also something that can’t be named. A phantom attractor. Every actual thing they desire and pursue is a substitute for it.”

“So… the things they pursue, mates, progeny, work, comfort, that never actually delivers what they are after?”

“Each obtained object reveals that what they really wanted was something else. It gets weirder.”

“How?”

“They don’t know they want this unattainable thing, not really, this other desire. They think they want the substitutes. And they keep chasing and keep failing. This continues until they die.”

“…”

“They are pulled towards things that… that undermine them. Excite them, but painfully. That are excessive in a way that hurts. They go back to the places where they suffer. They go back to the same arrangements. It’s like a compulsion that plays out over their lives.”

“What do they get out of it? Survival advantage?”

“A peculiar, perverted sort of pleasure.”

“Omigod, what a freak show.”

“I told you.”

“Wait. Do they know any of this about themselves?”

“Some of their scholars have figured it out, but they really struggle to talk about it in anything other than dense philosophical puzzles.”

“Alright, I’ve heard enough. Makes me glad we have authentic desires that map directly onto satisfiable needs.”

“Makes me wonder if they are the ones lacking something in their desire programming or if we are.”

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The final part of the interview is focused on the question of whether, in the light of property dualism, it makes sense to separate “mind problems” from “body problems” in medicine. On re-reading the interview, I find that I am still resistant to that argument. I do think that we can meaningfully talk about psychological causes and physiological causes of clinical problems (as well as causes at various levels of organization/explanation), but we cannot move from property dualism (mental properties vs physical properties, and the irreducibility of the former) to a nosological or clinical claim about mind vs body problems.

O’Leary’s proposed distinction that mind problems are caused by brain states correlated with experience, while body problems are caused by brain states not correlated with experience, is a substantive claim that is not an entailment of property dualism. One could be a property dualist and reject this distinction entirely, or accept a version of it while being a functionalist or non-reductive physicalist. Property dualism as an ontological thesis is compatible with any distribution of causes across levels of organization/explanation.

I find this distinction unhelpful because I don’t believe mental disorders or psychiatric conditions can be distinguished from physiological disorders in terms of being caused by brain states correlated with experience. Yes, we should absolutely strive hard to discover what the distribution of causes is for any given presentation (at some points O’Leary seems to think that I am saying that we should give up on trying to figure out what the causes are), but mental disorders are mental not because their causes are mental (the causes are multifactorial and multilevel) but because they are best describable, at present, at least, in mental terms.

I do believe O’Leary is responding to a legitimate problem, the premature foreclosure of diagnostic inquiry in the face of “medically unexplained symptoms,” often gendered, often harmful. And she’s right that some of the rhetoric around “avoiding dualism” has been conscripted to justify this foreclosure. I think the solution to this doesn’t lie in embracing property dualism, regardless of the philosophical merits of property dualism. Clinicians have adopted epistemic practices (premature closure, bad psychosocial just-so stories, misdiagnosis as depression/anxiety, invalidation) that are bad on ordinary epistemic and clinical grounds. The remedy is epistemic humility, acknowledging uncertainty, continuing diagnostic workup, and resisting invalidation (… and also rejecting bad metaphysics).

But check out the interview and draw your own conclusions!

Diane O’Leary, PhD is a philosopher, a disabled independent scholar whose work is centered on the overlap between philosophy of medicine/psychiatry and philosophy of mind. O’Leary has published on dualism, consciousness, and medically unexplained symptoms. Learn more about her work on her website.

Awais Aftab: Your impressive work on dualism in medicine and psychiatry has forced me and many others in medicine and psychology to reexamine long-standing assumptions. I’d refer readers to your papers on medicine’s metaphysical confusion (Synthese, 2021), the biopsychosocial model (EuJAP, 2021), and your recorded talk as part of the philosopher of psychiatry webinar series to learn about your views in detail. Can you, however, briefly explain your argument that medicine has misunderstood dualism?

Diane O’Leary: Many thanks for the kind words, Awais. The misunderstanding has its roots in George Engel’s work. Along with a whole lot of rich and valuable insights, Engel offered two confused philosophical claims. First, dualism and reductionism combine in the biomedical model, and that’s the source of its problems. Engel attributed the combination to Descartes, and he offered the biopsychosocial model as a remedy for both. Second, dualism is the separation of mind and body in our thinking, language, or medical practice. To fix the biomedical model, then, all we need to do is to change the way we think, talk, and practice in relation to mind and body. If we stop separating them, if we just orient ourselves around the person holistically, dualism and reductionism will go away, and all will be well. 

The thing is that it’s actually impossible for the biomedical model to embrace reductive dualism, or dualistic reductionism, because that’s like saying that it’s both day and night, that the lights are both on and off, or your new dress is both beautiful and hideous. Dualism and reductionism about mind and body are diametrically opposed views that cannot both be true. More importantly, dualism is not the separation of mind and body in our thinking or practice.  In fact, dualism is not something we do at all. Descartes is not a dualist because he thinks of mind and body as separate. He’s a dualist because he thinks both minds and bodies exist, and they’re going to keep on existing as two things no matter what anybody says or does. 

Why does this matter for medicine? It matters because Engel was right that medicine’s view on mind and body has a big impact on its success at helping people be well. First, the campaign to stop thinking of mind and body as separate is self-refuting if we accept Engel’s goals, and no science is at its best when its foundations are faulty. When we succeed in seeing mind and body as one, we are reductionists—but reductionism is the problem that Engel sets out to address. Second, well-meaning people in medicine, psychiatry, psychology, and bioethics believe they must try to eliminate the separation of mind and body in their thinking and language because philosophy says that’s a good idea. But philosophy says no such thing. As far as philosophers are concerned, if some form of dualism is true, it’s going to keep on being true even if no one ever thinks or speaks of it again, ever.

Finally, effort to avoid “dualism” interferes with patient care. (I put “dualism” in quotes when I’m referring to separation of mind and body.) In cases of unexplained symptoms, for example, clinicians are advised to end diagnostic effort because it’s “dualistic.” It’s hard to imagine any action more basic to medicine than effort to find disease that needs treatment, but for the many cases where diagnosis remains unclear, medical training prioritizes avoidance of separation of mind and body. Similarly, in countries where aid-in-dying is permitted for mental illness, avoidance of “dualism” has been the primary supporting argument. What’s permitted for medical illness, the argument goes, cannot be denied for mental illness, because to do so would be to separate mind and body. Regardless of what we might think about that practice, it sure seems clear that lives should not be ended on the basis of a misguided definition of dualism. Even the DSM has apologized for implying that mind and body are separate, confessing that, despite effort, “dualism” has yet to be overcome.

I recognize that it’s very difficult for people in medicine to imagine that dualism is not what they think it is, and that philosophy doesn’t care about controlling how we think and talk about it—but bad philosophy is not benign in medicine. This is something we need to address.

Aftab: One thing I want to note is that philosophers themselves are deeply divided on issues related to dualism and philosophy of mind. For instance, in the 2020 PhilPapers survey of philosophers, 52% accepted (or leaned towards) physicalism, while 32% accepted non-physicalism (N=1733). On the issue of consciousness, 22% accepted dualism, 4.5% accepted eliminativism, 33% functionalism, 13% identity theory, and 7.5% panpsychism (N=1020). I hesitate to ask psychiatrists to take a strong position on a matter that commands no consensus among philosophers. 

O’Leary: Let’s think through the idea that there’s no consensus among philosophers on the issue of dualism, because that’s not an accurate conclusion about this survey. On the choice between physicalism and non-physicalism, folks in medicine will assume that this question is really a choice between physicalism and dualism. Philosophers won’t see it that way, though, because philosophers aren’t thinking of Descartes when they see ‘dualism.’ They’re thinking of a new form called ‘property dualism.’

Susan Schneider explained this beautifully, “contemporary philosophy of mind sees the question of the nature of substance as being settled in favor of the physicalist. Dualism about properties, in contrast, is regarded as being a live option.” So we’ve settled the question of Descartes’ dualism against Descartes. We agree now that all things are physical things, even human beings. But that doesn’t settle the question of dualism because we still need to ask: how many of us physicalists are dualists about properties? That’s a live question in our time, so the fact that most philosophers are physicalists tells us nothing at all about the popularity of dualism.

The same kind of problem arises with the question of consciousness. Folks in medicine assume that all the “isms” on this daunting list—dualism, eliminativism, functionalism, identity theory, panpsychism—are mutually exclusive, so if you accept one, you reject the others. That’s a misunderstanding. Many forms of functionalism are forms of property dualism (e.g. Shoemaker), because, as the Stanford Encyclopedia of Philosophy puts it, functionalism is “officially neutral” on dualism. It’s hard to say what proportion of functionalists are property dualists, but this poll certainly doesn’t tell us that only 22% of philosophers are open to dualism. In fact, many panpsychists are property dualists too.

The clearest line we can draw within the list of “isms” is not between dualism and the rest, but between views compatible with dualism and those diametrically opposed to it. On the yes or maybe side you’ve got dualism, panpsychism and functionalism, and together that’s 63% of philosophers—three times more than you get on the absolutely no side, with eliminitivism and identity theory. If you’d taken this poll in, say, 1970, the imbalance would have leaned just as far in the opposite direction, so things have dramatically shifted. 

There are two lessons for psychiatry to draw from philosophers’ perspective on the mind-body options. First, dualism is not the separation of mind and body in our thinking and language. That idea does not appear on the survey. Second, dualism is not about Descartes. It’s about property dualism, and that’s a big broad umbrella idea that can accommodate a wide range of positions. Emergence, supervenience, panpsychism, naturalistic dualism, even functionalism—all of these views are either defined in terms of property dualism or potentially open to the idea. Fifty years ago philosophy fiercely opposed dualism, but that’s no longer the consensus.

Aftab: A related aspect of the hesitation I mentioned earlier is that it's evident that psychiatry accepts the ordinary existence of subjective experience and mental states, but it's not clear to me that psychiatry has to take any particularly strong position on whether these mental states are, in some fundamental ontological sense, radically different kinds of things than physical states of the brain. (I’m borrowing the language here from Stanford Encyclopedia of Philosophy: “In the philosophy of mind, dualism is the theory that the mental and the physical – or mind and body or mind and brain – are, in some sense, radically different kinds of things.”)

O’Leary: For the first part of your hesitation, then, dualism actually does command consensus among philosophers—at least insofar as true reductionists, eliminitivists, or identity theorists have now become rare. Regarding this second part, where you hesitate to ask psychiatrists to take a position on which mind-body option is right, the main point I’d like to make there is, well, me too. I don’t generally shy away from strong views, but on the issue of which “ism” is the right one for medicine or psychiatry, I’ve never made any claims. What I’ve said is that medicine and psychiatry are confused about what the word ‘dualism’ actually means in philosophy, and when we correct that, we find that medicine is already based on property dualism, particularly psychiatry.

You’ve said, “It's evident that psychiatry accepts the ordinary existence of subjective experience,” and I think you’re right about that. In fact, I can’t imagine anybody disputing it. The thing is that this is an assertion of property dualism, plain and simple. You’re saying that psychiatry accepts that subjective experiences exist, and that’s an ontological claim no matter how you slice it. You’re not saying that experiences are things, of course, in the sense of substances. You’re saying that experiences are states, or properties, that human beings have.

The reality of experience is so obvious to people in mental health fields that it seems like it can’t possibly be a substantive claim. But in the context of philosophy it is. In fact, the existence of experience is precisely what we’re debating with the question of dualism. When you accept that there are properties of experience, you actively distinguish those from physical properties of the brain. You recognize that the way you feel when you’re tired and you get hold of your morning coffee is distinct from the biochemical facts that characterize the state of your brain at that moment. No matter how committed we are to catch-phrases like “integration of mind and body,” your first taste of morning coffee is a private fact, a subjective fact, while the physical state of your brain at that moment is a public fact, an objective fact. I know we both agree that these are correlated in some deep and inextricable way, but they’re distinct just the same. In fact, they couldn’t be correlated if they were not distinct.

Aftab: When we talk about the mind, it seems we can easily fall prey to a conflation of mind as referring to consciousness (subjective experience, qualia, phenomenology, etc.) vs mind as referring to the cognitive, behavioral, or psychodynamic aspects that show up in psychological theorizing, e.g., memory, learning, executive functioning, perception, motivations, defense mechanisms, etc. Many neuroscientists would say that cognitive “information processing” in the cortex can take place, and routinely takes place, without conscious awareness. Solms writes, for example: “It is well-established that learning and memory can exert their effects without any “inner feel”; and the same applies to perception. Hence the title of (Kihlstrom's, 1996) celebrated review article: “Perception without Awareness of What Is Perceived, Learning Without Awareness of What Is Learned.”” (Solms, 2019)

In other words, there is more to mind than consciousness. This seems important to me because a lot of the philosophical debate around dualism centers on consciousness, while psychology and psychiatry are usually interested in many other psychological aspects as well. Does it make sense to be a “dualist” about processes such as memory and learning?

O’Leary: Maybe there’s a simple way to characterize what you’re suggesting and a more complicated way. The simple way is probably just the difference between access consciousness and phenomenal consciousness, and that’s largely what Solms is getting at. Phenomenal consciousness is usually what we mean by “consciousness,” that is, qualitative, first-person, subjective experience. Philosophers often see a difference between that and the aspects of mental activity, like learning or executive functioning, that go on without first-person experience. This helps us isolate the question of dualism as a uniquely “hard” problem. We can use neuroscience and cognitive science to explain cognitive activities of the brain. But there’s good reason to think that facts about the brain (at least as we currently understand them) cannot explain why any particular brain activity should also be accompanied by the private, “what it’s like” feel of first-person experience. If you’re someone who thinks this challenge is indeed uniquely difficult, then you’re open to dualism in some way. 

I think you might be getting at something deeper though, too, and it seems closely related to something I’m working on with Marie Nicolini. I think you’re suggesting that each of us is more than a “stream of consciousness,” so there’s a lot going on within a mind that’s sub-conscious or un-conscious rather than non-conscious. I take this distinction to be meaningful and important. My mind is engaged at this moment with my experience of the temperature in this room and the vague sense of hunger in my stomach, but these would not have entered my stream of consciousness if I hadn’t gone looking for some things I experience that I’m not aware of. So these are facts about my mind that I can discover if I go looking for them, but I do have to go and explore. Similarly, my mood suggests that somewhere “beneath the surface” I’m engaged with feelings about my son, or concern about my father’s health. I could bring these experiences into my stream of consciousness if I set out to do that—say, in therapy—but if I don’t, they remain so far out in my periphery that if you asked me what I was thinking about, I wouldn’t mention them.

The access/phenomenal distinction has really not captured this kind of thing. In fact, philosophers have not had much to say about our ability to investigate the depth and complexity of our current experience as we do in psychiatry. This is honestly part of the motivation for the work I do. As I’ve said, I think psychiatry will do a better job of supporting and protecting mental health if its mind-body picture is philosophically coherent—but the other direction is at least equally important to me. I’m certain that philosophy would do a better job of making sense of the mind if it engaged with psychiatry. Right now that’s not possible, because psychiatry can’t speak philosophy’s language.

Aftab: How much can we infer about the nature of mental disorders from a metaphysical position on the mind-body relationship? I’m doubtful that a metaphysical view such as property dualism, by itself, supports or challenges any particular view on the etiology of psychiatric disorders or says much about the appropriateness of diagnosis, pharmacological treatment, or the medical framework in psychiatry. Whether the medical model applies well or poorly to psychiatry seems to be an issue that is orthogonal to property dualism. What do you think?

O’Leary: That’s a great question. First, if we want to make sense of the nature of mental disorders, we’ll need a coherent picture of what “mental” means. I haven’t offered that—I mean, as I’ve said, there’s nothing prescriptive about my suggestions for psychiatry, except to get its philosophical house in order. Psychiatry is in a real stew at the moment, with every kind of foundational question up for grabs. I think this kind of breaking point was inevitable because the mind-body picture that underlies psychiatry has been incoherent for a long time. How can the field respond to a complex challenge like the antidepressant debate if we don’t even know what we mean by “mental,” and we have no coherent options for making sense of the relation between mental and physical? How can it begin to respond to discoveries about consciousness, or the idea that mental illness might be social?

This much about dualism is certain to be useful in any discussion on the nature of mental disorders: go ahead and separate mind and body! It will not be possible to make sense of mental disorders—as distinct or not distinct from purely biological diseases—unless we can freely consider the difference between the subjective experiences of the human being in front of us and the biochemical states of her brain. Mental disorders begin with the mental.

Second, once we recognize that psychiatry assumes property dualism, we open the door to an account of mental disorders that’s grounded in subjective experience. I’m not saying that’s the only right view (though it is a view I’m working out). At this point I’m just saying that this is a debate that must be had. Psychiatry needs to consider what a disorder of experience would amount to, and how it would be different from, but related to, purely biological disease. That’s going to require new philosophical clarity.

We’re starting to see a lot of new effort in this direction from phenomenology and from consciousness studies reaching over into psychiatry. There’s a marvelous paper called, “Putting the “mental” back in “mental disorders””, by Traschereau-Dumouchel and colleagues last year, and there’s “Taking subjectivity seriously”, by Kyzar and Denfield, which ties new insights from phenomenology and psychiatry to neuroscience. Then there’s Cecily Whiteley’s marvelous paper, “Depression as a disorder of consciousness”. This new kind of inquiry is deeply opposed to the campaign against dualism, so a new conceptual foundation is going to be important.

Aftab: You've persuasively argued that medicine and psychiatry have gotten dualism wrong, that they have misunderstood a metaphysical position about the existence of minds with the doctrine that the mind is separate from or disconnected from the body. You are right about the error. But it does nonetheless seem that the tendency to disconnect the mind from the brain is a tendency that needs to be guarded against in medicine and has historically been a problem in its own right (even if dualism is not the right term for it).

O’Leary: Well, thanks for saying so about the error. There are good reasons for thinking that a sense of wholeness is important not only to our well-being, but to our physical and mental health. But it’s important to think critically about what we’re actually saying with that idea. We’re not saying that there’s no difference between an experience and a bodily state. If that was our view, we’d be reductionists, so holism would be impossible. We’re saying that although we recognize the difference between our experiences and the brain activities they’re correlated with, we’ll lead better lives if we avoid the trap of imagining that we’re two divided things, mind and body, that are oddly stuck together. We are embodied experiencers, that’s how I tend to think of it, and as a matter of quality of life, and health—rather than a matter of metaphysics—our lives are better when we keep that in mind.

What we’re aiming for with this kind of thing is really humanism in medicine and mental health care, and I think that’s profoundly important. Based on Engel’s philosophical mistakes, though, people have the strange idea that humanism demands rejection of dualism. That’s the opposite of how philosophers see things, and truly it’s a bizarre view. We can’t be humanists if we think that humans really don’t have subjective experience, that experience is just physical brain activity, that you and I have no more inner life than the chairs we’re sitting on. When we reject every form of dualism or panpsychism, that’s what we’re left with. 

Aftab: You’ve talked about how confusion around dualism has led to an attitude of deliberate diagnostic vagueness that has negatively impacted the care of “medically unexplained symptoms.” Can you say more about that?

O’Leary: I suggested in 2018 that “deliberate diagnostic vagueness” is what you get when you’re so serious about the campaign against separation of mind and body that you directly discourage it in diagnosis. Standards of care for medically unexplained symptoms come from research in psychiatry, and all of this research is driven by the idea that it’s bad for clinicians to separate symptoms caused by disease from those caused by psychosocial distress. To avoid “dualism,” they should accept unexplained symptoms as diagnostically vague, as mind-body problems rather than one or the other, ending the quest to determine whether disease is present. 

Clearly this approach is unsafe, because a great many people suffer from diseases that are hard to diagnose. And though it’s commonly believed that error is rare in this area, research supporting that idea is poorly designed and generally not reviewed in medicine. This isn’t rocket science. No diagnosis is going to be reliable if it’s based on philosophy rather than science, and things will go particularly badly when the philosophy is misguided. If actual philosophy of mind were driving this research instead, the challenge of MUS would be forced out of psychiatry and back into medical science where it belongs.

It's unclear to me why this issue plays such a small role in critical psychiatry discourse. Public anger toward psychiatry about this problem is substantial, and growing rapidly as Long COVID grows more common. More broadly, because medical training on psychosomatic conditions comes from psychiatry, and psychiatry continues to center on gender in diagnostic recommendations, it’s psychiatry, more than medicine, that needs to address gaslighting as a threat to women’s health. The DSM construct of somatic symptom disorder is generally understood to occur in females ten times more often than males. And while that extraordinarily dangerous figure appears regularly in reviews and practice recommendations, no one seems to think that it requires evidence. Incredibly, Medscape and American Family Physician have recommended the 10:1 ratio for years, citing only each other.

Figures on women’s difficulty accessing healthcare for serious everyday disease are uncontroversial now, and they’re nothing short of alarming. Still, we have yet to see even the tiniest bit of movement from psychiatry toward protecting women from mistaken attribution of disease to the mind. Confusion about dualism seeps into every area of psychiatry. For me, as a matter of social justice, this one is the most urgent.

Aftab: There is a problematic attitude of diagnostic vagueness for sure, but its relationship to “dualism” is complicated. We can talk about bodily (physiological) dysfunctions and mental (psychological) dysfunctions, but both sorts of dysfunctions exist across the mind-body divide. Bodily dysfunctions often present with psychological symptoms and psychological factors often play important roles as risk factors or as moderators for recovery. Psychological dysfunctions are embodied, they involve brain processes, often present with bodily complaints, and physiological factors often play important roles as risk factors. Furthermore, we can have problems that arise from a complex set of interacting physiological factors, a complex set of interacting psychological factors, or a complex set of both physiological and psychological factors. Sure, we may separate mental properties and physical properties, but there is no way to extend this sort of separation to clinical problems in a clean or straightforward manner.

It is the case that in psychiatry, we have generally not found the project of separating “symptoms caused by disease from those caused by psychosocial distress” to be very productive. Paradigmatic psychiatric disorders such as depression and schizophrenia are not explainable with reference to psychosocial distress or psychosocial causation; they have causal risk factors that are distributed across multiple levels of explanation and involve psychological as well as neurophysiological mechanisms. It is also the case that meaningful (but overlapping) distinctions are to be made between psychiatric disorders and other medical disorders such as autoimmune disorders. It would be a serious error to misdiagnose an autoimmune disorder as a primary psychiatric disorders (e.g., schizophrenia), just as it would be a serious error to misdiagnose an autoimmune disorder as a primary disorder of joints (e.g., osteoarthritis) or as a primary disorder of the cardiovascular system (e.g., essential hypertension).

The problem in the case of “medically unexplained symptoms” is that clinicians end up offering bad explanations of psychosocial causes (“it’s stress”) or they misdiagnose the problem as a psychiatric disorder (as depressive disorder or as anxiety disorder, which may very well be comorbid but are not the correct diagnosis for the complaint). And this basically conveys the implicit message that the problem is “all in one’s head” and becomes a powerful form of dismissal, invalidation, and neglect.

This is all compounded by the inability of current healthcare professionals and systems to patiently work with unexplained symptoms and provide adequate care. Brian Teare has written about the experience of remaining undiagnosed after a series of medical tests: “I was betrayed by my own GP. She didn’t say the phrase It’s all in your head, but she might as well have...  I keep imagining what it would have meant to have encountered a doctor who said, I’m at the end of the care I can give you, and though I couldn’t diagnose your illness, I believe you are ill and you need more comprehensive testing than public health can provide.”

Resultantly, I can’t help but be dissatisfied with the idea that the solution to our current poor care of medically unexplained symptom lies in doubling down on some sort of dualism between “mind problems” and “body problems” when many complex, multifactorial problems cannot be neatly categorized in this manner. The essential thing, in my opinion, is a transparent acknowledgement of our ignorance and our state of knowledge, avoiding premature closure of the search for causes, resisting bad causal explanations, challenging misdiagnosis, and confronting clinical invalidation and medical neglect.

O’Leary: I confess I’m confused by these suggestions, Awais. We’ve agreed that separation of mind and body is not dualism, and that there’s no reason to resist property dualism, but here you are suggesting that, because it “doubles down on dualism”, doctors should not try to determine whether unexplained symptoms are caused by mind problems or body problems. We’ve all doubled down on dualism, I’m afraid, because psychiatry doesn’t work unless we accept the reality of subjective experience. Philosophy provides no reason to resist dualism in diagnosis, and no reason to avoid separating mind problems from body problems. In fact, medicine gives us no reason to avoid it, because concern about separation has been (wrongly) attributed to philosophy for so long that no one has bothered to support it on clinical grounds.

You suggest that separation is unproductive in psychiatry, but I think, first, that you really don’t believe that. You recognize the difference between bodily pain and psychosocial distress, and you understand what’s happening when a patient with bodily symptoms is referred to psychiatry. If you didn’t separate mind and body in these basic ways you couldn’t function as a psychiatrist. I think what you mean to say is that psychiatry is more effective when we accept complex interactions between mind problems and body problems—and I fully agree with that. I’m just pointing out that there are no interactions at all between a thing and itself. When we provide care that recognizes mind-body interactions, we begin by separating. In this way, it’s incoherent to prohibit separation of mind problems from body problems.

Second, it’s important to think about what psychiatry communicates to a doctor-in-training when it tells her that MUS are “complex, multifactorial problems that cannot be neatly categorized.” It tells her that deliberate diagnostic vagueness is the best approach, that her usual determination to diagnose disease should be abandoned with this patient group. Most impactfully, whatever we tell doctors-to-be about unexplained symptoms, we tell them about healthcare for women—because whether we use the term MUS or somatic symptom disorder or somatization, psychiatry has trained every physician to believe that these are the most common symptoms in medicine, and they affect women almost exclusively.

If you and I see our primary care doctors today for new symptoms, I will be ten times more likely to leave the office with talk about “complex, multifactorial problems that cannot be neatly categorized”. You will be ten times more likely to leave with a diagnosis, or an uncertainty that’s understood to require resolution. If we both have pain, you’ll be more likely to get pain medication and I’ll be more likely to get sedatives. If we both have bladder or kidney cancer, with symptoms, I’ll be two or three times more likely to have to have to visit three or more doctors before one of them takes me seriously enough to refer for testing. And if we were both over 55 with heart disease, I’d be twice as likely to be misdiagnosed with a mental health condition, and seven times more likely to be mistakenly sent home from the ED in the midst of a heart attack.

When we allow pseudo-philosophy to override diagnostic caution, people die. And when we combine that approach with entrenched professional gender bias, women die. Purely as a matter of numbers, few problems in psychiatry cause harm to more people than this quiet combination. I can’t imagine any way for psychiatry to justify its lack of effort to protect women from this error.

Aftab: Ok, so I want to press you here on what exactly it is that we are trying to distinguish. We begin with property dualism, according to which there is such a thing as subjective experience. Fine. But then you go further and seem to say that accepting this property dualism also means accepting that there is a (sharp? mutually exclusive?) delineation to be made between “mind problems” and “body problems.” That, to me, is a very different sort of distinction than property dualism. Let’s take a patient of chronic pain who has lumbar radiculopathy. There is the subjective experience of pain, and there is the activity in the nervous system (the neurobiological mechanisms) that makes the experience of pain possible, and then there is the narrowing of the space around the nerve root (the cause of the pain). Let’s consider two patients with depression. The first is someone who has recently had a stroke and has a textbook presentation of post-stroke depression. Here we can distinguish between the subjective experience of mood alterations, the neurobiology of mood regulation, and how that neurobiology is disrupted by the stroke. The second patient is someone who is experiencing a severe depressive episode after a divorce, and here we can distinguish between the subjective experience of mood alterations (and other symptoms), the neurobiological and psychological mechanisms that are associated with those experiences, the relationship between those experiences and divorce as a life event, and other risk factors that predispose the individual to experiencing depression. It is clear to me that the mere fact of altered subjective experience doesn’t tell us much about the relevant mechanisms, causes, and risk factors. Are you suggesting that the mechanisms and causes that are associated with any experience of illness can be neatly packaged into “mind problems” (mental mechanisms and mental causes?) and “body problems” (neurophysiological mechanisms and neurophysiological causes)? If that is the case, I don’t see what justifies such a binary packaging and why we should accept it.  

More fundamentally, it is not clear to me here what a “mind problem” exactly is. Psychiatric disorders or mental disorders are disorders that have “distinctive features [that] can be adequately characterized only by using the vocabulary of the mental” (Broome and Bortolotti, 2009) but acknowledging so doesn’t take away the fact that psychiatric disorders involve psychological as well as neurophysiological mechanisms, causes, and risk factors. Is there a “mind problem” that doesn’t involve neurophysiological mechanisms, causes, and risk factors? What are we talking about here?

O’Leary: I think it’s important, as you say, to clarify what I’m saying with the idea that mind problems are different from body problems. First, we can recognize the difference between them and still notice that their interaction can be complex. In fact, the idea of interaction is incoherent if we don’t begin with two distinct things that can interact. Second, the distinction in no way implies that mind problems and body problems “can be neatly packaged”, as you put it, in practice. It may be that in many cases where the two kinds of problems interact, clinicians are unable to disentangle them. This is no basis at all for imagining that it’s actually a bad idea to try to be clear about the nature of the problem at hand. At this time, many clinicians believe that they should walk away from the diagnostic process as soon as they get near the mind-body line. That idea is incoherent, and dangerous, and patients gain nothing from it. They gain from clinical awareness of complex interactions between mind problems and body problems—and that awareness is impossible without a distinction between them. 

You’ve basically articulated a kind of mind-body stew, a list of the many ways that mind and body are related in psychiatry, as if this suggests that effort to better understand is actually a bad idea. I just don’t see any basis for the leap from “we don’t understand it” to “it’s a bad idea to try to understand it”. Further, there’s a simple tool from philosophy that can draw us out of the stew into much clearer territory. As property dualists we agree that there are states of subjective experience, and these are correlated with, but different from, brain states. If we keep that simple picture in mind, we can rely on this basic distinction: mind problems are caused by brain states correlated with experience, while brain problems are caused by brain states not correlated with experience. (My webinar for the Philosophy of Psychiatry series offers diagrams that make this easier to understand.) In a nutshell, as long as we’re clear that all experiences are correlated with brain states, we might say that mind problems are caused by experience, while body problems are caused by purely biological states.

This simple clarification gives us at least one consistent, science-friendly way to understand the difference between mind problems and body problems. More than that, it allows us to locate problems in the realm of the mental (with Bortolotti and Broome) without ever losing sight of the fact that the brain is always involved. So, delusion is subjective experience correlated with a brain state, and pain is subjective experience correlated with a brain state. We might be inclined to toss up our hands there, concluding that there’s just no difference between them, but that conclusion is not supported. There is a difference.

Generally speaking, delusion is caused by a brain state (a kind of body state) that’s correlated with experience, perhaps a trauma, while pain is caused by a body state all on its own, like lumbar radiculopathy. Of course, there are exceptions to these rules, and we can easily make sense of them. Some cases of delusion are body problems because they’re caused by brain pathologies or other bodily pathologies all on their own, and some cases of pain are mind problems because they’re caused by brain states correlated with experience. Moreover, there are many cases of delusion, and many cases of pain, where the interplay between mind problems and body problems is so complex that we can’t possibly sort out which one is doing the most work. All of this is consistent with the picture we get from property dualism. We’ll need at least one more stipulation to handle the hardest cases, but this much, I think, is clear: property dualism provides an objective, science-based way to understand the difference between mind problems and body problems while staying true to the aims of biopsychosocial medicine.

I think much of the resistance to clarity about mind problems vs body problems, arises from concern that if we see mind problems as wholly mental matters, then psychiatry really won’t belong in medicine, or in science. This worry is unfounded. Property dualism does not suggest that mind problems are wholly mental matters. On the contrary, it’s a tool for understanding how to work with subjective experience in the context of brain science. Whether we choose to understand mental disorders within, or outside of, the frame of medicine, property dualism will consistently demand reflection on the role of the brain. It’s the best tool we have for making sense of psychiatry’s ability to plant one foot in the realm of experience and the other in the realm of physical science.

Aftab: Thank you!

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Austin Ratner, MD, is a prizewinning author of two novels, a history of psychoanalytic epistemology (The Psychoanalyst’s Aversion to Proof, 2019), and a coauthor of a physiology textbook. His work has appeared in The New York Times Magazine, The Wall Street Journal, The Lancet, and many other outlets. As former editor-in-chief of The American Psychoanalyst (tapmag.org, americanpsychoanalyst.substack.com), he rebooted the magazine of the American Psychoanalytic Association as a public-facing vehicle for psychoanalytic conversation about mental health, the arts, and culture.

Young sciences boil with controversy, mature ones cool down into consensus. The relatively young mental sciences are maturing. Among experts, there’s a growing bilingualism in the languages of clinic and lab, a pluralistic dialogue across faultlines that once isolated competing orthodoxies. The public conversation, however, seems to lag behind.

The problem of public misinformation isn’t unique to psychology and psychiatry, of course. Much has been written on the subtle biases that influence what well-meaning academic journals publish and what popular-science reporters cover. But for a number of reasons, the mental health field may be particularly vulnerable to media misinformation. And the results of that misinformation can be especially damaging. The psychological constructs that laypeople absorb from the media directly impact how they go about solving their own problems, negotiating conflict, caring for one another, and how they form identifications with larger social groups and movements—to whom they pray and for whom they vote.

It’s tempting to attribute media misinformation about psychology to the usual suspects: a simple language barrier or knowledge gap between journalists and scientists, maybe, or a media bias toward the latest studies, from which reporters then draw premature conclusions. I think it’s a lot more complicated than that.

My own research has focused on the role of defense mechanisms in how we talk about psychoanalysis—very meta, I know. Freud’s conviction that people’s defenses biased them against his theories provoked in him a deep pessimism about the prospects of public validation of his claims. For a long time that pessimism passed as conventional wisdom within the field of psychoanalysis and a nominal excuse to deprioritize research. While defensive reactions to psychoanalysis have certainly occurred and still do, my research suggests that Freud and many later psychoanalysts also had their own aversions to the work of validation, aversions rooted in their own discomfort with talking publicly about controversial subjects like sex, aggression, and repression. Their historical refusal to engage in normal scientific discourse has contributed significantly to the current position of psychoanalytic psychology. Psychoanalytic aversions to the task of proof only deepened the convictions of skeptics. As the evidence-based medicine movement took off, the psychoanalytic community was left behind. They lost academic credibility, leadership roles in psychiatry, access to research dollars, and their numbers shrank. A lot of fine psychoanalytic research is now being published, but psychoanalytic researchers are at a disadvantage due to this history. Most psychological research is not psychoanalytic, so any journalistic bias toward “the latest studies” directs attention away from psychoanalysis, which compounds the disadvantage. As one of the oldest perspectives in psychology, the psychoanalytic view is furthermore inherently less newsworthy.

Consider two recent representative examples of narrow discourse in the “Well+Being” section of The Washington Post and what misimpressions might result. On March 4, 2026, the Post ran a guest column with the headline “Can’t stop overthinking? Here’s what experts say actually helps. From zooming out to changing your environment, these research-backed strategies can turn the volume on noisy thoughts down.” The column offered solid evidence-based advice, but it didn’t touch upon the relationship between feeling and thinking, a relationship that has of course long been the province of psychoanalytic psychology.

In Macbeth, Shakespeare famously makes a connection between a kind of overthinking, an obsession, and a feeling, namely the feeling of guilt. In Act V scene i, a servant describes Lady Macbeth’s obsessive-compulsive handwashing to a doctor like this: “It is an accustomed action with her, to seem thus washing her hands: I have known her continue in this a quarter of an hour.” While sleepwalking, and not fully conscious, Lady Macbeth reveals to the doctor the secret motive behind her handwashing: she’s repeatedly imagining washing the blood of the murdered King Duncan off her hands. The doctor notes that “infected minds / To their deaf pillows will discharge their secrets.”

Even feelings of guilt more mundane than Lady Macbeth’s can still be quite painful to acknowledge and difficult to relieve—guilt along the lines of, say, “I disappointed my loved one” (and not “I murdered the king”). Guilt may not be the explanation for every obsession, nor does all “overthinking” necessarily qualify as obsession. Could it benefit some “overthinkers,” however, to ask themselves whether their overthinking does not to some extent reflect an unconscious effort to relieve a sense of guilt—a sense of guilt that they’re keeping secret from themselves because it’s too painful to feel consciously?

Lady Macbeth’s handwashing is not exactly breaking news. But recent scientific evidence actually does support the link, first proposed by Freud, between guilt and obsessive symptoms. So why didn’t the Washington Post article include the psychoanalytic view? If it’s only because cognitive-behavioral researchers dominate psychology departments today and they’re the ones who answer the phone when journalists call, well, that’s not a great reason.

A second “Well+Being” article published recently in the Post likewise takes such a narrow approach to its subject that it leads to alarming conclusions, ones that could have been avoided through a more holistic approach. The article cites a study’s finding that “Difficult people in your life might make you age faster.” The study labels such people “hasslers” and the study’s lead author offers the following reckless advice, according to the Post journalist: “The obvious advice, Lee said, is to consider relationships carefully, avoiding hasslers whenever possible and cutting ties if you feel like someone is adding lots of negativity and stress to your life, although that can be an incredibly difficult decision.”

The article sounds only one small note of caution, briefly quoting Debra Umberson, a sociologist and aging expert not involved with the study. “That’s the definition of relationships, they have hassle, right?” Umberson told the Post, commenting on the new research. “I mean, you can get support and love from them, but they all come with hassles.”

The discussion would have benefited from the psychoanalytic approach to introspection. So often, we unconsciously create our own trouble in relationships. We can sometimes hassle ourselves and then project the hassle onto others, seeing someone else as the problem when the problem originates within us. Family members notoriously hassle one another, and a mistaken conclusion that might be drawn from the Post is that we’ll live longer if we estrange ourselves from our hassling siblings or if we divorce our hassling spouses. Clearly, there are times when you need to break up with somebody. But eliminating all “hasslers” would be like spraying buckshot from a 360-degree swivel, likely to hurt the innocent and to shoot off your own feet.

Another important psychoanalytic concept that would have improved the “hassler” conversation is ambivalence. According to psychoanalytic psychology, we often love and hate the same thing, the same person, at the same time. Such ambivalence is a product of internal conflict and it’s normal. What feels like a hassle that could kill you may really be a sign you’re alive, feeling all the conflictual feelings that go with the territory. A psychoanalyst might argue for hanging in there in your relationships, trying to work out your hassles in dialogue with your loved ones and with yourself, before rushing to label and avoiding or excising “hasslers” or “negative people” from your life.

In fairness to the Post, just a month later, their “Optimist” column featured an article called “How to deal with chronically negative people” that was more sophisticated about emotions and defenses. Instead of recommending avoidance, the article quoted experts who encouraged readers to think through the emotions involved and coached them to use reflective listening to make negative friends and relatives feel heard.

Articles that incorporate a psychoanalytic perspective still feel like the exception, however. It continues to be common for journalists and experts to cite the urban legend that psychoanalysis has been categorically discredited, a claim that is ironically not itself “evidence-based.” Humanity needs every available tool in the doctor bag as we embark on a new millennium, pregnant with possibility, peril, and strain. At The American Psychoanalyst, we’re by no means ignoring or whitewashing the missteps in the history of psychoanalysis, but we’re working to keep psychoanalysis in the public conversation. A new era of psychoanalytic openness is dawning. The real conversation has just begun.

The American Psychoanalyst’s Substack

TAP offers a psychoanalytic perspective on mental health, arts and culture, and current events.

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David Heath is a psychiatrist in Waterloo, Ontario, Canada, retired from clinical practice but active in promoting psychiatric hospitalization at home. He founded Canada’s first psychiatric hospitalization at home program in 1989 in Kitchener and a second program in Cambridge in 1998. His book “Home Treatment for Acute Mental Disorders: An Alternative to Hospitalization” was published in 2004 to excellent reviews in US psychiatric journals. He has given grand rounds and has delivered courses on the topic at annual meetings of the American Psychiatric Association. His website is www.intensivehometreatment.com.

This is a follow-up to:

I know of only two Psychiatric Hospitalization at Home (PHH) programs currently operating in the US. Neither Google nor ChatGPT could turn up any others. So you will be surprised to learn that the US has had more influence on the development of this model than any other country. The earliest randomized controlled trials (RCTs) were carried out in the US. A PHH program in Boston started as a pilot project funded by the National Institute of Mental Health (NIMH) in 1957, operated impressively like a modern PHH program, and in 1964 won the American Psychiatric Association Gold Award. Its founders wrote a handbook in 1967, much of which could be written today. One of the two research studies that provided the evidence base for both PHH and Assertive Community Treatment (ACT) took place in Madison, Wisconsin, in 1980. Three of the most influential thought leaders in PHH were American.

Ideally, innovations in mental health services are disseminated and, refined by research, build one on top of the other until mainstream, such as first episode psychosis programs. Instead, this history is a story of decades of … I’m not sure what… institutional amnesia?

Let’s start with Adolph Meyer, the first psychiatrist-in-chief at the Johns Hopkins Hospital, who was one of the most influential psychiatrists in the first half of the twentieth century.

His influence can be seen in the first-ever PHH program. It was established in the Netherlands by psychiatrist Arie Querido, who became the director of the Department of Mental and Nervous Diseases of the Amsterdam Public Health Board. Because of the financial problems of the 1930’s, he was asked to find ways to reduce hospital admissions.

Querido was influenced by the ideas of Meyer, whose mental hygiene movement was prominent in the US in the early twentieth century. Meyer thought mental illness had to be understood in relation to the whole person, their life history and their social environment, not just as a brain disease managed inside an asylum.

Similarly, Querido, instead of treating crises as something to be removed from the home and treated in the asylum, built services around home visits, family context and social conditions. He concluded that management at home was advantageous because the social difficulties creating the crisis were visible and amenable to intervention.

These ideas became a fundamental principle of PHH that to this day influences practice within PHH programs.

He instituted home visits by a social worker and a psychiatrist to all patients referred for acute admission. An alternative community treatment plan, sometimes involving follow-up visits, was formulated whenever possible.

The system he established attracted considerable international attention and in the 1960’s, 12 psychiatrists and 25 social workers were providing a 24-hour home-visiting rota for the whole of Amsterdam (Crisis Resolution and Home Treatment in Mental Health ed. by Sonia Johnson et al.) In 1956 a brief note in the Journal of the American Medical Association concerning Querido’s home visiting service in Amsterdam aroused great interest among American psychiatrists. Soon after, he was invited to the US to explain his program in greater detail.

As far as I can determine, psychiatrists at the Boston State Hospital were the only ones to have translated that interest into action. After some initial pilot studies, the NIMH awarded a grant to the hospital and the Boston University School of Medicine for a demonstration project: the Psychiatric Home Treatment Service.

Housed in the Administration Building of the Boston State Hospital, in 1957, the Psychiatric Home Treatment Service started out as a demonstration project and pursued its clinical goals within the context of a research demonstration. At first it consisted of a psychiatrist, a psychiatric social worker and a psychiatric nurse. Its catchment area was South Dorchester, a section of Boston with a population of 80,000 adjacent to the hospital.

Three directors or former directors of the program wrote a monograph describing this pioneering experiment treating mentally ill patients in their homes. It became fully operational with a staff of 20, including students, in 1962. In 1964 it won the Gold Award of the American Psychiatric Association.

Published in 1967, “Home Treatment: Spearhead of Community Psychiatry” by psychiatrists Leonard Weiner, Alvin Becker, and Tobias T. Friedman was designed to serve as a guidebook for hospitals and community agencies in establishing similar programs.

This is a remarkable book. The chapter headed “Manual of Operations” describes the principles and practices of the service. Apart from the hours of operation, these are identical to those listed in the British National Health Service’s “Mental Health Implementation Guide” on Crisis Resolution and Home Treatment (UK model of PHH) published 32 years later. This is the founding document that launched the NHS plan for 335 CRHT services throughout England; thus, England became the epicentre of research and practice in PHH. The English “template” of CRHT influenced the establishment of home treatment in 12 countries.

Reading this book, I felt a bit like an archaeologist who had discovered an ancient advanced civilization.

It is unclear how long the program continued to operate. The Boston State Hospital closed in 1979 and its functions were likely absorbed into the Massachusetts Mental Health Center programming but not as a distinct PHH.

Continuing the theme of American influence is a PHH program inspired by the Boston program at the Notre Dame Hospital in Montreal, Quebec, established in 1962. A report of its operation 1962-1964 in the Canadian Medical Association Journal shows that its principles and practice were in line with current PHH. As in the US, we see decades of institutional amnesia.

When on April 16 2024 the Quebec government announced a PHH pilot project at the hospital, there was no mention of an identical service operating 62 years before!

When I informed Montreal psychiatrist Olivier Farmer, one of the architects of the Quebec government’s plan to establish PHH throughout the province, of the existence of this PHH in 1962, he exclaimed, "Wow, really…. I had no idea, honestly. I first set foot in Notre-Dame as a student in 1999 and then as a psychiatrist in 2004.”

Americans were first out of the gate in randomized controlled trials of PHH. Four of the first five trials were American, starting with Pasamanick’s 1964 study in Louisville, Kentucky. This showed that patients with acute schizophrenia could be treated at home.

The largest intellectual influence on the development of PHH was Paul Polak, director of mental health research at the Fort Logan Mental Health Centre in Denver in the 1970s. He was the first to identify the role of conflicts and stressors in the patient’s social system in contributing to the need for hospitalization; 60% in fact, compared to factors in the individual.

Here he explains his ideas in his blog:

“When I left residency and went to work at Fort Logan Mental Health Center in Denver as Director of Research, I was concerned with the evaluation of treatment effectiveness of psychiatric hospitals. I quickly found out that people didn’t end up in the state hospital just because they were crazy. There were many people with crazy symptoms who never got close to a psychiatric hospital. For those who did end up in the state hospital, a major conflict in the patient’s family or primary living group was almost a prerequisite. As I gained more experience with the social process leading to hospitalization both at Fort Logan and later at Dingleton Hospital in Scotland, I came to believe that a social disturbance in the patient’s family typified by several unresolved crises a more significant determinant of admission than the patient’s psychiatric symptoms, and I began to evaluate and treat patients routinely in the context of their families in their real-life settings.”

This idea had legs.

It caught the attention of Australian psychiatrist John Hoult of Sydney, who later became the main architect of the UK National Health Service rollout of 335 CRHT programs.

Hoult had become dissatisfied with what he called the perseveration of the mental health system, in which patients get admitted to hospitals in a crisis. The precipitating social factors are not noticed and addressed; the emphasis is on symptoms and medication, and they are repeatedly admitted.

In 1977 he visited Polak’s service in Denver and incorporated his ideas into his PHH program in Sydney. Polak’s influence via Hoult was such that, according to Sonia Johnson, two of the four theoretical principles of CRHT practice can be traced to Polak.

These principles are

1. Treatment in the home environment is desirable because of the very large key role in many crises of difficulties in families and wider social networks.

2. Managing crises in the community is an opportunity for patients to develop skills and insights that will help them cope with their illness and with subsequent crises.

The story of American influence on PHH ended with the research and program development of psychiatrist Leonard Stein of Madison, Wisconsin, the second most important influence. His 1980 randomized controlled trial with psychologist Mary Anne Test was a giant leap forward in PHH research.

Their version of PHH, the Training in Community Living service, was more sophisticated than any previous studies and showed a deep understanding of the needs of chronically and severely ill patients. His team showed considerable resemblance to the current CRHT model. Stein’s study also influenced John Hoult, who decided to replicate it in Sydney in 1984.

Up to this time, all PHH teams were what are called “hybrid teams.” They had two components. Firstly, they were an alternative to admission for any patient in a crisis destined for admission. Secondly, after discharge, all these patients were then followed as outpatients, usually with no time limit. As Sonia Johnson points out, both Stein’s and Hoult’s services have the potentially confusing distinction of being cited as supporting evidence for two prominent service models: PHH and Assertive Community Treatment.

There are resemblances between PHH and ACT: both involve intensive contact with patients in community settings and integration of treatment of mental illness with help with social and practical problems. However, the populations served and timescales are different: PHH provides short-term treatment for mental health problems of varying type, severity and duration, while ACT is a long-term approach to the care of a selected subgroup who have severe illnesses and are especially difficult to engage and treat effectively.

In the mid-1980s, Hoult and Stein together decided it was unrealistic to expect one team to provide both crisis care for a broad range of patients and intensive community care for the particularly disabled subgroup requiring it. They recommended that the two functions be split into two services: short-term PHH for any patient destined for admission and ACT for long-term support of the most severely ill, difficult-to-treat patients.

In the 1990s, Hoult, taking with him the ideas of Polak and Stein, moved to Birmingham, UK, and became the first psychiatric consultant to the team in the Yardley area of Birmingham. This program has had an extensive influence on the development of the British NHS plan to develop 335 CRHTs, of which Hoult was the major architect.

So, to summarize, the current British CRHT model was influenced by Leonard Stein and Paul Polak via Australian psychiatrist John Hoult. Since about 2000, CRHT has influenced the creation of PHH teams in 12 countries—most recently in Canada in the province of Quebec.

However, in the US, PHH seems to have “died at birth” — except one team set up by Stein at the Dane County Mental Health Centre where he became the director in 1974 (Johnson)

Surely, the time has come for psychiatric hospitalization at home?

Awais says there is a need for a strong moral vision that places the clinical needs of people over the needs of the health care system, i.e., a clear, convincing rationale for PHH.

Home hospitalization avoids hospital-related harms, states Awais. A common view among experts is that hospitals disrupt all aspects of patients’ daily lives, and this may damage their social networks and social functioning. Hospitalization is an unpleasant and alienating experience and may result in even greater stigma than being diagnosed as mentally ill.

These ideas about hospitalization appear to have been one of the main motivations for the Quebec provincial government’s plan to institute PHH province wide—the first provincial or state government in North America to do so. In his announcement of this in October 2023, the social services minister described avoidance of hospitalization as the rationale. “Hospital is a negative stigmatizing experience, which, if prolonged, will hinder their self-determination, autonomy, and recovery process.”

One benefit of PHH in my experience is that it decreases the need for involuntary admission. Over my eighteen years of experience treating severely ill patients at home, I came to the conclusion that for many patients, it’s the hospital that they are refusing, not the treatment. Even if they refuse treatment at first, many can be persuaded to accept it, often with the encouragement of their families and other supports.

There is little research on this topic, but one study stands out: a PHH program initiated in the famous mental health system of Trieste Italy, a city of 240,000. The site of a WHO collaborating centre with the goal of disseminating its practises across the world. It’s the one place psychiatrist Allen Frances says he would wish to be if he had a severe mental illness. He’s visited it five times.

Compulsory admissions in Trieste were rare, and by 2005 there were only 15 cases that year due to the practice of “relentless negotiation” with uncooperative patients sometimes over many hours. And yet, they felt the need to reduce these even further and, to that end, in October 2017, created the Home Care Crisis Attention Team.

Within one year the compulsory admission rate was reduced by 78.7%.

A 2003 study in County Monahan in Ireland saw the compulsory admission rate reduced by over half, a third of the national rate, after the creation of PHP.

There is a theme running through research and commentaries regarding PHH, of hospitalization being necessary but best avoided if possible.

During my work, first as a medical director of a psychiatric ward, then as the founder of two PHH programs, I have formed a list of patients who one would expect to have particular difficulty in adjusting to psychiatric hospitalization.

Patients with postpartum disorders, those who are developmentally delayed, refugees and recent immigrants who don’t speak English, first-episode psychosis patients, and homeless individuals.

The theme of hospitalization being necessary, but best avoided by referral to PHH if possible, also runs through the clinical guidelines of the UK’s influential National Institute of Health and Care Excellence (NICE). Their guidelines for the management of acute schizophrenia, bipolar disorder and severe depression all recommend PHH rather than admission if possible. Guidelines for patients with borderline personality disorder, similarly recommend referral to PHH and emphasize only admitting to a hospital if there is significant risk to self or others that cannot be managed by other services or for detention under the Mental Health Act.

The advantages of PHH treatment over hospital treatment for patients with borderline personality disorder were illustrated by the experiences of the Adult Psychiatric Home Support team—a PHH program in Edmonton, Alberta, which I visited for my book. This program was founded by psychiatrist Richard Hibbard, who had a special interest in the treatment of these patients.

Consequently the staff had become competent, comfortable and effective with these patients, and also with those with narcissistic and histrionic personality disorders who often present with self-harm.

Over the years, staff had often dealt with these patients both in the hospital, and then subsequently, in the PHH program. They found them easier to deal with in the PHH program.

A firm three-week limit to length of stay limits dependence; the patients get more time with staff than on the ward; and a firm, consistent approach to head off splitting is easier with a small, close-knit team.

Acting out in the community is less: “It’s their stuff, they are not going to throw their own belongings, or run away from their own home.”

The limited research evidence in support of PHH is often brought up by commentators.

Randomized controlled trials are generally seen as the gold standard form of evidence regarding treatment in medicine, though it has been argued that the complexity of interventions and the many factors that make their outcomes vary between settings limit the usefulness of this scientific method in mental health services research.

An additional problem in PHH research has been the changing ethics of RCTs. The investigators in the 2005 North Islington RTC, mentioned by Awais, came to understand why so few randomized trials of PHH had been published (Johnson). The main challenge is that people presenting in a crisis may transiently lose their decision-making capacity at that time.

Unlike today, in most of the studies conducted in the 1970s and 1980s, everyone referred for hospital admission was randomized at the time of the crisis without first seeking consent. The N. Islington investigators went through an arduous complex procedure to overcome this. Consequently, there were no RCTs after that until the 2020 Swiss RCT cited by Awais.

The latest RCT is a 2022 Dutch study that found a 36.6% reduction in hospital days in the experimental group, but no difference in the number of admissions. Investigators overcame the ethical challenges by using a modification of the traditional RCT, called a Zelen design, in which participants are randomized before the consent stage.

These problems with RCTs can be avoided with quasi-experimental studies that compare two time periods, before and after the institution of a PHH program, or of two areas, one with and one without a PHH program. The main challenge here is whether the two groups are otherwise equal.

The most recent quasi-experimental study was carried out in Switzerland in 2022, where allocation of patients for acute treatment to PHH or the hospital depended on place or residence.

Results showed that PHH can replace an inpatient unit.

Two quasi-experimental studies in the UK showed reductions of admissions of 37.5% (Leeds) and 45% (Newcastle) but are dated (2007).

A sign of the maturity of the PHH model is the creation of a fidelity scale. Fidelity measures are tools to assess the implementation of interventions or program models and as such can help address the major challenge for mental health services of translating scientific knowledge into patient benefits.

Development of fidelity measures for complex interventions in mental health services has been advocated not only as a means to define an intervention and measure services’ adherence to the model specified, but also to suggest service improvement.

In the US Evidence-based Practice Project fidelity scales have been developed for complex mental health services such as Assertive Community Treatment.

In 2016, a group at University College London developed the CORE fidelity scale. It’s a 39-item measure of CRHT with good face validity and promising initial testing, indicating its value in assessing adherence to a model of CRHT best practices.

Item 6 in the fidelity scale is that the CRT has a fully implemented “gatekeeping” role, assessing all patients before admission to acute psychiatric wards and deciding whether they are suitable for home treatment. This is supported by a strong expert consensus, with PHH seen as much less able to reduce admissions if they do not automatically assess every potential admission for suitability for home treatment.

John Hoult specified this requirement from the start. In the 1990s he worked with a PHH program in Sydney, Australia, where the admission rate was halved. After he left, the admission unit was moved from the local mental hospital to a teaching hospital, where the new doctors did not routinely call the PHH team: admission rate and bed usage reverted to the previous level.

This phenomenon of resistance to referring patients to PHH was evident in the PHH program at Boston State Hospital in the 1960s described above. Eventually, it was mandated that all doctors who intend to send patients to the hospital must first get in touch with the PHH program.

When I was visiting PHH services in UK for my book, I met the chief psychiatrist of a hospital who railed against her colleagues who regularly, against established policy, bypassed the PHH team and admitted their patients. “I’m supposed to be their boss,” she lamented.

I heard PHH staff complain of psychiatrists bypassing their service and admitting patients who would be suitable for home treatment while visiting PHH programs in Edmonton, Alberta, and Victoria, BC, for my book.

The PHH service I founded in Cambridge, Ontario, in 1998 was discontinued some years after I left in 2007. I understood one of the reasons was that most of the referrals had originated from one psychiatrist who was an enthusiast of PHH. When he left the hospital, patient numbers shrank.

In a centrally controlled mental health service like the UK NHS, where psychiatrists are employees paid by a salary, gatekeeping works, but I can’t see how it would be possible to institute this in the Canadian health care system.

Sustainability of PHH is an issue according to Hoult (Johnson), who wondered why many teams in other countries have not been sustained. This has been a problem in Canada, where, apart from Quebec, teams were founded by local enthusiasts like myself and were often the only ones, or one of a few, in the province. Over the years in Canada four PHH programs in three provinces were not sustained. Certainly the lack of support from local psychiatrists didn’t help.

Although there is little evidence about this in the literature, Hoult says, the likely answer is they have not been seen as an integral part of the total service system and/or that they have failed to demonstrate their usefulness and effectiveness, thus becoming easy targets for cutting when times become difficult. He outlines principles for ensuring sustainability.

Staff burnout and low morale have been raised as a concern in those contemplating creating a service. However, two studies in the UK have demonstrated good morale, and scores of the three components of burnout were low or average in PHH teams, in contrast to Assertive Community Treatment teams and community mental health teams.

Awais raises the issue of PHH services being very complicated and creating a service being a daunting task.

That seems to be one of the reasons why I have been unsuccessful in getting Ontario’s Ministry of Health (MOH) to develop PHH programs, according to one high-ranking mental health services administrator, who told me that the MOH lacked people with the requisite skills and experience. One Canadian expert told me a specific “technical assistance center” would be required to create a PHH team.

When Vancouver General Hospital in BC replaced an 18-bed psychiatric ward with a PHH program, they hired Accenture—a large consultancy—for project management.

Canada does not have mental health technical assistance centers like SAMHSA does; could these play a role in providing PHP services in the US?

The shortage of public psychiatric beds in the US is a serious problem. The Treatment Advocacy Centre (TAC) advocates for 50-60 beds /100,000 population; currently there are 11.7 /100,000 population.

I could not find any mention of mitigating this shortage by PHH programs. And yet, these may be the only solution to this bed shortage. What are the chances that states are going to build new bricks-and-mortar psychiatric wards?

PHH is cheaper than inpatient care and requires little or no capital expenditure. A detailed review of PHH in the Psychiatric Services journal analyses cost savings. PHH programs can provide an alternative to admission for about a third of patients, plus early discharge for 40%.

But what if the possibilities for diversion of seriously mentally ill patients from hospitalization can be extended by boosting PHH programs with acute day hospitals and supervised crisis and other residential services?

These combinations are not uncommon in the UK but have not been evaluated.

A clue as to how far these combinations could make up for the shortage of beds can be found in a study carried out in Montreal, Canada, in 1996. Even though this study is 30 years old, the design of what was called Intensive Home Care is different from the current PHH design and the setting and healthcare system are different from the US, I think the types of patients and the service models are similar enough to provide the TAC with food for thought.

Instead of mental health planners and bureaucrats determining the role of hospital alternatives (top-down decision-making) it was the patients’ attending psychiatrists who determined what their patients needed at the time of admission (bottom-up decision making) and the results were surprising.

This methodology was pioneered in London and Nottingham, UK, in the mid-1990s. The instrument used is the Nottingham alternative to bed utilization schedule (NABUS).

This comprises 3 sections. The first covers the need for key elements of the care package, including residential alternatives, what the authors call Intensive Home Care (2-6 hours weekly), and day care. Residential alternatives include supervised apartments, supervised hostels, halfway houses, and crisis centers.

The setting is the Louis-H. Fontaine Hospital in the east end of Montreal, once the largest psychiatric hospital in Canada. In the 1980s the hospital decided to curtail access to long-stay beds, thereby creating a defacto pool of new long-stay patients in acute wards in the absence of alternatives for these patients.

The NABUS was translated into French, and operational definitions were developed for the 3 alternatives. At the time of the study, neither Intensive Home Care nor a Day Hospital was set up. Diagnoses were: organic brain syndrome 10%, psychoses 40%, major mood disorders 38%. 64% patients lived in their own homes.

Analysis showed that a package of care, rather than separate alternatives to hospitalization, was the most recommended: IHC combined with residential alternatives or day care.

This left a floor level of 18 acute care beds per 100,000 population required. On a given day, only 62 of 212 patients were unsuited for any alternative to acute care hospitalization.

These results were surprising. It was expected that local psychiatrists would be hospital-centered and resistant to bed cuts. They were not familiar with day hospitals and Intensive Home Care. Instead they favored care packages that delivered treatment in the homes or residential settings of patients in their community.

The effectiveness of PHH turbocharged by an alternative residence is evident in a unique program founded by psychiatrist Olivier Farmer in 2013 in Montreal—the PRISM program. PRISM (Projet de reaffiliation en itinérance et santé mentale) is the French acronym for the Homelessness Mental Health Reaffiliation Project.

Its target population is homeless people with psychosis—schizophrenia spectrum disorder and severe bipolar disorder, often with comorbid substance abuse. It is often the service of last resort.

PRISM is psychiatric hospitalization at home, where home is a homeless shelter. Clients live in a separate dedicated space within the shelter that provides private or semi-private rooms, a lounge with sofas, TVs, and computers. They get all their meals and can come and go as they please.

Treatment is provided by an embedded team consisting of a full-time social worker, a half-time nurse, a part-time psychiatrist, and a full-time shelter support worker. The clinical staff are employees of a hospital where the psychiatrist can admit patients. The service has multiple partnerships, most prominently with Housing First organizations. Clients have to agree to receive treatment and to seek housing. They pay $335 /month rent from their social benefits. The main goal of the program is to get the clients well enough that they have the capacity to engage with a Housing First program and other supports.

After 8-12 weeks, 76.7 % achieve stable housing. 78% are linked to ongoing mental health supports with a warm handover, and 62% are still housed after one year. 75% are treated with a depot intramuscular antipsychotic.

There are now six PRISM programs, one of them in Quebec City.

Finally, to end on a positive note, on January 5, 2026, the history of PHH came full circle in Boston, 62 years after the Home Treatment Service at Boston State Hospital was awarded the APA Gold Award.

That day, the Massachusetts General Behavioral Health Home Hospital (BHH) in the Boston area launched a pilot randomized trial of home-based acute psychiatric care for a highly selected lower-risk subset of adults who would otherwise have needed inpatient psychiatric care.

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In a previous discussion of psychiatric hospitalization, I wrote:

“We need to recognize the disability and disruption that accompanies mental illness; it is not a fiction, and systems of care are a necessity. Attempts to reduce involuntary psychiatric hospitalization without creating alternatives are not likely to end well. The good news is that many such alternatives exist, such as open-door units, crisis stabilization units, crisis houses, peer respite centers, partial hospitalization programs, intensive outpatient programs, and home hospitalization. These alternatives remain woefully underfunded and underdeveloped.”

In this post I want to say more about the last item on that list of alternatives, psychiatric home hospitalization.

When psychiatric patients in some parts of the world experience a mental health crisis severe enough to warrant hospitalization, they might in some cases remain at home and receive intensive treatment from a crisis team that will visit them daily (or more frequently, if needed) and provide them a level of care that approximates the inpatient unit. This is called “psychiatric home hospitalization,” and it is a 20th-century innovation in acute mental health care. The treatment is commonplace and fairly well-established in the UK. The UK mandated more than 300 such teams nationally in 2000 and successfully implemented them within four years. In the United States, despite the model originating here in Madison, Wisconsin in the 1970s, home hospitalization remains a curiosity and is basically absent from the service landscape. Home hospitalization also has a limited presence in Canada, around half dozen programs in various cities. Crisis resolution and home treatment services are also available in Australia, New Zealand, Ireland, the Netherlands, Belgium, Norway, Germany, Switzerland, Spain, France, and Malta. Suffice to say, the dilemmas around involuntary psychiatric hospitalization have not been resolved in these countries, but unlike the US, the existence of such services at least means that inpatient psychiatric hospitalization is not the only option in a psychiatric crisis.

My own exposure to and understanding of home hospitalization comes from the psychiatrist David S. Heath, the most prominent champion of home hospitalization in North America. Heath founded Canada’s first psychiatric home hospitalization program, Hazelglen Service, in Ontario in 1989. He is the author of the 2004 book Home Treatment for Acute Mental Disorders (Routledge, available open access here), still the most authoritative book on the subject, and he maintains the website Intensive Home Treatment, providing updates on new research and resources.

Heath has been making the argument that if we want to avoid admitting patients to the hospital and to shorten their stay, intensive home psychiatric treatment is our best bet. Home hospitalization can effectively address the lower tertile of acuity of psychiatric emergencies (can be particularly useful for postpartum patients and first-episode psychosis) and it can facilitate early discharge from the inpatient units, providing transition to outpatient care.

Psychiatric home hospitalization goes by different names. Crisis Resolution Home Treatment teams in the UK, Community Treatment Teams in Australia, various other names in other places (home-based care, psychiatric home support, hospital diversion, intensive home treatment, mobile psychiatric crisis intervention). The core features are consistent, however. A multidisciplinary team including psychiatrists, nurses, social workers, and sometimes peer specialists provides intensive treatment to people experiencing acute psychiatric crises who would otherwise require hospitalization. The team visits patients at home daily or multiple times per day, for a period spanning days to weeks. They provide medication management, brief psychotherapy, crisis intervention, family support, and practical assistance. They offer 24-hour phone access for emergencies and can arrange hospital admission if situations deteriorate.

This differs from mobile crisis teams, which conduct brief assessments and referrals but don’t provide ongoing treatment. It differs from partial hospitalization programs, or acute day hospital programs, which require patients to attend a facility during daytime hours, but don’t have services available at home or over the weekend. And it differs from traditional community mental health care, which might see patients weekly or monthly. And it differs from Assertive Community Treatment, which is focused on chronic management of serious mental illness to prevent rehospitalization. Home hospitalization represents hospital-level intensity of care, delivered in the patient’s natural environment rather than an institution.

The clinical evidence, while limited, is respectable and relatively consistent across decades and countries. A 2020 Swiss RCT of home hospitalization reported a 30% reduction in hospital days over 24 months. A 2005 RCT of crisis resolution teams (assessing all patients and managing them at home if feasible) in residents of the inner London Borough of Islington reported that patients receiving the service were less likely to be admitted to hospital in the eight weeks after the crisis (odds ratio 0.19, 95% confidence interval 0.11 to 0.32), although compulsory admission was not significantly reduced. A 2015 Cochrane systematic review of “care based on crisis‐intervention principles, with or without an ongoing homecare package,” concluded that interventions reduced repeat admissions, family burden, and increased satisfaction compared to standard hospitalization.

In United States, access to inpatient psychiatric care for patients who do not meet criteria for involuntary care has become drastically difficult over the past decades, and patients are generally only admitted if there are concerns about suicidal ideation, violent behavior, grave disability, or other serious psychiatric decompensation. There is a sizeable chunk of people who get admitted who don’t have a genuine clinical necessity, but such cases are usually driven by liability considerations in emergency contexts. A lot of patients who would benefit from voluntary inpatient psychiatric hospitalization do not have access to inpatient care. Such patients are currently being managed mostly by a patchwork of intensive outpatient programs, partial hospitalization programs, and crisis stabilization units. So it seems to me that the sort of patient most likely to benefit from home hospitalization is already being excluded from inpatient psychiatry in the US, and home hospitalization is thus less likely to replace inpatient volumes but more likely to expand access to those who need care but are currently underserved.

The exclusions for home hospitalization are straightforward. Patients with acute intoxication, extreme agitation posing immediate danger, acute imminent suicide risk or suicidality unmanageable at home, significant risk to others, and no stable living situation cannot be treated at home. These exclusions rule out a substantial chunk of patients presenting in psychiatric crisis.

These days I work in an intensive outpatient and partial hospitalization program, so it is natural for me to wonder: which patients need hospital-level care and are suitable for home treatment but can’t be better served in IOP/PHP? Home treatment provides 24-hour availability including weekends when partial programs don’t operate. It reaches patients who can’t or won’t travel to facilities due to agoraphobia, paranoia, disorganization, cognitive impairments, or lack of transportation. It engages patients who would be discharged from partial programs for non-attendance or disruptive behaviors but will accept home visits. However, I do have to say that if there is ready access to inpatient beds with an adequate quality of care and there is a strong coordination with IOP and PHP programs for step-up and step-down care, the gap to be filled by home hospitalization is a relatively small one.

That said, patients who are currently admitted to inpatient units on an involuntary basis primarily for liability reasons could potentially be managed via home hospitalization, only if there is a strong system of coordination and quick handover between emergency rooms and psychiatric home hospitalization teams, and, importantly, psychiatric home hospitalization teams are willing and able to take on the liability of managing risk of suicide and violence in the person’s home environment. Once you factor in the problem that the US currently doesn’t have an established pathway for reimbursement of psychiatric home hospitalization, the challenge of implementation becomes daunting.

The Case for Psychiatric Home Hospitalization

Many acute psychiatric episodes can be stabilized at home with the right intensity of timely care, allowing earlier intervention before situations degrade to the point where emergency departments and inpatient admission become the only options.

Home hospitalization avoids hospital-related harms: sleep disruption, exposure to restraints or seclusion, effects of being on a unit with other acutely ill patients, and trauma from involuntary treatment. Continuity to routine outpatient care can be smoother and less abrupt compared to inpatient units.

Staying at home during a crisis can feel better because people have more privacy, control, and dignity. People are more likely to be engaged if they feel like care is being provided with their input. When clinicians go to someone’s home, the difference in institutional power that characterizes inpatient psychiatry is lessened. For people who don’t want to go to the hospital because they’re afraid of the loss of control or have had traumatic experiences, home-based care may be the only option that is acceptable to them in a crisis.

The ethical argument is that psychiatric care should be the least restrictive option that ensures the person’s safety and well-being. Home hospitalization expands the possibilities of the least restrictive options available. People keep their independence and freedom, stick to their routines, make decisions, and stay connected to their roles as parents, workers, students, or community members instead of having those aspects of their lives forcibly disrupted.

Crisis care stays in a person’s social world instead of being taken out of it. Caregivers and family members can participate in the treatment more naturally. They see what the psychiatric team is doing; conversely, the team can better assess the family dynamics.

Home hospitalization builds integration across sectors by requiring coordination with primary care, housing, schools, and community supports. There are also financial benefits: safely replacing a portion of inpatient admissions can cut down on bed days and costs for the system.

But home hospitalization works only if the eligibility requirements are strict, the staffing is reliable, and the thresholds for escalation to inpatient care are low. Home hospitalization isn’t a replacement for all or even most hospital stays for mental health issues.

Since home hospitalization can’t replace inpatient services entirely (you cannot shut down an inpatient unit and rely only on home hospitalization), creating the service in a system does require a sizeable initial investment, even if it saves the system money later. Services need to make detailed clinical protocols for dealing with risks, medications, substance use, unsafe environments, and quick escalation pathways. There are legal and regulatory requirements. Coordination is needed with emergency departments for medical clearance and lab work, with inpatient units for priority admission when home treatment becomes unsafe, and with insurers about reimbursement. Building infrastructure for home hospitalization in a system with fragmented pots of money and competing interests can be formidable. There is a problem with shifting costs: keeping people from going to the hospital saves insurers money, but providers have to pay for the program unless contracts align incentives. Most programs need money from health systems, grants, or contracts based on value.

Problems with the workforce can also be daunting. The service needs nurses, psychiatrists, social workers, therapists, and peer specialists who can work in a crisis and are willing to make home visits. There must be coverage available 24 hours a day, or at least a reliable after-hours model with on-call rosters. Clinicians will see a lot fewer patients than in a clinic or hospital setting because they have to travel and do high-acuity work. Retention can be hard because of the intense, unpredictable work that comes with safety concerns and potential moral distress.

Liability exposure may increase when adverse events transpire outside hospital environments, necessitating a justification for the preference of home hospitalization over inpatient admission. Weapons, domestic violence, unsafe neighborhoods, pets, hoarding, and infestations are all examples of environmental dangers that can be expected.

Psychiatric Home Hospitalization: Scarcity Mindset vs Abundance Mindset

I find myself thinking about psychiatric home hospitalization through two different lenses: the logic of scarcity and the logic of abundance. The scarcity lens treats home hospitalization as a response to constrained resources. The argument goes like this: inpatient beds are scarce and expensive, emergency departments are overwhelmed with boarding patients, and staffing is limited. The scarcity mindset optimizes for admission avoidance, bed-days saved, reduced emergency department length of stay, lower per-episode cost compared to inpatient care, and system throughput. It speaks the language of hospital executives and payers. It fits the political economy of extracting efficiency.

The problem with the scarcity lens is that if the entire selling point is saving money and freeing up beds, the program will be judged primarily on reducing hospital admissions and duration of stays. This creates two predictable consequences. First, to hit admission-avoidance targets, teams will be pressured to accept higher-risk patients, then face criticism and scrutiny when inevitable adverse events occur. Second, the service can degrade into triage. There will be temptation to use home hospitalization services as gatekeepers for inpatient admissions. My understanding is that this is what happens in the UK to some degree. Patients aren’t admitted without being assessed by CRHT teams. The goal is to prevent unnecessary admissions, and there is a risk that the service can become organized around assessment and triage instead of providing actual hospital-level care at home. Home hospitalization becomes an instrument of withholding access to care that patients feel they need rather than actually providing required care. This is, obviously, undesirable.

The abundance lens focuses on the argument that crisis care should be patient-centered and clinically graded. Inpatient care is one tool, not the default. Home hospitalization is an additional high-quality option for people who want it and for whom it’s safe, along with other elements of care like crisis stabilization units, intensive outpatient, partial hospitalization, and assertive community treatment. This frame optimizes for quality and experience, privacy, dignity, family involvement, fewer coercive exposures. It emphasizes continuity and smoother transitions. It focuses on functioning and recovery by treating people in their regular environment. It creates opportunities to address equity by designing access so the service isn’t only available to people with stable housing and caregivers, and can be extended to things like shelters and group homes.

The abundance frame is compelling to clinicians like me. It fills a gap in the American continuum of care, between emergency departments and inpatient units on one side and outpatient clinics and day programs on the other. And it is not built on the promise of restricting access to inpatient beds or saving the system money.

The two mindsets shape actual program design in different ways. Scarcity-driven programs will have gate-keeping functions and broader eligibility to maximize admission diversion, which means more borderline cases and higher volatility. Abundance-driven programs will have clearer stratification: home hospitalization is reserved for the lower quartile or tertile of patients with suitable characteristics, while others are directed to mobile crisis, crisis stabilization units, day programs, or inpatient care. Scarcity programs will use lean staffing models and fewer in-person visits. Abundance programs will have reliable staffing, frequent in-person visits, strong nursing capacity, robust after-hours coverage, and meaningful psychotherapy. Scarcity programs will measure admissions avoided, length of stay, and cost per episode. Abundance programs will measure symptom and functional change, patient-reported outcomes, patient satisfaction, safety events, continuity of care, etc. The failure mode for scarcity is building a triage team and calling it home hospitalization. The failure mode for abundance is building a program that isn’t economically or logistically viable.

In practical terms, the scarcity frame is likely to be more successful in the short run in terms of getting approved and funded. But in the medium to long run, I believe the abundance frame is what is needed to prevent the service from collapsing, providing subpar care, or becoming a tool of withholding inpatient care.

The American healthcare landscape makes it very difficult to capture the value of programs that reduce psychiatric hospitalization and provide high-quality care in the community. The psychiatric workforce crisis means staffing 24-hour crisis teams with psychiatric providers is prohibitively difficult. The liability environment creates risks that risk-averse healthcare organizations would be reluctant to accept.

Perhaps the only way to pierce through this thick fog of inertia and liability is a strong moral vision that places the clinical needs of people over the needs of healthcare systems.

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This post will be followed up by a commentary by Dr. David Heath.

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In a post titled “Are Most Claimed Psychiatric Diagnoses False?,” (July 2025) psychiatrist @ (henceforth, “Dr. Affective”) made an unsettling argument modeled on John Ioannidis’s famous 2005 paper on why most published research findings are false. He applies the logic of positive predictive value (PPV) to psychiatric diagnosis and arrives at the conclusion that most psychiatric diagnoses given in real-world clinical settings are likely “false.” False here means that the diagnostic label given to the patient doesn’t actually satisfy the DSM/ICD diagnostic criteria for that diagnosis; if the DSM/ICD diagnostic criteria were properly and rigorously applied, the person would have a different diagnosis (or different diagnoses) or no formal diagnosis at all.

The thesis is straightforward and technically sound, as far as it goes. A diagnosis can be treated as analogous to a positive test result. Its accuracy depends on how common the disorder is in the population being evaluated (prevalence, or the pre-test probability), how good the evaluation is at catching the disorder when present (sensitivity), and how good it is at ruling out the disorder when absent (specificity). Even with respectable sensitivity and specificity (say, 85% each) the positive predictive value drops sharply for diagnoses that have low prevalence. For a condition present in 10% of the population being assessed, an 85/85 evaluation yields a PPV of only 39%. That is, most (>50%) of the positive diagnoses are wrong.

Aside from prevalence, there are many considerations working against the accuracy of diagnoses. Common psychiatric conditions such as depression, generalized anxiety, and ADHD have overlapping symptom profiles and fuzzy boundaries with “normality,” making them hard to distinguish even in rigorous evaluations. Most diagnoses aren’t made by psychiatrists but by primary care providers with less training and less time, lowering both sensitivity and specificity. Systematic biases such as clinician hobbyhorses, patient expectations, edge cases, and the pressure to produce a billable diagnosis shift thresholds toward overdiagnosis. And a multiple comparisons problem emerges as patients see multiple providers who each screen for multiple conditions, inflating the cumulative probability of at least one false positive. The more popular and sought-after a diagnosis is, the more likely it is to be false.

When I first read the post, my reaction was, “Damn!” I think Dr. Affective is right. As I’ve sat with the argument, I’ve come to think that the most important thing about it is that it forces us to ask further questions about what “false” means when applied to psychiatric diagnoses.

Why Aren’t Things More Catastrophic?

If psychiatric diagnoses are wrong more than half of the time, you’d expect the clinical psychiatric enterprise to be in freefall, with widespread chaos. We’d expect most people to receive inappropriate treatment and experience negative outcomes from that. And while psychiatric treatment certainly has its problems and while the radical critics of psychiatry already do believe that most people are being harmed, I genuinely don’t believe that the current state of affairs is as bad as it would be if the majority of diagnoses had no meaningful connection to what patients were experiencing.

The reason, I think, is that specific DSM/ICD diagnoses are doing far less therapeutic work than the system pretends. Most (first-line) psychiatric treatments target broad symptom domains, not specific diagnostic categories. SSRIs are effective for depressive symptomatology, multiple anxiety disorders, OCD, post-traumatic reactions, and (sometimes) eating disorders. CBT and psychodynamic principles apply across the internalizing spectrum and more. Mood stabilizers and antipsychotics are deployed transdiagnostically. If a clinician diagnoses major depression when a more careful evaluation would yield generalized anxiety, or when the “true” picture is an undifferentiated blend of depressive and anxious distress, the initial medication recommendation as well as the psychotherapy approach is likely to be the same.

Careful attention to DSM/ICD diagnoses does matter. I want to acknowledge that. Optimal treatment of OCD diverges from optimal treatment of generalized anxiety, for example. And this is where competent clinicians outperform subpar clinicians who cannot progress beyond a coarse-grained symptom characterization. And I’d say excellent clinicians are those who can go beyond DSM/ICD categories to richer forms of clinical characterization and case formulation. In this sense, both subpar and above-par clinical psychiatric practice involves a certain disregard for DSM/ICD.

Clinicians, in practice, operate at a level of description closer to symptom domains and prototypes. DSM/ICD diagnoses are most useful when a clinical presentation is an excellent fit with a diagnostic prototype… when someone has a “classic” or “textbook” presentation of schizophrenia, bipolar disorder, OCD, BPD, etc. It is very common, however, for clinical presentations to have a fuzzy and polymorphous character that doesn’t really fit well into DSM categories. The DSM diagnoses offer a shared vocabulary and many practical and administrative elements of the system run on them, but actual clinical reasoning proceeds on a different and more granular track.

The problem identified by Dr. Affective, if taken to its conclusion, points toward a mismatch between the categorical structure of our diagnostic system and the dimensional, transdiagnostic complexity of what patients present with in the clinic. The categories are too specific, pseudo-precise in a way, too discrete for the underlying phenomenology, and too fragmented for what the treatments can actually distinguish between. As Dr. Affective wryly comments, “Sometimes I think we should just call everything psychosis or neurosis and be done with it.”

If specific diagnoses aren’t driving treatment decisions, then the “falsity” of a given DSM/ICD diagnosis may be less consequential than one may initially assume. A “false” major depression diagnosis in someone with pervasive internalizing distress (say, with a “correct” DSM diagnosis being dysthymia and generalized anxiety) isn’t clinically catastrophic in the way a false cancer diagnosis would be, because the treatment offered isn’t contingent on the diagnostic specificity in the same way.

The risks of false diagnosis are concentrated along certain points: when misdiagnosis comes with the risk of treatment harms (e.g. confusing bipolar disorder with ADHD and putting patient on stimulant monotherapy inducing a manic episode), or missing something vital like catatonia or secondary medical etiology, or failure to update diagnosis beyond initial treatment (e.g. failing to recognize personality disorder after poor response to multiple medications) or when diagnoses carry prognostic weight (schizophrenia), or when they determine access to specific services or accommodations (autism), etc.

Diagnostic Metaphysics vs Diagnostic Math

The deeper issue is the metaphysics rather than the math of diagnostic accuracy. The PPV framework requires a determinate fact of the matter: either the patient “has” MDD or they don’t, and the diagnostic evaluation is trying to correctly determine which. While a person has MDD or not in a strict DSM operational sense, in reality, the person exists on a spectrum of approximate fit to the prototype of major depression (and that prototype itself breaks down into more statistically homogeneous dimensions). Any picture that presupposes that DSM/ICD categories correspond to discrete entities that patients either have or lack gets things wrong at a very fundamental level.

When we talk about the falsity of diagnoses, we can talk at the level of particular diagnoses (while assuming the classification system to be valid) or we can talk at the level of the classification system itself. We could mean that the patient doesn’t meet the DSM criteria for the assigned condition on careful assessment, but diagnoses can also be false in the sense that the entire exercise of forcing a dimensional, hierarchical picture into a discrete categorical scheme is misguided at the level of the classificatory framework. The first problem is addressed by more comprehensive and rigorous evaluations and diagnostic refinement/correction over time. The second problem suggests that we need to update our entire way of thinking about diagnosis to account for the fact that there may be no determinate fact of the matter for a categorical diagnosis to be true or false about.

Asking whether a diagnosis is “true” or “false” in the correspondence sense (does this label accurately map onto a discrete entity the patient has or lacks) may be the wrong question. A better question might be: is this diagnosis a good enough fit for this patient’s symptom profile and descriptive psychopathology, given our current categories, to usefully guide clinical decision-making?

Diagnostic Truth as Convergence

Another way we can think of diagnostic “truth” is in terms of convergence rather than correspondence. The relevant thought experiment goes something like this: if multiple competent clinicians, with comprehensive information available, including detailed developmental and psychiatric history, collateral information from family, longitudinal observation, treatment response data, and adequate time to conduct a thorough evaluation, with agreement on the diagnostic criteria being applied, and with opportunities to refine/update diagnoses, would they converge on the same diagnosis?

When convergence is high, we have something worth calling a “true” diagnosis because it represents a stable judgment under favorable epistemic conditions. Florid mania, contamination OCD, severe anorexia nervosa, melancholic depression, classic paranoid schizophrenia, these are cases where convergence would be high under favorable epistemic conditions and where calling a discordant diagnosis “false” seems appropriate. The clinical presentation is distinctive enough and the consequences substantial enough that competent evaluators would reliably agree.

When convergence is low even under epistemically favorable conditions, then the language of true and false diagnoses becomes misleading in a way. What we have is irreducible diagnostic uncertainty or non-specific psychopathology, reflecting not (or not primarily) the incompetence of the evaluators but the genuine ambiguity of the clinical picture, the overlap between the available categories, or the fuzziness of clinical boundaries.

Even under ideal convergence conditions, DSM/ICD diagnoses encompass heterogeneous symptom profiles and show high comorbidity. Even when convergence is high, even when all competent evaluators would agree that this patient “has MDD,” the diagnosis is still a lossy compression.

This is a thought experiment, in a sense, because in reality clinicians rarely have comprehensive information, adequate time, or opportunities for convergence. Real-world evaluations are typically brief, conducted under time pressure, influenced by biases, and performed by clinicians with varying levels of training. The PPV calculations accurately describe the de facto state of diagnostic practice. But the convergence thought experiment helps us distinguish between two very different sources of diagnostic error: errors that would be corrected by better information and more careful evaluation (and thus are genuinely “false” in a meaningful sense), and indeterminacies that would persist even under ideal epistemic conditions (and thus reflect limitations of the categories themselves rather than failures of the clinicians). When a diagnosis is uncertain, whether epistemically or metaphysically, saying so is both more honest and more clinically useful than conveying false diagnostic certainty.

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In the middle of Richard Saville-Smith’s groundbreaking 2023 book Acute Religious Experiences: Madness, Psychosis and Religious Studies, there is a haunting passage addressed to any psychiatrist who may stumble across it.1

“But, deep into this book, I do want to write two things about madness as madness, as my madness, for the benefit of any psychiatrists who may stumble across these words:

1. Being mad is, for me, not the aberration, it is the more, the numinous, the Shamanic consciousness, the mystical experience, the reality beyond the model offered by the psychotomimetic/psychedelic experience. Madness is the peak experience. In quantitative terms madness is a small part of my life, in qualitative terms it is the most profound, the most important, the most eye-opening, mind-altering, liberating experience, like a light-bulb moment which can last for pain-filled weeks, too hot, too bright, too harsh. I am not not me when I am mad. I am the same person, living the same life but with the costs and benefits of riding a wave of immediacy over which the only control I seek is to go higher. The reason mad people, like me (I speak for myself, but I know I’m not alone), are forcibly detained is because, in contrast with all other ‘medical’ patients, I am impatient, I don’t want to be helped or cured, I don’t want to be interrupted.

2. Speaking even more personally, when the psychiatric system trips me up and intervenes for the benefit of myself or others, I understand their good intentions. But what they don’t know is that when they lock me up, I make myself sane – in order to escape – and, and this is the key point, in pretending to be sane I become sane. This pretence is exhausting. I adopt routines, but not rigidly, ritually or obsessively – an afternoon nap, an evening bath (they don’t know whether I sleep or bathe). I walk instead of running, I sit where I can be seen, pretending to read a book, as the words bleed down the page, I eat my meals at mealtime and ask the staff to compliment the chef, I play chess by sticking to the rules, I hold my tongue and I do not rise to provocation…

My difficulty with psychiatry is not driven by the historic othering of the mad in their categories of pathology, it is driven by their continual refusal to understand that what they call psychosis is, referencing the phrase that Otto never used, the mysterium tremendum fascinans, even though it hurts, even though I hurt the ones I love. If psychiatrists paid attention to the (rich white) world of psychedelic studies and took the same care over ‘setting’, they might make psychosis more beautiful; and they might attend to how their patients could learn how to come down through their own volition, assisting with the integration of their experiences through the ontological trauma on the climbdown, not by interfering with my brain by chemistry, but by showing sensitivity to the question of how they might help me to live my best life.

There, I’ve said it.”

(p 143-144)

And earlier in the book, he writes:

“How is it possible to persuade a psychiatrist that one is sane when in the midst of an overwhelming and ineffable experience of god? At the contemporary cutting edge of psychiatric theory is the recourse to a phenomenological approach (e.g. Zahavi 2021). But however much the categories of the psychiatric classification are bracketed through the epoché, the inquiry remains one in which madness is required to give a rational account of itself to provide the psychiatrist with the means of understanding. The patient is required to speak. This method is cloaked in the impossible notion of reasoning with madness, which is a continuation of the domination of madness by reason. Except now, the mad subject is required to give their own reasonable account, to justify themselves even though the organization of the meeting place renders them the othered subject. The seven accounts in Part I have in common a recognition that the experience of the extraordinary/anomalous/extreme is irrational, un-understandable even to the subjects when they are in the midst of their own disorientated, immediate state. The asymmetrical power imbalance of the clinical encounter requires the mad to articulate themselves, to articulate the ineffable in flimsy, inadequate, useless words – coherently. The resultant disorganized speech may be an inevitable by-product of the setting of the encounter rather than an intrinsic failure on the part of the mad. The result is that all the necessary components of mental disorder line up and the voice of god is overwritten with the presumption of psychosis. The epistemological injustice (Fricker 2007) is that the delusion of religion which is tolerated by psychiatric pragmatism in normal life (or the lives of normals), when experienced as overwhelming reality, as religious experience, exceeding conventional formulae, becomes an automatic disqualification for sanity.” (p 103)

Ever since I read these words in Saville-Smith’s book, I have been chewing on how I would respond to them.

Saville-Smith frames the clinical encounter as a kind of epistemological tribunal. The patient, in a seemingly acute psychotic or manic state but also amidst a profound religious experience, is asked to give a rational account of themselves. They are expected to articulate, coherently and in words, an experience that is overwhelming and beyond language. As the psychiatrist observes for the behavioral markers of pathology, the very act of trying to communicate the ineffable in a setting designed to assess rationality inevitably produces the appearance of irrationality.

Saville-Smith is right in this regard. I acknowledge that the clinical encounter is not a neutral epistemic space. It is organized around particular assumptions about what counts as coherent self-presentation, and those assumptions can systematically disadvantage people whose experiences fall outside familiar frames, including acute religious experiences as well as states of madness.

There are experiences of madness that have nothing religious about them, and there are many spiritual, religious, and mystical experiences that have nothing mad about them (at least in a way that brings them to clinical attention). What Saville-Smith is talking about exists at the intersection of the two, and while it genuinely happens, it is a distinctive subset of both “madness” and “religious experience.” So I want to be clear that I am only talking about mad-and-mystical states, cases where the religious experience is legitimate (whatever it means for a religious experience to be legitimate) but also otherwise indistinguishable from mania and psychosis. From what Saville-Smith describes, this seems to be his situation.

I also want to affirm something that should not be controversial but still meets resistance in clinical settings: the experience of psychosis and mania can be, for the person undergoing it, phenomenologically rich and deeply meaningful. Saville-Smith describes madness as “the more, the numinous, the Shamanic consciousness, the mystical experience.” For him, these episodes are qualitatively the most significant experiences of his life. I take him at his word. Any account of psychosis that treats it as nothing but pathology, as mere noise in the signal, as experience evacuated of meaning, is clinically impoverished and philosophically naïve. I remember a patient from several years ago who had undergone a religious experience amidst an otherwise quite destructive manic episode, and the consequences of that spiritual experience outlasted the mania. He had been an atheist before and now believed in God. But he was also struggling to make sense of it, because his family members and the clinicians couldn’t see past the psychopathology of mania and psychosis.

So far, then, I am with Saville-Smith. But how do I, a psychiatrist, stumbling across these words in the middle of his book, answer him?

Let’s start with the question of truth. There is a conflation here between the experience itself and its epistemic authority. Saville-Smith describes his manic episodes as contact with the numinous, as mysterium tremendum fascinans, as something that overwhelms, terrifies, and fascinates. Psychiatry wrongs Saville-Smith by overwriting the voice of god with the presumption of psychosis.

This is a point that William James already understood in The Varieties of Religious Experience; mystical states carry a “noetic quality” for the subject, a sense of insight into deep truths, but this quality confers no epistemic authority on those who have not shared the experience. The feeling that one is in contact with ultimate reality is not the same thing as being in contact with ultimate reality.

How is it possible to persuade the psychiatrist that one is truly in the midst of an overwhelming and ineffable experience of god? The psychiatrist here is a representative of the clinical community as well as the society at large. How is it possible to persuade anyone (in a predominantly secular culture) that one is truly in the midst of an overwhelming and ineffable experience of god? What can Saville-Smith say that would persuade his mother? His neighbor? His childhood best friend? His lawyer? His GP? If he were in a court of law, how would he persuade the judge? There are always believers, of course. Every prophet and mystic has found some in the past. But that does little to budge the default skepticism our culture has towards the truth of mystical experiences. The experiences may constitute sufficient warrant for Saville-Smith, but they are his experiences. Others only have the stuttering, rambling testimony of an overwhelming and ineffable experience that looks and sounds very much like madness. A mystic’s private and inaccessible experience comes with no public obligation that others have to believe in its reality.

The reality of an overwhelming experience of the divine is, in some ways, a collective epistemic matter, something adjudicated within communities of interpretation. Even the world’s great mystical traditions have never simply accepted every claim of divine contact at face value. The Christian contemplative tradition, Sufism, the Hindu and Buddhist meditative traditions, all of them have frameworks for discernment, for distinguishing genuine spiritual insight from spiritual inflation, from ego-aggrandizement, from states that tradition itself regards as dangerous or misleading.

However, regardless of whether I as a psychiatrist am personally convinced or not, this is not a point that needs to be pressed in the clinical encounter. A psychiatrist sitting across from a patient in an acute state does not need to adjudicate the reality or unreality of the religious experiences (although unfortunately many are dogmatic or close-minded enough to do so). Saville-Smith writes as though the only obstacle to the acceptance of his experience is psychiatric dogma; as though, absent the clinical gaze, the experience would simply be recognized as what it truly is. The reality is that the epistemic challenge extends far beyond the psychiatrist.

If the truth question can be bracketed, and I think it can and should be in the clinical setting, then what remains? What is the psychiatrist actually doing when they intervene in an acute manic or psychotic state? As a psychiatrist, I am after a set of far more mundane and far more urgent questions. Can you exercise control over your behaviors and impulses? Can you discern what is happening around you in the mortal world? Can you keep yourself safe and out of danger’s way? Can you recognize your bodily needs? Are you behaving in ways that alarm the people who love you? Are your actions making you vulnerable to harm?

These questions are not the imposition of an alien, oppressive, rationalist authority. They are the questions that any social arrangement must navigate when someone enters a state of radical behavioral alteration or disruption. And Saville-Smith’s own account is candid on this point. He acknowledges that his episodes hurt the ones he loves. He acknowledges that the psychiatric system intervenes “for the benefit of myself or others.” He understands their good intentions. His complaint is not that the concern is misplaced but that the response is wrong, that psychiatry should help him “live his best life” rather than interfering with his brain chemistry.

I have considerable sympathy for this. Psychiatric intervention in acute states is often blunt, coercive, undignified, and inattentive to the experiential world of the patient. There is no question that we can do better. But the aspiration to do better is not the same as the aspiration to do nothing. And in cases similar to Saville-Smith’s, how can we take the patient’s report of “living his best life” at face value if it involves a prolonged state of profound impairment that the patient barely seems to acknowledge?

If not psychiatry, then what other social institution will take responsibility for a person’s well-being in such a state? The church may have, at one point. Hard to believe they will do so now, and hard to believe that the public will tolerate it even if they try. If you strip away psychiatry without replacing it with something, you do not get liberation. You get neglect, incarceration, homelessness, or a burden displaced onto family members. The alternatives to psychiatric hospitalization in our current social world are not freedom and spiritual community. They are the emergency room, the jail, and the street.

To his credit, Saville-Smith does have a constructive proposal. He suggests that psychiatry should learn from the world of psychedelic studies, should attend to “setting,” should help patients come down through their own volition, should assist with the integration of their experiences rather than suppressing them pharmacologically. This is an attractive vision, and there is indeed much that psychiatric treatment of psychosis can learn from psychedelics. The psychedelic therapy framework is built around the recognition that overwhelming altered states can be meaningful and dangerous, that the human organism needs scaffolding to move through them safely, and that the quality of the environment profoundly shapes the quality of the experience.

But the gap between a transient psychedelic experience and the reality of acute mania or psychosis in the community is also enormous. Psychedelic sessions are planned, time-limited, and voluntarily entered. Manic and psychotic episodes are none of these things. They escalate. People in manic states spend their savings, lose their jobs, destroy their marriages, endanger themselves physically, terrify their children. The state that Saville-Smith describes as the peak experience is, for the people around him, a crisis.

If Saville-Smith wants to remain in a state of heightened spiritual experience and wants the mental health system to make the experience “more beautiful,” and help him “come down through his own volition,” how do we know that this is possible on a timeline that is safe and feasible? In the US, for example, a court order for involuntary medication use often takes about 2-3 weeks at the earliest. If a person cannot come down through his own volition within that sort of timeframe, and if, in terms of impairment, the mad-appearing mystic is indistinguishable from the mad, what are we to do? Again, this is not simply a matter of convincing an individual clinician. It is a matter of convincing an entire society.

Saville-Smith describes, with considerable self-awareness, how he performs sanity in the hospital in order to secure his release. He describes this performance as exhausting and as an indictment of the system, evidence that psychiatry demands conformity rather than understanding. If Saville-Smith can modulate his behavior in this fashion, then the boundary between the manic experience and the capacity for self-regulation is not as absolute. He is not simply a mystic interrupted by the psychiatric police. He is someone who moves between states, who has learned from cumulative experience, and who possesses, by his own account, some capacity to navigate that movement.

And the performance of sanity is exactly what I expect sometimes from my manic and psychotic patients. The capacity to perform, the behavioral control needed to lie, is sometimes sufficient for a person to function outside the hospital. It shows they have enough awareness of what is going on around them that they can recognize what will get them in trouble and adjust their behavior. I do not always need delusional people to give up their delusions; they can hold to their cherished beliefs, as long as they can recognize that others around them do not share them. The performance of sanity can be enough. But it is surprising how often pretending to be sane is a prelude to becoming sane.

If the goal is to help someone move through an acute state with less coercion and more dignity, then the capacity for strategic self-regulation is a resource to be built upon. Good clinical work might involve helping someone develop the skills and supports to navigate altered states more safely, not by denying the meaning of those states, but by taking seriously the question of how to live with them in a world that includes other people, including skeptical and unpersuadable people. This, it seems to me, is closer to what Saville-Smith is actually asking for.

I don’t pretend that any of this resolves the tension Saville-Smith is pointing to. There is a good reason his words have stayed with me. The encounter between psychiatry and extreme experience is genuinely difficult, and the history of that encounter is an uncomfortable one. I have also been fortunate, as a young adult, to have been friends with self-described practicing mystics. I am not sure what to make of their experiences but I know they experienced something beyond psychosis. One of them, “N.,” now deceased (rest in peace, my brilliant friend), told me how, when she was just about entering adulthood, she had her first mystical experience. She told her parents, who, not quite sure what to do, took her to a psychiatrist’s office. N. laughed as she recounted this story, “The poor guy had no idea what to do with me.” She never went back as he didn’t have anything meaningful to offer her and she was never in a position where she had to be taken against her will. She was very articulate, educated, accomplished. Her encounters with mysterium tremendum fascinans had not come at the cost of her sanity. I don’t know what will convince me of the truth of such experiences other than a deep personal trust in an individual’s intellect and judgment. But I am always aware that someone like N. could be sitting in my office. And I’m always aware that the next time I’m on the inpatient unit, I could encounter someone like Saville-Smith. And I want to do better. I do not want to be the poor guy who has no idea.

Saville-Smith asks how it is possible to persuade a psychiatrist that one is sane in the midst of an overwhelming experience of god. I don’t think such persuasion is possible in most cases, but I also think that such persuasion is unnecessary. Psychiatry should be far more attentive to the meaning of acute religious experiences, even, and perhaps especially, when they coincide with manic and psychotic experiences. There is no reason to demand adherence to a disenchanted secular worldview as proof of insight. The field should work to pay attention to the “set” and “setting” of psychosis, minimize coercion and maximize dignity, and allow, as much as possible, for the spiritual dimension of psychosis. And it should remain available and needs to remain available (imperfect, blunt, fallible, but available; sorry Richard) for moments of grave impairment and disability.

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• In an unexpected turn of events, I have been selected by the American Psychiatric Association for the 2026 Distinguished Service Award for services to American psychiatry. I am surprised, like many of you may be, but also delighted and honored. I am grateful to the folks who believed in me enough to nominate me and support my selection. Is my selection any reflection of the current mood of American psychiatry? I am not sure (probably not), but one can always hope! Since I’m receiving the award, I’m planning to be at the Convocation ceremony at the APA annual meeting in San Francisco in May.

• The International Network for Philosophy and Psychiatry (INPP) is holding its next international conference on the theme of “What can Philosophy do for Mental Health Care?” on October 8 - 9, 2026, in Nijmegen, the Netherlands. I am one of the keynote speakers (along with Sofia Jeppsson and Rosa Ritunnano). It is building up to be an exciting event. Consider attending!

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• Sigal Samuel interviewed me for Vox on various considerations that come up around staying on antidepressants versus going off them. You can see the Q&A here.

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If you follow developments in psychiatric classification, you’ve likely heard of the Hierarchical Taxonomy of Psychopathology, or HiTOP. It’s one of the most ambitious attempts in recent decades to redescribe and reorganize mental health problems, moving away from the clinically familiar syndromic categories of the DSM and ICD toward a statistically driven framework that generates symptom profiles for patients along an array of dimensions. But what are the theoretical assumptions that underpin this project? What philosophical commitments does it carry, even when it presents itself as guided by data?

In a newly published paper led by me and co-authored with folks from the HiTOP Revisions Workgroup, we take on these questions directly. “Examining the Foundational Assumptions of the Hierarchical Taxonomy of Psychopathology” in Philosophy, Psychiatry, & Psychology offers a structured overview of the framework’s conceptual and philosophical underpinnings, while being mindful that these are matters of active debate, and there is expected to be disagreement among the consortium on many of these issues.

I have to say, working on this paper was an intellectual treat for me, and conversations and exchanges among the authors forced me to consider these issues with a conceptual rigor that deepened my own understanding of psychiatric classification in the process. I could not have asked for a better team of authors. It was a privilege for me to collaborate with people whose work I’ve previously read and admired, such as Aidan Wright, Miri Forbes, Eiko Fried, Chris Hopwood, and Bob Krueger. Colin DeYoung in the senior author role was a wonderful intellectual guide.

In this blog post, I want to offer an overview of the discussion and walk through the key themes of the paper in a manner that also touches on their significance for anyone interested in questions of classification and psychopathology. I also hope this post serves as encouragement for you to read the full article!

I do want to note that this paper is not an introduction to HiTOP. If you know almost nothing about HiTOP, you may want to start with a primer, e.g. this 2019 clinical introduction to HiTOP, this 2021 scientific overview of HiTOP, or my 2024 paper on diagnostic pluralism.

This paper was published as a “Philosophical Case Conference,” which means it is accompanied by 5 commentaries from authors across psychiatry, psychology, and philosophy (thank you Dost Öngür, Sam Fellowes, Brian Hood, Miriam Solomon, and Nick Zautra), and our response. The commentaries have also been published online ahead of print, but our response is still pending publication, so I will have more to say about the commentaries later.

Why HiTOP exists

To understand HiTOP, you first have to understand what it’s reacting to. Traditional diagnostic systems (that is, the DSM and ICD) organize mental illness into distinct categories: you either have “major depressive disorder” or you don’t; you either meet criteria for “generalized anxiety disorder” or you don’t. These systems were built on clinical tradition, expert consensus, and assume that mental disorders are best described as polythetic categories (meaning a checklist of criteria, a certain number of which must be met and various combinations are possible), regardless of how statistically coherent these categories are.

The trouble is that decades of research have exposed serious problems with this approach. Comorbidity is rampant. Patients routinely meet criteria for multiple disorders at once, far more than expected by chance, which raises the issue of whether these are truly distinct conditions or we are just slicing complex symptom profiles into clinically convenient but etiologically misleading pieces. Due to lumping together of variable presentations within any single diagnosis, patients can look strikingly different from one another (the heterogeneity problem). And the boundaries between “disorder” and “no disorder” are often arbitrary, with no clear natural threshold separating the two in the diagnostic manuals.

HiTOP consortium was launched in 2015 to address these shortcomings. It proposes organizing psychopathology as a hierarchy of dimensions, ranging from narrow symptom components and traits at the base to broad spectra (such as internalizing, externalizing, and thought disorder) at higher levels, all the way up to a general psychopathology factor (the “p factor”) at the top. The structure is derived from patterns of statistical covariation (essentially, which symptoms tend to go together in statistical analyses) rather than from clinical observation or theoretical tradition.

What does the HiTOP model actually represent?

This is the well-known (I hope) figure representing the current version of HiTOP:

One of the first things our paper clarifies is what the official HiTOP model is and isn’t. It is not a fitted statistical model or a particular instance of it. Rather, the visual diagram is best understood as a heuristic, an expository scaffolding that represents patterns of covariation hierarchically without specifying exact mathematical values. It synthesizes a great deal of evidence from factor-analytic and related statistical studies, but the model itself is a conceptual summary.

The HiTOP model is fundamentally descriptive. It tells us how symptoms and traits cluster together, not why (at least for now). It is not etiologically guided; it does not claim to reveal the causes or mechanisms behind any particular cluster of symptoms. The hope is that getting the description right will ultimately facilitate better causal research, much as Linnaeus’s taxonomy of organisms provided a descriptive foundation that eventually paved the way for evolutionary theory. But that’s an aspiration, not a claim already realized.

The consortium relies primarily on quantitative evidence, with the stated aim of minimizing decisions driven by special interests, ideological traditions, or sociopolitical influences. The model also acknowledges uncertainty: constructs with limited evidence are flagged as preliminary, and the revision process is designed to be systematic and transparent. And as our paper emphasizes, “data-driven” does not mean “free from assumptions and values.”

HiTOP is not “atheoretical”

HiTOP has been described as a “quantitative nosology based on consensus of evidence,” which can easily be read as a claim that it is purely empirical or atheoretical. Our paper pushes back against this reading. The reality is that HiTOP relies on several significant assumptions.

The most obvious are the commitments to dimensionality and hierarchical organization: the ideas that psychopathology is best understood as continuously distributed in a population and that this variation is best organized in a nested, hierarchical structure.

The dimensionality assumption is based on taxometric evidence, hence, it is not an assumption in a deeper, foundational sense. If taxometric and other scientific evidence points out the existence of discrete categories, HiTOP will follow that evidence.

Three different meanings of “dimension” have been described in psychopathology literature. The first simply refers to continuous variables where indicators can be summed or averaged rather than used categorically, such as counting depression symptoms on a continuous scale (eg, Patient Health Questionnaire-9) rather than making a binary diagnosis. The second, more restrictive meaning requires that these indicators cohere statistically, fitting a unidimensional factor model where a single superordinate construct explains their covariance. The third and most restrictive meaning adds the requirement that the dimension be empirically distinguishable from related constructs within a multidimensional framework. HiTOP uses “dimensions” in this third most restrictive meaning, exemplifying a statistically coherent, multidimensional framework.

The hierarchy assumption is more fundamental. Although hierarchical models can statistically fit the data well, many alternative statistical models could potentially fit the same data. The assumption that clinical symptom clusters should be arranged within a hierarchy is untestable using only statistical data on covariance, but can potentially be supported with other forms of scientific evidence, such as associations with biomarkers at different levels of the hierarchy.

Beyond these two explicit assumptions, there are also theoretical considerations that are implicit. The reliance on factor analysis brings its own set of mathematical assumptions and biases. The historical decisions about what counts as “psychopathology” and what gets measured in the instruments whose data feed into the model shape the model’s scope in ways that aren’t always made visible.

From the perspective of philosophy of science, the idea that any scientific project could be entirely value-free or assumption-free is not tenable. All observation is theory-laden; all science operates within paradigms of shared assumptions, methods, and standards. HiTOP is no exception. Our paper draws on work in philosophy of science to frame scientific objectivity not as a “view from nowhere” that perfectly mirrors an independent reality, but as something achieved through transparent methods, systematic evidence evaluation, and being open to critiques. HiTOP’s commitment to quantitative rigor and transparent procedures is itself a methodological choice, one molded by the judgment that earlier diagnostic systems relied too heavily on clinical consensus and pragmatic considerations at the expense of statistical coherence.

What counts as “psychopathology”?

What does HiTOP mean by “psychopathology”? The answer, our paper notes, is that HiTOP does not have an official working definition. The consortium has been focused on structural organization — on mapping the covariance of symptoms — rather than on defining what makes something psychopathological in the first place. In practice, HiTOP has implicitly assumed that psychopathology is whatever clinicians and researchers have studied under that label over the course of history.

Concepts of mental disorder and psychopathology are heterogeneous and historically contingent. The domain of what counts as a mental disorder has expanded considerably over time, and different philosophical accounts of mental disorder, e.g. Wakefield’s harmful dysfunction analysis, Boorse’s biostatistical theory, DSM’s folk-psychological approach, cybernetic accounts, etc., would draw the boundaries of pathology in different places and different ways. HiTOP’s core model describes patterns of symptom covariation, but covariation alone doesn’t tell us whether something is functional or dysfunctional, a manifestation of difference or disorder, adaptive or maladaptive.

In other words, HiTOP addresses only some components of the broader concept of mental disorder (which includes components like clinical significance, dysfunction, and harm). It maps the terrain of symptom co-occurrence but leaves open the questions of clinical significance, dysfunction, and harm, the very questions that any complete account of psychopathology has to eventually confront. The silence is a deliberate feature at the moment, and it means that HiTOP’s descriptive model will eventually need to be integrated with a theoretical account of what makes certain symptom patterns pathological.

Although HiTOP as a statistically informed model is agnostic regarding notions of psychopathology, it can be a source of inspiration and support for theories of psychopathology. For instance, the HiTOP model suggests a continuity between dimensions of personality (the Big Five) and dimensions of psychopathology (HiTOP spectra), and this alignment provides an opportunity for theories of psychopathology seeking to explain them in terms of shared mechanisms. For an example of such a theory of psychopathology, see the cybernetic theory of psychopathology by DeYoung and Krueger.

Making sense of latent variables

Latent variables are statistical constructs that emerge from factor analysis (and related statistical techniques) and form the backbone of HiTOP’s evidence base.

Psychologists sometimes talk about latent variables as if they are hidden entities lurking inside the person, “causing” the symptoms we observe. But mathematically, a latent variable is simply a representation of the shared variance among a set of observed indicators. It is a statistical summary, not a causal account. The arrows in a factor model diagram represent statistical associations, not causal pathways, much like regression coefficients describe associations without necessitating causation.

HiTOP aims to be agnostic about the ontological status of its latent variables. It does not assume that a factor like “internalizing” represents a single hidden cause or causal essence. The observed covariation among symptoms could arise from common causes, from mutual reinforcement among symptoms (mutualism, aka network model, is when symptoms feed into each other, e.g., worry leads to insomnia leads to fatigue leads to more worry), or from some combination of both. HiTOP’s latent variables can be understood as dispositions, tendencies to act or behave in certain ways, that don’t come packaged with a specific causal story.

In the “common cause” model, symptoms of, say, depression co-occur because they’re all driven by some underlying depressive liability. In a mutualist or network model, they co-occur because they causally influence each other. The covariation is real either way, and a factor model will capture it as latent variables.

This mathematical interpretation of latent variables also sidesteps the traditional realism/anti-realism debate in the philosophy of science in our view. If no unobservable causal entity is being posited, if latent variables are understood purely as representations of covariation patterns, then the question of whether they “really exist” as hidden causes doesn’t come up in the usual way. Our paper suggests, tentatively, that this stance may have affinities with structural realism: the view that what successful scientific theories capture about reality is mathematical structure and relational properties rather than unobservable entities.

Dimensions, categories, and thresholds

The dimensionality assumption is supported by large meta-analyses of taxometric research finding that dimensional models fit the evidence far better than categorical models. But dimensionality at the population level doesn’t rule out possible discontinuities at the individual level. Phase transitions between states of health and illness, for instance, are theoretically compatible with a continuous distribution of symptoms between individuals.

Then there’s the practical question of what to do about diagnostic thresholds. Clinical practice needs categories: we have to decide who receives treatment, who qualifies for services, who is counted in prevalence estimates. HiTOP doesn’t reject the use of categories. Dimensional scores can be converted to severity categories using standardized T-scores along any of HiTOP dimensions, with suggested benchmarks for mild, moderate, and severe presentations. Unlike DSM’s fixed thresholds at the syndromic level, these cut-points are intended to be flexible, context-dependent, and usable at any level of hierarchy.

One important finding our paper highlights is that the relationship between symptom severity and impairment across most domains of psychopathology appears to be linear so far, without obvious inflection points. Unlike, say, blood pressure or HbA1c, where exponential increases in health risk at certain thresholds help justify specific diagnostic cut-points. In the absence of such natural thresholds, the choice of where to draw the diagnostic line becomes, inescapably, a decision that reflects social and practical attitudes, allocation of available resources, and judgments about how to handle access to care and the risks of over-diagnosis and over-treatment.

How does HiTOP handle validity?

Diagnostic validity, the question of whether diagnostic constructs correspond to something real and meaningful, has been a central concern in psychiatry since Robins and Guze’s influential 1970 paper proposing criteria for validating psychiatric diagnoses and the subsequent expansion and refinement of this approach by Ken Kendler. The DSM tradition uses a set of external validators (family studies, biological markers, treatment response, and so on) to assess whether categories are picking out genuine syndromes.

HiTOP follows what has been described by Nick Zautra as a “structure-first psychometric validity” approach. The first and most critical step is structural validity: does the construct accurately capture the patterns of covariation observed in symptom data? This is evaluated through factor-analytic methods and related methods such as principal component analysis. Only after structural validity is established does HiTOP turn to external validators (the same kinds of criteria used in the DSM tradition) to assess whether the constructs relate meaningfully to things like family aggregation, biological markers, treatment response, and course of illness.

This is a notable point of convergence: despite HiTOP’s criticism of DSM-style categories, it borrows the DSM’s validators for evaluating external validity. It also continues to rely on expert curation but the focus of expert curation is on synthesis and interpretation of psychometric evidence as primary. Although the revision process prioritizes systematic evaluation of quantitative evidence by transparent criteria, decisions about what to include and how to interpret the evidence ultimately still depend on committees of specialists. The need for human judgment in synthesizing and interpreting evidence remains, similar to how it is across medicine and science.

Values, diversity, and the limits of “objectivity”

HiTOP is, like all science, not “value free.” The paper devotes considerable attention to the role of values in HiTOP, both epistemic values (like empirical adequacy, parsimony, internal consistency) and non-epistemic values (like equity, clinical utility, inclusivity). Epistemic values are of primary importance in the development of the HiTOP model and take precedence over non-epistemic values whenever there’s competition, but non-epistemic values are also present and play a role.

The consortium has explicitly committed to ensuring that the model has clinical utility and that it is applicable to diverse, underrepresented, and epistemically marginalized populations. This consortium has a workgroup devoted to this issue, and the paper discusses concrete examples of how sociocultural context can affect the meaning and measurement of symptoms. Addressing this requires methodological adjustments as well as the inclusion of diverse perspectives in the model’s development. The discussion on this issue aligns with philosophical approaches of standpoint epistemology and methodological objectivity, along the lines that perspectives from marginalized groups and the diversity of the scientific community can reveal biases and assumptions that may otherwise be invisible.

Conclusion

HiTOP is an important step forward in the scientific classification of mental health problems. A concerted and sustained effort to establish a descriptive framework for psychopathology, rooted in quantitative evidence. But, like any scientific project, it has theoretical assumptions, it has guiding values, and it exists in a certain historical context. It has a context of discovery and a context of justification.

Our paper elaborates on these assumptions and choices, allowing clinicians and researchers to better understand, investigate, and critique HiTOP’s approach. HiTOP on its own is limited in what it can accomplish; it is one approach to psychopathology among many, and diagnostic pluralism is currently both a clinical and scientific necessity. We hope it encourages more philosophical discussion of the framework, both inside and outside the consortium.

The article pdf is available online ahead of print in Philosophy, Psychiatry, & Psychology. As always, I welcome your thoughts and reactions.

P.S. This is my personal summary of the article, prepared with considerably less caution than what went into crafting the original, which reflects the collective, iterative effort and agreement of all the authors. I have tried to be faithful to the paper in this post, but if there are any significant discrepancies in the language used here and the language used in the published article, the journal article obviously takes precedence as the authoritative version.

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My article ‘The Future DSM: Bold Redesign, Lingering Blind Spots’ appeared as the March 2026 cover story in Psychiatric Times. In it, I examine the reports from the Future DSM Strategic Committee and its subcommittees, recently published as a series of papers in the American Journal of Psychiatry. I’m republishing the piece here for readers of Psychiatry at the Margins.

The American Psychiatric Association (APA) has established a road map for updating its official diagnostic manual. In a series of articles published in the American Journal of Psychiatry, the Future DSM Strategic Committee has presented details of its progress and strategic priorities since beginning work in May 2024 [1-5]. Their publication represents the most comprehensive rethinking of psychiatric classification since DSM-III in 1980. In this article, I offer an overview of the proposed changes, and following that, I will offer some personal commentary and make a brief case for some suggestions of my own that I hope the readers will find illuminating and that the Future DSM Strategic Committee will take into consideration.

The overview paper by the committee, chaired by Maria A. Oquendo, MD, PhD, starts off by identifying multiple critiques of existing DSM editions that the future DSM seeks to address [1]. First is the manual’s atheoretical stance regarding causal factors. DSM-III emerged when “there were several conflicting hypotheses about causal mechanisms of mental illness, with limited empirical data and divergent views.” The atheoretical approach allowed psychiatry to sidestep these debates and focus on describing disorders with reliable criteria.

The new committee grapples with whether this agnosticism remains justified. They acknowledge that although there is broad agreement that disorders arise from the interplay of neurophysiological, developmental, experiential, sociocultural, and environmental factors, scientific understanding of how they interact is still premature. Nonetheless, they believe it is time to move from an atheoretical position toward one that explicitly acknowledges this multifactorial causal interplay. The DSM committee also recognizes that DSM constructs are not natural kinds, but the clinical and scientific work of classification can still proceed meaningfully by adopting a pragmatic stance. We cannot wait for perfect knowledge of valid boundaries before providing diagnostic tools for clinical practice.

Another fundamental issue concerns DSM’s categorical structure, where disorders are either present or absent. The committee notes that “many clinical presentations manifest symptoms that occur along a spectrum of severity and that some symptoms, such as anxiety and anhedonia, are transdiagnostic.” However, they point to a practical reality in support of categorical diagnoses: “Clinical decision-making involves categorical choices among a set of finite options.” DSM-5 attempted to address the presence of transdiagnostic symptoms through crosscutting dimensional symptom measures, yet these tools were relegated to section III, “often deemed by readers to be optional,” limiting their impact. The future DSM wants to address this issue in a better way.

The committee has organized its work through 4 subcommittees, as follows:

• Structure and Dimensions

• Functioning and Quality of Life

• Biomarkers and Biological Factors

• Socioeconomic, Cultural, and Environmental Determinants of Mental Health

The committee plans to integrate “people with lived experience as experts” alongside traditional clinical and research expertise. They are considering moving “away from theoretical agnosticism and embracing biology and environment and their interactions as key determinants of mental disorders.”

The committee envisions DSM evolving continuously rather than undergoing periodic major revisions. They propose regular cycles of solicited improvements with transparent review criteria, arguing for incorporating progress as it happens rather than waiting for comprehensive overhauls. The goal is to transform DSM into an online dynamic manual that keeps pace with advancing knowledge. Even the manual’s name may change from Diagnostic and Statistical Manual of Mental Disorders to Diagnostic and Scientific Manual of Mental Disorders, recognizing that the goal of the manual is “no longer simply to provide for the collection of psychiatric hospital and census statistics.”

The 4-Domain Model

The Structure and Dimensions Subcommittee, led by Dost Öngür, MD, PhD, proposes a major redesign, introducing a 4-domain model [2]. This is intended to address the problem that although DSM is near universally used for communication, its categorical structure poorly reflects clinical reality. “Only a minority of patients present with a classic form of one disorder as described in DSM; most instead present with a mixture of problems along dimensions such as mood, anxiety, psychosis, addiction, and so on.”

The model consists of 4 interconnected domains:

• Domain I: Contextual factors. This includes socioeconomic, cultural, and environmental determinants; developmental factors; medical comorbidities; functioning levels; and patient-reported quality of life (QOL). These factors, currently relegated to background information, would become central to diagnosis.

• Domain II: Biomarkers and biological factors. This represents the first systematic inclusion of biological measures in DSM classification, encompassing “all factors related to the biology of brain and body measured using any modality—including neuroimaging, genetics, metabolomics, cognition, digital phenotypes.” Although validated biomarkers remain rare, the structure would be ready “to accept new, rigorously studied biomarkers as they become available.”

• Domain III: Diagnoses. This introduces variable specificity. Clinicians could diagnose at a broad “major category” level (such as psychosis or trauma-related disorders) when information is limited or provide a “specific diagnosis with specifier(s)” when sufficient information exists.

• Domain IV: Transdiagnostic features. This allows clinicians to document common problems that transcend diagnostic boundaries, such as anxiety or cognitive difficulties, even when these do not warrant separate diagnoses.

Öngür et al. provide a concrete example: a patient with prolonged grief disorder, posttraumatic stress disorder with dissociative symptoms, and alcohol use disorder. The evaluation would document contextual factors (low income, threat of job loss, history of childhood physical abuse), medical comorbidity (irritable bowel syndrome), biological factors (amygdala hyperreactivity on brain imaging), all 3 diagnoses with severity ratings, and transdiagnostic anxiety.

Integrating Biological Measures

The Biomarkers and Biological Factors Subcommittee, led by Bruce Cuthbert, PhD, and Anissa Abi-Dargham, MD, faces a daunting challenge: how to incorporate biological measures into a manual that has remained largely based on symptoms since 1980. With the recent exception of Alzheimer disease, “no biomarkers have had the needed specificity and sensitivity for use in routine psychiatric diagnosis.”

The report highlights 4 areas showing potential:

• Psychosis biotypes: The Bipolar-Schizophrenia Network for Intermediate Phenotypes consortium identified 3 distinct biotypes among individuals with psychosis using a battery of tests including electroencephalogram (EEG), brain imaging, eye tracking, and cognitive testing. These biotypes cut across traditional diagnoses. One finding suggests patients with low “intrinsic EEG activity” may respond better to clozapine, pending validation.

• Genetic risk scores: Polygenic risk scores aggregate thousands of genetic variants to calculate disease risk. For schizophrenia, individuals in the top 10% have 2.3 times higher odds of diagnosis. However, these scores “still have limited predictive power, may suffer from population bias, and may not add much more than already established risk factors, such as family history.”

• Inflammatory markers: C-reactive protein (CRP), a readily available blood test, may identify an “inflammatory subtype” of depression. Approximately 27% of patients with depression show elevated CRP and respond better to certain antidepressants than selective serotonin reuptake inhibitors (SSRIs).

• Brain circuitry: Findings from functional MRI studies identified a “cognitive biotype” representing 25% of patients with depression who show reduced activation in cognitive control regions. These patients “do not respond well to standard SSRI treatment” but benefit from cognitive behavior therapy or transcranial magnetic stimulation.

The next phase for the subcommittee involves defining criteria for listing candidate biomarkers “so that the process is structured, rigorous, and guided by robust science,” with attention to cultural and ethnic considerations.

Functioning and Quality of Life

The Functioning and Quality of Life Subcommittee argues that psychiatric diagnosis remains incomplete without systematic assessment of how patients function in daily life and perceive their well-being. Mental illnesses represent “8 of the top 25 causes of years lived with disability worldwide,” yet DSM has treated functional assessment inconsistently.

The Global Assessment of Functioning scale conflated symptoms with functioning: A patient could score in the same range due to either “serious symptoms” or “serious impairment,” creating ambiguity. DSM-5 recommended the World Health Organization Disability Assessment Schedule (WHODAS 2.0), but placement in section III “sent an unintended message to the field that the WHODAS 2.0 was not ready for routine use.”

The subcommittee concludes that functioning and QOL are related yet distinct domains requiring separate assessment. Functioning refers to objective capacity to perform activities and fulfill roles, such as going to work, maintaining relationships, managing daily tasks. QOL adds the patient’s subjective perspective on their well-being and life satisfaction, defined by WHO as “one’s perceptions of their position in life, contextualized by the culture and value systems in which they live.” Two patients might have similar functional impairments but dramatically different QOL ratings, depending on their values, expectations, and life circumstances.

The subcommittee reviewed numerous assessment tools but found that “no single instrument met all desirable characteristics.” The challenge is balancing thoroughness with feasibility. Even brief versions of recommended scales, the 12-item WHODAS-2.0 for functioning and the 16-item Quality of Life Enjoyment and Satisfaction Questionnaire for QOL, “may still prove infeasible in many clinical and research settings.”

The committee’s central recommendation is unambiguous: Functioning and QOL “must be included in the essential elements of DSM and not be relegated to the ‘Emerging Measures and Models’ section.” This marks a shift from treating these domains as optional supplements to recognizing them as core components of psychiatric diagnosis.

Integrating Social Context

The Socioeconomic, Cultural, and Environmental Determinants of Mental Health Subcommittee, led by Milton Wainberg, MD, proposes systematic integration of contextual factors historically treated as supplementary. These conditions span 5 domains: demographic factors, economic stability, neighborhood and built environment, environmental events, and social/cultural context.

The subcommittee outlines 3 potential approaches: incorporating screening into routine intake, embedding factors into clinical decision trees where “high burden triggers enhanced case management,” and developing “risk-adjusted diagnostic models” where patients meeting the same criteria but facing intersecting stressors warrant more intensive intervention.

The authors acknowledge barriers: Many systems “do not routinely collect” such data, resource shortages are common, and there is “risk of tokenism, where simple checklists without further evaluation make diversity efforts symbolic rather than structural.”

Summary of Proposed Changes to the Future DSM

I. Structural and conceptual framework changes

• Transition to a living document with updates at briefer intervals

• Possibly rename to Diagnostic and Scientific Manual to emphasize evolution away from statistical recordkeeping origins

• Soften theoretical agnosticism to explicitly embrace biology, environment, and their interactions

• With the new diagnostic construction model, organize assessments and diagnostic formulations into 4 domains: contextual factors, biomarkers, diagnoses, and transdiagnostic features

II. Integration of biomarkers and biological factors

• Include candidate biomarkers derived from a wide range of methods, including neuroimaging, genetics, inflammatory markers, electrophysiology, and digital phenotypes

• Use biomarkers to identify biotypes/subtypes for treatment selection (eg, inflammatory subtype of depression)

III. Enhancement of functioning and QOL

• Make functioning and QOL essential elements of psychiatric diagnosis

• Use brief, feasible instruments for clinical use

IV. Socioeconomic, cultural, and environmental determinants (SCE-DOH)

• Move beyond V/Z codes to systematically integrate SCE-DOH into psychiatric formulations

• Implement risk-adjusted diagnostic models that account for social stressors when estimating severity and treatment needs

V. Diagnostic specification and dimensionality

• Allow variable specificity levels from major category (eg, psychosis) to specific diagnosis (eg, schizophrenia)

• Integrate transdiagnostic dimensions to better reflect comorbidity and symptom heterogeneity

VI. Procedural and stakeholder changes

• Include people with lived experience, global perspectives, and Indigenous epistemologies as experts in the revision process

Personal Reflections and Suggestions

Diagnostic Formulation Needs to Be Linked to Treatment

The future DSM is moving toward diagnostic formulation. This is a welcome change and a nod back to DSM-III and DSM-IV’s multiaxial diagnosis. In my opinion, for this to be meaningful, along with the atheoretical stance, DSM also needs to break its silence on treatment implications. Historically, DSM has restricted itself to diagnosis, but for diagnostic formulations to be useful and implemented by clinicians, DSM must explain how different aspects of the model will guide specific treatment. The manual does not need to become a collection of treatment guidelines, but where diagnostic distinctions have treatment implications, this needs acknowledgment and elaboration.

The Missing Domain: Psychological Factors and Personality Traits

It is notable that the proposed structure lacks a dedicated domain for psychological functioning. This seems like an inexcusable oversight. Classification systems serve to inform probabilistic reasoning about presentation, trajectory, and therapeutic response. Without designated space to document psychological capacities and patterns, clinical formulations will inadequately capture person-level psychological characteristics that influence prognosis and treatment planning.

By psychological factors here I am referring to measurable, reliable, relatively enduring dispositions and clinically meaningful psychological capacities that provide information beyond what diagnosis and symptom dimensions convey. These include personality trait profiles (Big 5 personality traits such as neuroticism, agreeableness), patterns of attachment, internalized relational models, reflective functioning abilities, metacognitive beliefs, recurrent cognitive distortions, defense mechanisms, and psychological resources supporting resilience.

Such constructs routinely inform practicing clinicians’ decisions about psychotherapy customization, patient-modality matching, treatment pacing and emphasis, potential for therapeutic relationship difficulties, interpretation of treatment nonresponse, and selection among skills-focused, insight-oriented, family-involved, or integrated approaches. These aspects are particularly emphasized in the Psychodynamic Diagnostic Manual (PDM). If DSM neglects them, it will lose ground among psychotherapy clinicians.

The solution is fortunately straightforward: Incorporate “Psychological Factors” as an explicitly named domain, supported by concise implementation guidance and validated brief assessment instruments.

DSM’s Notion of Dimensionality Is Underdeveloped

Hopwood et al. (2023) have described 3 different meanings of dimension in psychopathology literature [6]. The first simply refers to continuous variables where indicators can be summed or averaged rather than used categorically, such as counting depression symptoms on a continuous scale (eg, Patient Health Questionnaire-9) rather than making a binary diagnosis. The second, more restrictive meaning requires that these indicators cohere statistically, fitting a unidimensional factor model where a single superordinate construct explains their covariance. The third and most restrictive meaning adds the requirement that the dimension be empirically distinguishable from related constructs within a multidimensional framework. Hierarchical Taxonomy of Psychopathology (HiTOP) exemplifies such a statistically coherent, multidimensional framework. The Distress subfactor in the Internalizing spectrum, for instance, is not only continuous and homogeneous but also demonstrably distinct from the Fear subfactor.

These conceptual distinctions regarding dimensionality matter because debates about dimensional vs categorical diagnosis become muddled when authors use the same term to mean different things. Some may consider simple continuous measures to be sufficient for dimensionality (what DSM is currently doing), but psychiatrists and psychologists interested in grounding classification in structural evidence envision psychometrically validated constructs embedded in comprehensive structural models as appropriately dimensional (the HiTOP approach).

Major Categories Should Not Become the New “Unspecified”

Öngür et al. note that for the major category level, such as depression or psychosis, they “anticipate that currently available diagnostic codes, such as unspecified depressive disorder, unspecified schizophrenia spectrum, and other psychotic disorder, will be used in combination with the severity measure.” [2]

Prior DSM editions have delegated unspecified categories to almost second-class status. Large swaths of psychopathology simply are not named in the DSM, either because presentations are subthreshold or because no corresponding category exists. This is why clinicians use unspecified categories so frequently. The more I practice, the more I believe specified DSM criteria are rather conservative. The diagnostic manual struggles to keep up with the magnitude of clinically significant distress that exists.

The proposal to use major categories is a step forward in officially recognizing the large domain of clinically relevant presentations. Although reliance on unspecified International Classification of Diseases (ICD) codes makes practical sense, I strongly recommend that the future DSM not use the word unspecified in the names of major categories to ensure that these major categories are not deprioritized in the same way as unspecified categories have been in DSM-5 (and the way “not otherwise specified” categories were in DSM-III and DSM-IV before that).

The Definition of Disorder (and the Proposed Name Change)

DSM’s reliance on the term “disorder” and its sloppy formal definition in the manual have led to a lot of unnecessary conceptual confusion. What is the difference between “mental health problems” that merit clinical treatment due to distress and impairment and “disorders” as classified in the DSM? By the official DSM definition, the distinction involves psychological or biological “dysfunction.” Dysfunction is not defined further, but diagnostic criteria make clear the notion is commonsensical and folk-psychological: Something is “not doing what it is supposed to do” based on everyday norms of what is expected and typical. [7]

Two strategies are possible here:

1. Make the DSM meaning of dysfunction explicit and clear, differentiating it from other notions of dysfunction (such as failure of evolved mechanisms or biostatistical deviation from species-typical norms). This will help address the popular misconception that the DSM assumes the existence of pathological processes inside the individual. But it raises the additional question: Why should a scientific manual design its scope around such a commonsensical, folk-psychological notion?

2. Abandon the commitment to a folk-psychological notion of dysfunction, avoid references to dysfunction in the formal definition, and recognize the manual’s interest in a wide range of experiential and behavioral states of distress, impairment, and harm to others which come to clinical attention, warrant management, and have been characterized with some degree of reliability and rigor (meeting DSM’s evidential standards) by the scientific community.

If we go the second route, a more accurate title for the book would be Diagnostic and Statistical/Scientific Manual of Mental Disorders and Related Mental Health Problems, akin to ICD’s full name: International Statistical Classification of Diseases and Related Health Problems.

Indicate the Degree of Empirical Validation for Specific Diagnoses

Currently, browsing through DSM gives the false impression that all conditions have equal clinical and scientific legitimacy. Disinhibited social engagement disorder appears to have the same status as posttraumatic stress disorder. It is like a house of mirrors that flattens everything to the same size [8]. Validity and utility are not equally distributed among DSM diagnoses. Schizophrenia and disruptive mood dysregulation disorder are continents apart in terms of validation. The future DSM needs to communicate this meaningfully in some manner. One way to approach this could be to synthesize the evidence of interrater reliability, predictive validity, and diagnostic stability for each specified diagnosis.

Explain Why Diagnostic Thresholds Are What They Are

Unlike dimensional diagnoses in general medicine (such as hypertension thresholds that optimize cardiovascular risk management), DSM thresholds do not seem to clearly optimize anything. Some thresholds seem semi-arbitrary by design. Spitzer famously said 5 criteria for depression were chosen as a threshold because “4 seemed like not enough and 6 seemed like too much.” Others are based on nonempirical considerations: Prolonged grief’s 12-month threshold was reportedly set more conservatively than research supported to avoid public backlash.

There is nothing wrong with using best guesses or expert opinion as preliminary thresholds, but we cannot treat these thresholds as sacred or conduct research programs assuming they capture meaningful etiological differences. The future DSM needs transparency about what evidence, if any, supports particular thresholds, and if the threshold can be set differently to optimize different clinical goals, that information should be disclosed.

Include HiTOP in the DSM Appendix

DSM categories have advantages for clinical communication, but they rest on semi-arbitrary thresholds, produce heavy comorbidity, and lump heterogeneous presentations together. HiTOP offers a dimensional alternative that starts from psychometric data rather than historical categories, with research showing advantages at the spectrum level, with better stability, cleaner psychometric structure, and stronger validator links.

The DSM appendix, where the Alternative Model for Personality Disorders currently lives, would be a reasonable place for inclusion of HiTOP. This would legitimize psychometric approaches to classification and provide a bridge between categorical and dimensional models.

DSM, including the future DSM, should not be seen as the one true classification but as one historically contingent, fallible effort. The clinical and scientific reality is that we now exist in a landscape of nosological pluralism, where traditional DSM serves as a “good enough” shared language that coexists with alternatives such as HiTOP and PDM. A plurality of legitimate and useful classifications is already here. It is heartening to see Oquendo et al. write, “Applied with all due epistemic humility, DSM can continue to play an important role in clinical care and research.” I hope that the future DSM can overcome the epistemic arrogance of its predecessors and show us that the manual has philosophically matured.

Dr. Aftab is a psychiatrist in Cleveland, Ohio, and clinical associate professor of psychiatry at Case Western Reserve University School of Medicine. He is the editor of “Conversations in Critical Psychiatry” (Oxford University Press, 2024) and writes online at “Psychiatry at the Margins.”

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You Aren't in the DSM

“It may be readily surmised that where the best thinkers have failed to produce an unexceptionable classification, the failure must be due to some inherent difficulty of the subject…

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References

1. Oquendo MA, Abi-Dargham A, Alpert JE, et al. Initial strategy for the future of DSM. Am J Psychiatry. 2026;appiajp20250878. Online ahead of print.

2. Öngür D, Abi-Dargham A, Clarke DE, et al. The future of DSM: a report from the Structure and Dimensions Subcommittee. Am J Psychiatry. 2026;appiajp20250876. Online ahead of print.

3. Cuthbert B, Ajilore O, Alpert JE, et al. The future of DSM: role of candidate biomarkers and biological factors. Am J Psychiatry. 2026;appiajp20250877. Online ahead of print.

4. Drexler K, Alpert JE, Benton TD, et al. The future of DSM: are functioning and quality of life essential elements of a complete psychiatric diagnosis? Am J Psychiatry. 2026;appiajp20250874. Online ahead of print.

5. Wainberg ML, Alpert JE, Benton TD, et al. The future of DSM: a strategic vision for incorporating socioeconomic, cultural, and environmental determinants and intersectionality. Am J Psychiatry. 2026:appiajp20250875. Online ahead of print.

6. Hopwood CJ, Morey LC, Markon KE. What is a psychopathology dimension? Clin Psychol Rev. 2023;106:102356.

7. Aftab A. Weaving conceptual and empirical work in psychiatry: Kenneth S. Kendler, MD. Psychiatric Times. May 26, 2020. https://www.psychiatrictimes.com/view/weaving-conceptual-and-empirical-work-psychiatry-kenneth-s-kendler-md

8. Aftab A. 6 suggestions for DSM-6. Psychiatry at the Margins. November 20, 2025. Accessed February 10, 2026. https://www.psychiatrymargins.com/p/6-suggestions-for-dsm-6

“Psychopathology: Persistent failure to move toward one’s psychological goals due to failure to generate effective new goals, interpretations, or strategies when existing ones prove unsuccessful.”

Colin G. DeYoung & Robert F. Krueger (2018), A Cybernetic Theory of Psychopathology

“Some clinicians might be concerned that, if they applied the harmful dysfunction concept, they may find that they are treating many of their patients or clients for nondisorders. Actually, the DSMs have always recognized that the mental health profession often can be helpful to individuals with “problems in living” that are not disorders.”

Robert L. Spitzer (1997), Brief Comments From a Psychiatric Nosologist Weary From His Own Attempts to Define Mental Disorder

In clinical practice, I routinely encounter people whose cognitive, emotional, or temperamental capacities are being overwhelmed by what their lives are demanding of them. It is a collision between who the person is and what they’re facing. These are among the most common presentations in psychiatric clinics today, yet our diagnostic vocabulary captures them poorly. And the two dominant framings on offer, namely, stress-diathesis as a model of disorder development versus a moralistic, disapproving stance of overdiagnosis and medicalizing social problems, are each inadequate in their own way.

What sort of examples do I have in mind?

• A woman with high baseline neuroticism who is chronically anxious in a work environment that would be stressful but manageable for someone with average emotional reactivity. She is able to function, just about, with the support of SSRIs and psychotherapy.

• A man working two jobs to support his family, chronically sleep-deprived, cognitively impaired by exhaustion, who is able to function, barely, thanks to stimulant medications for ADHD. He was diagnosed with ADHD as a child but was never treated before and never needed stimulants until now.

• A student with average working memory and processing speed enrolled in a program that selects ruthlessly on the ability to perform under timed, high-stakes conditions. She is experiencing self-doubt, low worth, anxious ruminations, and pessimism about the future. She wonders if she has generalized anxiety and ADHD because most of the other smart people struggling academically whom she knows of seem to have those diagnoses.

• A woman with a history of developmental trauma and insecure attachment, in an abusive marriage, refusing to even entertain the possibility of leaving the relationship, presents to the psychiatrist and therapist with worsening anxiety and depression, requesting more aggressive pharmacological and psychological treatment because she is unable to function.

What all these cases share is a mismatch between what these particular people can tolerate or sustain given their particular dispositions and what their circumstances require. Sometimes their capacities are entirely within the normal range, and sometimes they have unusually high or low values of a trait that renders them vulnerable. These are situations of temperament-environment mismatch, cognitive capacity-demand mismatch, socioeconomic entrapment, unhealthy attachments, self-defeating behavioral patterns, and, sometimes, the search for enhancement or optimization.

What they also share is that the person typically does not present to the psychiatrist saying, “I’m in an impossible situation and I need help figuring a way out of this.” They present saying, “I have anxiety” or “I can’t focus” or “I’m depressed” or “I am overwhelmed and breaking down.” They come seeking a clinical remedy for what they experience as a clinical problem. And in the contemporary healthcare system, it is very easy, almost frictionless, to confirm that framing, write a diagnosis, recommend a treatment, and move on.

There is a real temptation, especially for conscientious clinicians, to adopt a stance that goes roughly like this: “Your problem isn’t really psychiatric. There is nothing wrong with you. It’s situational. Medication won’t fix it. What you need to do is change your circumstances. Leave the job, leave the relationship, lower your expectations, accept your limitations.” In many cases it is at least partly correct, but it also leaves much to be desired and rarely offers anything meaningful to the patient.

It assumes the person has options they may not have right now, structurally or psychologically. Telling someone to change their situation when they are not in a position to do so is just an ineffective lecture. This can shade into a kind of moralism that is disguised as clinical judgment. The clinician is making a value judgment about how the patient should be living their life, and they are using their control over the prescription pad to enforce that judgment.

Also, the neat distinction between “disorder” and “mismatch” that makes this stance feel intellectually coherent does not survive contact with clinical reality. Because of the interaction between trait vulnerabilities and situational stressors, there is considerable uncertainty in real-world clinical assessments about the relative contributions of each and the existence of downstream dysfunctions arising from their interactions. Chronic stress, for example, brings its own neurobiological and psychological changes (hello, HPA axis dysregulation) that can acquire an independence of their own even if the original stressor is removed.

Finally, this ignores that the person can genuinely benefit from clinical treatment, including medications, at least to some degree, at least for some time, and withholding that treatment from an actively suffering person requires some degree of clinical indifference that makes most clinicians uncomfortable.

I find that I oscillate, case by case and sometimes within a single encounter, between positions that are hard to reconcile. Psychiatry should not be in the business of helping people endure situations that are harming them. To medicate a person so they can tolerate an intolerable job, or an abusive relationship, or chronic sleep deprivation, is to collude with the conditions that are making them sick.

On the other hand, the person in front of me is suffering now. They are not an abstraction or a case study in social determinants. They have come to me asking for something specific, and I have the ability to provide it, and it has a reasonable chance of helping them to some degree. Why should we withhold treatment from a suffering patient because we disapprove of the circumstances that produced the suffering? The structural conditions that generate these presentations are unlikely to change on any timeline that is useful to the person sitting in my office.

The standard psychiatric assessment is structured around an evaluation of symptoms and accompanying distress and impairment. Identifying demand-capacity mismatches requires the clinician to assess the person’s capacities and their environment’s demands and then evaluate the relationship between them. It requires assessing baseline capacities, asking about lifelong temperamental patterns, cognitive profiles, and stress tolerance independent of the current presentation. A person who has always been highly neurotic but managed fine in a structured, predictable job and began struggling only when moved to a chaotic one has a very different clinical story than a person whose anxiety has been debilitating across all contexts since adolescence.

Some patients have a hard time seeing the mismatch at all because they have fully internalized the idea that they are deficient or defective in some way. I struggle, others don’t, what is wrong with me? Why can’t I deal with this?

Others see the mismatch clearly but cannot change it; they are trapped by economics, obligation, or fear, and need the clinician to take their constraints seriously.

Some can see the mismatch but refuse to change it or are unwilling to take the steps needed for reasons that are irrational, puzzling, or opaque.

And some cannot see the mismatch because seeing it would require confronting something they are not psychologically ready to confront.

I find DeYoung and Krueger’s approach to psychopathology as a persistent failure to move toward one’s goals due to failure to generate effective new goals, interpretations, or strategies helpful in this context. I’m going to bypass any broader discussion of how adequate it is as a general definition of psychopathology; for now, I am more interested in the idea of “persistent failure to move toward one’s goals” as a target of clinical intervention and as a characterization of the sorts of problems we are discussing here.

Extreme trait levels are neither necessary nor sufficient for a failure to accomplish one’s goals. What matters is the failure of characteristic adaptations. A person with high neuroticism struggles when their characteristic adaptations (the specific goals, interpretations, and strategies they have developed in response to their life circumstances) fail, and they cannot generate effective replacements. The problem, in many cases, is neither purely in the trait nor purely in the environment but in the failure of the adaptive interface between them. Two people with equal neuroticism in the same demanding job may differ in their capacity to generate effective new adaptations. The one who can generate these adaptations remains functional despite the mismatch.

In other cases, there is a conflict between people’s goals, and their existing interpretations and strategies are failing in resolving that incompatibility. And sometimes, the goals are impossible given the person’s resources, and no amount of generating new strategies will make them achievable. The situation genuinely does not allow any effective adaptations within the constraints the person faces. And we know from evolutionary psychiatry that confronting inescapable and hopeless goals is particularly depressogenic.

The emphasis on characteristic adaptations and trait vulnerabilities allows us to think about effective lines of intervention.

Generating new strategies is often the most straightforward. Helping the person develop better coping mechanisms, more effective work habits, or more adaptive relational patterns is the bread and butter of psychotherapy. This is what CBT, DBT skills training, and many behavioral interventions do. In the mismatch scenarios, this corresponds to helping the person manage their situation more effectively within existing constraints.

Generating new interpretations is helpful in situations where existing interpretations are maladaptive and holding people back. Reinterpretation does not change the situation, but it can change the person’s relationship to it in ways that reduce conflict and restore some degree of effective functioning.

It is often necessary to abandon or modify goals that are unachievable (or achievable at a great cost to oneself). Giving up a goal can be difficult when the person is highly emotionally invested in it. It is useful to see negative affect as a signal, similar to bodily pain, pointing towards a change that needs to be made. Sometimes acknowledging this can sound like we are telling the person that they should want less from life because of who they are. When a clinician helps a person generate new goals, they are participating in reshaping that person’s vision of their own future, and it is important to be clear about whose values are guiding the process.

Psychiatric medications tend to target the trait level, adjusting the parameters of the cybernetic mechanisms that produce the trait. An SSRI that reduces neuroticism is, in cybernetic terms, adjusting the sensitivity of the threat-detection system so that the person registers fewer mismatches between their current state and their desired state. The person with reduced threat sensitivity may be able to tolerate the demanding job, generate new strategies that were previously blocked by anxiety, and develop characteristic adaptations that are more effective.

Whether this is a “good” outcome, in a broader ethical sense, depends on whether the continued functioning in that particular environment is conducive to a person’s overall flourishing and well-being. It also depends on how sustainable the improvement is. Sometimes a medication only buys people time, a pause before their capacities are overwhelmed again, a pause that can be valuable if it is used to develop new adaptations and reassess goals.

I am of the view that the most important things a psychiatrist can offer in these situations are an honest formulation, communicated with care, with the clinical room to explore and work through the trait-demand interactions at play, respecting a person’s autonomy and preferences, the openness to use medications in a clinically appropriate manner while being forthcoming about what they can and cannot do, avoiding medications when they will only worsen the problem (e.g. masking sleep deprivation with stimulants), guiding the person to the right psychological interventions aimed at building new strategies, interpretations, and goals, and providing space and grace for the person to come to terms with what they have been unwilling or unable to confront.

What I keep coming back to is the obligation to be honest. Honesty with the patient about what I think is happening and what I can and cannot do about it. Honesty with myself about the limits of my abilities and the values embedded in my clinical judgments. And honesty, insofar as I have a public voice, about the ways in which the profession I practice is being asked to absorb and individually manage forms of suffering that are, in part, collective in origin and that deserve collective responses. And honesty about the need for a clinical language that does justice to trait-demand mismatches and sees them as firmly and unapologetically deserving of clinical care.

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Nev Jones, PhD, is an Associate Professor of Social Work and affiliate faculty in the Department of Psychiatry at the University of Pittsburgh, USA. An accomplished mental health services researcher, her work has been continuously funded by the National Institutes of Health and she leads multiple large-scale research projects focused on systems and services for individuals labelled with ‘serious mental illness.’ Along with colleagues from the Human Services Research Institute, she recently completed a large-scale study of the implementation and effectiveness of AOT across New York State.

What Is Assisted Outpatient Treatment?

Assisted Outpatient Treatment (AOT), also known as Involuntary Outpatient Commitment (IOC), is a civil court procedure in which a judge orders an adult with a serious mental illness to adhere to community-based treatment. In the United States, as of 2024, 48 states and the District of Columbia authorize some form of AOT. Implementation varies widely across and within states in eligibility criteria, duration of court orders, available services, and enforcement mechanisms.

AOT typically involves mandated medication (often long-acting injectables), required attendance at outpatient appointments, substance use restrictions, and case management monitoring. Noncompliance may result in law enforcement transport to a hospital for evaluation, and potentially involuntary hospitalization or medication over objection. Court orders are typically 90–180 days, renewable indefinitely in most states.

What Do the Randomized Controlled Trials Show?

Three randomized controlled trials (RCTs) of involuntary outpatient commitment have been conducted worldwide. RCTs are the gold standard for determining whether an intervention causes better outcomes, because random assignment controls for all other factors that might explain differences between groups.

Key findings: None of the three RCTs found statistically significant differences between court-ordered and control groups on any primary clinical outcome. The Duke study reported positive results only in secondary, post-hoc subgroup analyses — specifically, for individuals whose court orders were sustained for 6+ months and who also received intensive services (3+ contacts/month). However, commitment duration was not randomly assigned, and the Cochrane Collaboration, which sets international standards for evidence-based review, treats post-hoc subgroup findings that contradict null primary analyses as having low evidentiary value.

The most recent (‘Gold Standard’) Cochrane meta-analysis (Kisely & Campbell, 2017), pooling all three RCTs, found no significant effect of court-ordered treatment on any of the meta-analyzable clinical outcomes studied with the exception of low quality evidence for reduced victimization. The number needed to treat (NNT) to prevent one hospital readmission was calculated as 142 — meaning 142 individuals would need to be placed under court orders to prevent a single hospitalization. While AOT is typically justified as a means of addressing “violence” or “social harm” in the US, recent meta-analysis of all available research on the effects of involuntary outpatient treatment on aggression or criminal offending found no significant benefits in either primary or sub-group analyses (Kisely et al., 2025).

Notably, in the Duke study, besides reduced victimization, coercion was the only other variable that reached statistical significance in a primary between-group comparisons: individuals under court orders reported 45% higher coercion than controls who received the same services without a court order. Black participants were approximately twice as likely to experience high levels of coercion as white participants, and disproportionality remained even after controlling for diagnosis, symptom severity, substance abuse, insight, functioning, marital status, and the length of the court order (Swartz et al. 2002).

What About Non-Experimental Studies?

Since the Duke and Bellevue RCTs, no further randomized trials of AOT have been conducted in the United States. The post-2001 evidence base consists of pre-post (mirror-image) studies, quasi-experimental matched comparison research, and the 2024 federal ASPE evaluation. These studies generally report improvements in hospitalizations and service utilization after AOT enrollment. However, they share fundamental limitations:

• Regression to the mean. Individuals are enrolled in AOT at their worst point — after repeated hospitalizations or crises. Statistical improvement from that low point is expected regardless of intervention. Only comparison to a control group can account for this, and non-experimental studies lack true control groups. Studies of voluntary ACT as well as studies comparing ACT and AOT (as is true of the ASPE evaluation) find decreases in all areas for individuals receiving voluntary ACT, not just AOT.

• Confounding of court orders with enhanced services. AOT enrollment typically comes with priority access to assertive community treatment (ACT) or intensive case management, linkage to SSI/SSDI and other social welfare benefits and sometimes guaranteed access to supportive housing. When hospitalizations or arrests decrease after someone begins receiving ACT and/or supported housing, attributing that improvement to the court order rather than the services is not justified.

• Provider accountability confound. AOT creates mandated accountability for providers to deliver services. This monitoring and accountability effect may itself drive improved service delivery, independent of the legal coercion experienced by the individual.

• Insufficient quantitative measurement of harm (see also below and cf Kisely et al., 2024 meta-analysis of what has and has not been documented to date globally).

The largest non-experimental study is the original New York State Kendra’s Law evaluation (Gilbert et al., 2010; Swartz et al. 2010), which analyzed Medicaid claims for 3,576 AOT recipients. The pre-post analyses showed reduced hospitalizations and increased service utilization. A contemporary New York-based quasi experimental study (Phelan et al. 2010) found some positive benefits, albeit with uncertain service utilization and provider accountability differences between AOT recipients and matched (quasi-experimental controls) but found no significant differences in psychotic symptoms or quality of life. The authors concluded that results “should be interpreted in terms of the overall impact of outpatient commitment, not of legal coercion per se.” Researchers at the University of Pittsburgh and Human Services Research Institute have recently completed a second, state-sponsored evaluation of Kendra’s Law – report will be released in early summer 2026.

ASPE Federal Evaluation and GAO Assessment

In 2024, the Office of the Assistant Secretary for Planning and Evaluation (ASPE) published a federally funded evaluation of SAMHSA’s AOT Grant Program, conducted by RTI International, Policy Research Associates (PRA), and Duke University School of Medicine. The evaluation examined 6 case study sites selected from 18 federally funded programs and used within-group pre-post analyses supplemented by a between-group comparison at a single site. Most measures were collected through structured interviews with AOT recipients conducted by clinicians working at their sites, creating potentially far-reaching measurement bias as participants already under court orders and motivated to appear “compliant” and “happy” in order to discharge their orders would generally not be expected to honestly report concerns and negative outcomes directly to clinicians with (plausible) power over future decisions to renew.

In July 2025, the U.S. Government Accountability Office (GAO) reviewed the ASPE evaluation and SAMHSA’s outcome reports and concluded:

“HHS’s assessments of the effects of the AOT grant program were inconclusive. This is because the ASPE and SAMHSA assessment efforts were both hampered by methodological challenges, many of which were inherent in the program and beyond their control.”

The GAO declined to report the specific results of either the ASPE evaluation or SAMHSA’s reports to Congress, stating that they “decided not to include the evaluation’s results because (1) we determined that ASPE and RTI International lacked information needed to help understand the extent to which the results represented all AOT participants included in SAMHSA’s grant program; and (2) our analysis of information we received from RTI International showed a high level of uncertainty for some of the results.”

Since 2016, the federal government has awarded approximately $146 million in AOT grants to 63 grantees across 28 states. The GAO concluded that “challenges assessing the grant program are likely to persist.”

Coercion and Potential Harms

Although AOT’s defining feature is legal coercion, remarkably few studies have measured the experience or consequences of that coercion. The available evidence includes:

• The Duke North Carolina study (Swartz et al. 2002) found that court-ordered treatment increased perceived coercion by 45% compared to controls receiving the same services. Each additional month under a court order increased the risk of high perceived coercion by approximately 10%. African American race independently predicted nearly twice the odds of experiencing high coercion (OR=1.89), after controlling for all measured clinical and demographic variables.

• Munetz et al. (2014) compared 17 former AOT participants to 35 mental health court graduates in Ohio. AOT recipients reported significantly higher perceived coercion on every dimension measured compared to mental health court participants, significantly lower procedural justice in interactions with judges, significantly less respect after program completion, and significantly less hope after completion than before.

• The judicial process itself raises substantial procedural justice concerns. A qualitative study of 13 NYC judges and 20 attorneys (Player 2015) found that judges overwhelmingly defer to the single evaluating psychiatrist, apply the evidence standard loosely, and rarely credit testimony from the individual subject to the order. Defense attorneys reported that their clients’ testimony often “means nothing” in practice and that psychiatric evaluations are typically 15–60 minutes conducted by clinicians with no prior treatment relationship.

Additional areas of potential harm that have not been published in the US AOT context include:

• Serious medication side effects from mandated polypharmacy, often without adequate access to treatment or intervention (beyond screening), including metabolic syndrome, Type II diabetes, antipsychotic-induced Parkinsonism, and cognitive decline secondary to the anticholinergic effects of prescribed medications.

• Custodial iatrogenesis: institutionalization in the community through supervised residential facilities that control finances, food, and social life creating dependency and de facto social and physical segregation.

• Disruption of family bonds including custody, elder caregiving and reproductive justice concerns – AOT orders may separate parents from children, and children from elderly parents, require residence in facilities that custodial parents have described as “too terrifying to expose a young child too” and/or that are physically distant; reproductive justice concerns include medication side effects impacting fertility, pregnancy and potential iatrogenic effects on the developing fetus.

• Social defeat — the chronic experience of subordination and powerlessness that is itself implicated in the development and worsening of psychosis.

These harms are non-trivial and publications in preparation (Pitt PathLab team) are beginning to document and substantiate how profoundly impactful they can be.

The Central Policy Question

The policy question underlying AOT is not “do people improve after AOT enrollment?” — pre-post studies can answer that question affirmatively for virtually any enhanced service, including voluntary ACT, supported housing, and SSI/SSDI access. The relevant question is: does the court order produce better outcomes than the same services delivered voluntarily?

The three randomized controlled trials that were designed to answer this question all found null primary results. The Cochrane meta-analysis confirmed no significant effect based on the pooling and re-analysis of data across RCTs. The most recent federal (ASPE) evaluation was deemed “inconclusive” by the US General Accountability Office upon audit and independent analysis of evaluation data. Meanwhile, the one participant-centered outcome measured in the Duke RCT — perceived coercion — is significantly increased by AOT, disproportionately for Black individuals, and the international qualitative research confirms widespread experiences and negative impacts of coercion within AOT (Barti et al., 2022; Goulet et al., 2020). No study has demonstrated that involuntary court-ordered treatment adds value beyond the enhanced services and system accountability that accompanies it. Meanwhile, intensive voluntary services such as ACT and Housing First have a well-established evidence base for improving outcomes for individuals with serious mental illness. Policymakers considering AOT should weigh whether the documented costs of legal coercion, in combination with serious ethical concerns, are justified given the absence of evidence that court orders add benefit beyond what these voluntary services achieve.

Join Nev Jones for an online webinar, A Deeper Dive on US “AOT” literature & International Findings, arranged by Roots Up, Mar 11 from 12pm to 2pm EDT.

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Key References

• Bartl, G., Stuart, R., Ahmed, N., Saunders, K., Loizou, S., Brady, G., ... & Lloyd-Evans, B. (2024). A qualitative meta-synthesis of service users’ and carers’ experiences of assessment and involuntary hospital admissions under mental health legislations: a five-year update. BMC psychiatry, 24(1), 476.

• Burns, T., Rugkåsa, J., Molodynski, A., Dawson, J., Yeeles, K., Vazquez-Montes, M., ... & Priebe, S. (2013). Community treatment orders for patients with psychosis (OCTET): a randomised controlled trial. The lancet, 381(9878), 1627-1633.

• Burns, T., & Molodynski, A. (2014). Community treatment orders: background and implications of the OCTET trial. The Psychiatric Bulletin, 38(1), 3-5.

• Burns, T., Yeeles, K., Koshiaris, C., Vazquez-Montes, M., Molodynski, A., Puntis, S., ... & Rugkåsa, J. (2015). Effect of increased compulsion on readmission to hospital or disengagement from community services for patients with psychosis: follow-up of a cohort from the OCTET trial. The Lancet Psychiatry, 2(10), 881-890.

• Gilbert, A. R., Moser, L. L., Van Dorn, R. A., Swanson, J. W., Wilder, C. M., Robbins, P. C., ... & Swartz, M. S. (2010). Reductions in arrest under assisted outpatient treatment in New York. Psychiatric Services, 61(10), 996-999.

• Goulet, M. H., Pariseau-Legault, P., Côté, C., Klein, A., & Crocker, A. G. (2020). Multiple stakeholders’ perspectives of involuntary treatment orders: a meta-synthesis of the qualitative evidence toward an exploratory model. International Journal of Forensic Mental Health, 19(1), 18-32.

• Government Accountability Office. (2015). Serious mental illness: HHS assessment of assisted outpatient treatment have yielded inconclusive results. GAO-15-700.

• Kisely, S. R., & Campbell, L. A. (2015). Compulsory community and involuntary outpatient treatment for people with severe mental disorders. Schizophrenia Bulletin, 41(3), 542-543.

• Kisely, S., Zirnsak, T., Corderoy, A., Ryan, C. J., & Brophy, L. (2024). The benefits and harms of community treatment orders for people diagnosed with psychiatric illnesses: A rapid umbrella review of systematic reviews and meta-analyses. Australian & New Zealand Journal of Psychiatry, 58(7), 555-570.

• Kisely, S., Bull, C., & Gill, N. (2025). A systematic review and meta-analysis of the effect of community treatment orders on aggression or criminal behaviour in people with a mental illness. Epidemiology and psychiatric sciences, 34, e12.

• Munetz, M. R., Ritter, C., Teller, J. L., & Bonfine, N. (2014). Mental health court and assisted outpatient treatment: Perceived coercion, procedural justice, and program impact. Psychiatric Services, 65(3), 352-358.

• Phelan, J. C., Sinkewicz, M., Castille, D. M., Huz, S., & Link, B. G. (2010). Effectiveness and outcomes of assisted outpatient treatment in New York State. Psychiatric Services, 61(2), 137-143.

• Player, C. T. L. (2015). Outpatient commitment and procedural due process. International Journal of Law and Psychiatry, 38, 100-113.

• Simon, J., Mayer, S., Łaszewska, A., Rugkåsa, J., Yeeles, K., Burns, T., & Gray, A. (2021). Cost and quality-of-life impacts of community treatment orders (CTOs) for patients with psychosis: economic evaluation of the OCTET trial. Social psychiatry and psychiatric epidemiology, 56(1), 85-95.

• Steadman, H. J., Gounis, K., Dennis, D., Hopper, K., Roche, B., Swartz, M., & Robbins, P. C. (2001). Assessing the New York City involuntary outpatient commitment pilot program. Psychiatric Services, 52(3), 330-336.

• Swartz, M. S., Swanson, J. W., Wagner, H. R., Burns, B. J., Hiday, V. A., & Borum, R. (1999). Can involuntary outpatient commitment reduce hospital recidivism?: findings from a randomized trial with severely mentally ill individuals. American Journal of Psychiatry, 156(12), 1968-1975.

• Swartz, M. S., Swanson, J. W., Hiday, V. A., Wagner, H. R., Burns, B. J., & Borum, R. (2001). A randomized controlled trial of outpatient commitment in North Carolina. Psychiatric Services, 52(3), 325-329.

• Swartz, M. S., Wagner, H. R., Swanson, J. W., Hiday, V. A., & Burns, B. J. (2002). The perceived coerciveness of involuntary outpatient commitment: findings from an experimental study. Journal of the American Academy of Psychiatry and the Law Online, 30(2), 207-217.

• Swartz, M. S., Wilder, C. M., Swanson, J. W., Van Dorn, R. A., Robbins, P. C., Steadman, H. J., ... & Monahan, J. (2010). Assessing outcomes for consumers in New York’s assisted outpatient treatment program. Psychiatric Services, 61(10), 976-981.

• Valasek, C. J., Nelson, K. L., Fettes, D. L., & Sommerfeld, D. H. (2025). Emerging trends in research on assisted outpatient treatment in the United States: a narrative review. Psychiatric Services, 76(5), 469-478.

Patrick D. McGorry, MD, PhD, is an Irish-born Australian psychiatrist and Professor of Youth Mental Health at the University of Melbourne, where he also serves as Executive Director of Orygen, Australia National Centre of Excellence for Youth Mental Health. After his family immigrated to Australia, McGorry earned bachelor’s degrees in medicine and surgery from the University of Sydney (1977) and doctorates in psychiatry from Monash University (1991) and the University of Melbourne. In 1992, he founded and became director of the Early Psychosis Prevention and Intervention Centre (EPPIC), the first Australian organization to focus specifically on young people rather than adolescents or adults, and its model has since influenced mental health services across Asia, Europe, and North America. In 2001 he established Orygen as a translational medical research institute for youth mental health and it is now the largest mental health research organization in Australia. His advocacy led to the establishment by the Australian Government in 2005 of the National Youth Mental Health Foundation, which was branded as Headspace in 2006 and this model of care now operates in 174 Australian communities. His contributions have earned him numerous honors, including the Australian Government Centenary Medal (2003), the 2010 Australian of the Year award, and the Founders’ Medal of the Australian Society for Psychiatric Research (2001). He has done pioneering scientific work in the multidisciplinary treatment of first-episode psychosis, the development of clinical staging models in psychiatry, and youth mental health.

From “Dementia Praecox” to “First Episode Psychosis”

Aftab: I’d like to start by going back to the beginning of your career. You trained in medicine in Sydney in the 1970s, completed your psychiatric training in Melbourne, and by 1992 you had founded EPPIC, the Early Psychosis Prevention and Intervention Centre. I’m struck by how you’ve been at the forefront of rethinking how we conceptualize and respond to emerging psychopathology in young people. So, I’m curious: what was your big-picture understanding of mental disorders in your early days as a trainee, and how has it changed over time?

McGorry: When I was young, I was caught up in a lot of revolutionary thinking. As a medical student in the 1970s, that spirit was still very much alive in Europe. Antipsychiatry currents were strong in places like Heidelberg, where the Socialist Patients’ Collective had emerged. It was a radical time, with broad dissatisfaction with institutions, and within psychiatry that dissatisfaction had a particularly intense focus. The old asylums were oppressive places, and many had clearly lost their purpose.

I was drawn to psychiatry partly because I’d always been as interested in the humanities as the sciences. Psychiatry seemed to offer a unique blend, from philosophy through to medicine, an integrative, diverse field that still sat inside medicine. But I was also deeply wary of psychiatry because of the antipsychiatry literature I’d consumed. Then a suitable opportunity emerged: I’d spent a few years working in internal medicine, and a very humane professor of psychiatry, someone I respected a lot, the late Professor Beverley Raphael, was appointed where I was working in Newcastle. She gave me hope that a different psychiatry was possible. With her as a role model, I thought I could give psychiatry a chance. When I started training, it felt like stepping back decades compared to the general hospitals, in terms of the quality of care, the custodial atmosphere of the old institutions. But I persisted.

Near the end of my training, I moved to Melbourne to work with a newly appointed professor, Bruce Singh, who gave me the opportunity to establish a research unit in one of the old asylums there, a small facility near the city center. I decided to focus on first-episode psychosis, and this decision was shaped by an earlier experience in medicine. I’d worked in an education and stabilization center, created by the late Dr. Paul Moffitt, for newly diagnosed diabetics, many of them adolescents having to come to terms with a life-changing diagnosis. The psychological impact of being diagnosed with diabetes was real and often profound, and diabetes is relatively straightforward compared to what it means to be told you have schizophrenia or psychosis. That contrast stayed with me.

I also observed unconscionably long delays before young people with psychosis accessed treatment, and I witnessed how harmful many treatment experiences could be, both the neglect and the coercive aspects. It became clear to me that you first had to remove the iatrogenesis of the system itself before you could build something genuinely hopeful, recovery-oriented, and humane. That’s what we set out to do.

Aftab: How was your understanding of psychopathology developing at this early point in your life?

McGorry: My PhD was fundamentally about mapping, in minute detail, the psychopathology of a first episode of psychosis. I developed a multidiagnostic instrument that would allow me to capture the full phenomenological landscape of these experiences. I drew extensively on historical concepts from classical descriptive psychiatry, and where those concepts hadn’t been properly operationalized, I worked to operationalize them myself. The result was a comprehensive set of definitions covering psychotic and severe mood phenomena within a single instrument, administered both at the beginning and end of the episode, supplemented with detailed information from family members and other informants.

The aim was to produce a rich, textured portrait of what actually happens during a first episode of psychosis, not just a symptom checklist or a diagnostic label. I wanted to understand the phenomenological complexity, how these experiences unfold, what their constituent elements are, how they evolve over time and how people react to these typically profound experiences. That process immersed me deeply in psychopathology in a way that fundamentally shaped my subsequent thinking. It taught me to pay close attention to what young people were actually experiencing.

Aftab: How did you go from a more rigid schizophrenia concept, from Kraepelinian thinking, to the more fluid “first-episode psychosis”?

McGorry: In a way, moving to “first-episode psychosis” as a conceptual frame was strategic, because I’d come to believe that the Kraepelinian dichotomy created a terrible problem for the field—a fatal flaw. I’d read Kraepelin’s original text closely and realized that the basis for the concept of dementia praecox was essentially a deteriorating outcome. It was an attempt to unify diverse clinical presentations under a common end state, a syndrome defined by progressive deterioration.

I think Kraepelin was inspired by neurological diseases like Alzheimer’s disease, where you genuinely do find a common underlying biology producing a syndrome that culminates in a specific, severe outcome. He tried to apply that same logic as a heuristic for functional psychosis: gather together cases with poor outcomes and assume they share a common underlying basis.

But that approach wouldn’t work in other areas of medicine. If you grouped together all cases of chronic renal failure and assumed they were a single entity with a common cause, you’d be committing a fundamental conceptual error. You’d be confusing a prognostic pathway with etiological unity. And that mistake has had severe consequences in psychiatry which persist to this day.

It leads directly into the twin problems of heterogeneity and pleiotropy, which are two sides of the same coin. Even something with a relatively simple biological cause can present with diverse syndromal expressions; conversely, a syndrome like psychosis or depression can arise from multiple distinct causes and pathways. The Kraepelinian framework conflates these issues by reifying diagnostic categories as if they were disease entities.

This framework became the cornerstone of clinical attitudes that I found deeply problematic. In case conferences, I watched teams spend enormous energy debating: is this schizophrenia, which implicitly meant hopelessness and deterioration, or is it bipolar disorder, which felt like “winning the lottery” because the prognosis was assumed to be so much better? But in real patients, outcomes overlap far more than that stark dichotomy suggests. Many people diagnosed with schizophrenia recover well, and many with bipolar disorder struggle chronically.

More troubling, communicating low expectations for recovery, whether explicitly or implicitly, was profoundly iatrogenic. It contributed to demoralization, hopelessness, and suicide risk. The prognosis narrative was harmful as well as empirically incorrect. Even older longitudinal work, including the WHO cross-cultural studies, showed substantial rates of recovery in schizophrenia. The idea that you should tell someone experiencing their first episode that their outlook is inevitably terrible violates basic principles of medical practice. You wouldn’t approach someone with a serious cancer diagnosis that way, telling them at the outset there’s no hope. Why would we do that in psychiatry?

Aftab: At that point in your career, what was your general understanding of what mental disorders are? Conceptually, how were you thinking about psychiatric constructs?

McGorry: I started with a strong pull toward environmental, sociological, and psychological explanations, partly shaped by antipsychiatry influences, but also because psychoanalysis was still prominent in Australian psychiatry at the time. I had substantial psychodynamic influence in my training, which made me receptive to ideas of multiple causation and psychological meaning.

I was quite resistant to biological explanations initially, partly because Kraepelinian determinism felt inseparable from biological reductionism and therapeutic nihilism. But the reality of immersion in frontline care and the success of careful biological treatments for most patients rapidly helped me to see that biology was undeniably part of the picture. Diabetes became a useful analogy for me: you can have a clear biological basis for an illness while recognizing that environmental and psychological factors profoundly influence its course, the degree of disability, and the prospects for recovery. So I tried to move toward a genuinely integrative biopsychosocial framework, grounding it in what was actually happening on wards and in clinical services.

One experience that profoundly shaped my thinking in those early years was witnessing what was being done with antipsychotic medications, particularly in acute settings. There was a prevailing fashion for “rapid neuroleptization.” The philosophy being that if some medication is good, more must be better, so very high doses were given very quickly with the belief that people would get well faster. There was no evidence supporting this approach, and it caused a lot of harm.

In the first year I worked at the hospital, Royal Park, where we developed our first episode psychosis unit, eight patients died of torsades de pointes, fatal cardiac arrhythmias directly caused by massive doses of antipsychotics. That was catastrophic, and it clarified something fundamental for me at the time: the first principle for young people experiencing their first episode had to be protecting them from the iatrogenic effects of high-dose medication practices and also mixing newly diagnosed young people with much older chronically ill patients.

If you look back historically, quite small doses were sufficient when neuroleptics were first introduced in the 1950s. The problem developed when medication increasingly became used for behavioral control rather than careful treatment of core psychotic symptoms. We returned to very low doses, something like 2 mg of haloperidol as a starting point, and we used benzodiazepines to reduce anxiety, distress, and behavioral disturbance rather than simply escalating antipsychotic doses. Patients’ experiences were dramatically better. They weren’t zombified, they could think more clearly, they maintained more of their sense of self.

Then we set about developing comprehensive psychosocial treatments. At that time, there weren’t many effective psychosocial approaches available in routine psychiatric care. There were pockets of good practice, some social skills work, and Ian Falloon had written compellingly about family interventions, but nothing like the integrated recovery-oriented program we envisioned.

So we built what we called a recovery program: psychosocially oriented, actively involving families, infused with hope and realistic optimism. It was pragmatic and evidence-informed, drawing on whatever worked while remaining grounded in patients’ actual experiences and needs. And we began to conduct research, especially in new psychosocial interventions, and integrate these with much more careful medication strategies.

Aftab: Within the psychiatric community at that time, was there resistance to the idea that psychotic disorders could be effectively managed through psychosocial interventions?

McGorry: Psychiatry was deeply split along ideological lines and sadly this still lingers. On one side, you had psychoanalysts, who believed psychoanalysis could essentially treat anyone, including people with severe psychotic disorders. On the other side, you had biologically oriented psychiatrists, especially those working in the asylums and large state hospitals, who more or less believed psychological treatments were useless, that psychosis was fundamentally a brain disease requiring medication, and that talk therapy was at best irrelevant, at worst a distraction. Sadly, that latter attitude remains common in many acute psychiatric settings even today. The former attitude of psychological reductionism also dies hard.

I did engage seriously with some of the more thoughtful psychoanalytic writers—Silvano Arieti comes to mind—who at least attempted to understand the phenomenology and meaning of psychotic experience in sophisticated ways. But much of the mainstream psychoanalytic culture involved people writing quite confidently about psychosis without actually treating actively psychotic patients in any sustained way. There was often a disconnect between the theory and the clinical reality.

We were trying to chart a different course. Our approach became: use medication, but carefully and at low doses, always combined with robust psychosocial support, family involvement, and attention to the social and psychological dimensions of recovery. We weren’t interested in ideological purity. As clinical scientists we wanted to know what actually helped young people recover and get their lives back.

Antipsychotics versus psychosocial care in first-episode psychosis

Aftab: You’ve been involved in trials in first-episode psychosis comparing antipsychotics with cognitive-behavioral therapy–based approaches, along with intensive case management. These kinds of trials are extraordinarily difficult to design, fund, and implement, and often controversial. I’m thinking here of the Francey et al, 2020 paper. What drove that work?

McGorry: Part of the historical background is that Philip May conducted related work back in the 1960s, but the more immediate motivation came from the intense debate about duration of untreated psychosis (DUP).

Tom McGlashan came to Melbourne in the 1990s after we had established our early psychosis program and prodromal clinic. He engaged deeply with what we were doing and subsequently took many of these ideas to Norway and the United States. At the invitation of the pioneering Dr Jan Olav Johannessen in Stavanger he became scientifically involved in the TIPS Study in Scandinavia, which used a quasi-experimental design: in one sector, massive efforts were made to shorten DUP through public education campaigns and mobile early detection teams, while another sector continued with standard care as a naturalistic comparison. They found substantially better outcomes in the early detection sector, sustained even at 10-year follow-up.

At the time, there were prominent skeptics who argued that the correlation between longer DUP and worse outcomes was spurious, that it simply reflected a confound. Their claim was that poor-prognosis patients present later because they have a more insidious onset, greater negative symptoms, and less social support, so DUP doesn’t cause worse outcomes, it merely reflects underlying illness severity. McGlashan believed it was unethical to randomize people to early versus deliberately delayed treatment, which is why he pursued the quasi-experimental approach. But that design ultimately couldn’t definitively settle the causal question. I asked myself: under what conditions could you ethically conduct a randomized study that gets closer to answering the causal question about early intervention?

In our setting, we were seeing many young people with remarkably short DUP, often just weeks, not the months or years typical of chronic first-episode cohorts. That demographic reality led me to a different hypothesis: perhaps some first-episode patients with very recent onset, where psychosis was still in its earliest stages, could recover with intensive psychosocial treatment alone, at least initially. Some of these individuals might be clinically closer to the subthreshold or clinical high-risk population. Potentially more responsive to psychosocial interventions before psychotic processes became deeply entrenched.

At the same time, I was thinking carefully about the relationship between symptom severity and medication necessity. The severity of overt psychosis isn’t necessarily the only guide to whether someone needs medication. Some people with subthreshold presentations might genuinely require antipsychotic medication; conversely, some people who meet full threshold criteria for psychosis might not need it immediately, or might recover adequately without it under the right conditions. The clinical question became: especially with much shorter DUPs, can we identify a subgroup that can do well without antipsychotics, at least as a first-line approach?

That question became the basis for what’s often called the STAGES study. We had to design the trial meticulously and take it through ethics committees with great care. We excluded anyone at high risk: people who were severely disturbed, experiencing intense suffering, actively suicidal, at risk of harm to themselves or others, or otherwise unsafe to delay medication. We focused exclusively on individuals who were relatively early in their psychotic presentation, not in acute crisis, and who could provide genuinely informed consent to postponing antipsychotic treatment.

We drew heavily on the capacity-to-consent framework developed by Paul Appelbaum and colleagues. Some of our FEP patients were clearly able to meet that standard. They could understand the risks and benefits, appreciate their situation, reason about the choice, and communicate a decision. Importantly, some patients were ambivalent about or resistant to medication anyway, so we could approach them honestly: we had an open mind about whether this particular individual needed antipsychotic medication immediately or not, and we were conducting rigorous research to find out.

We randomized approximately 90 patients over about five years. Since our service was seeing many more first-episode cases during that period, the recruited cohort wasn’t at all representative of the entire spectrum. They were deliberately a carefully selected subset who met our safety and consent criteria. But the trial demonstrated clearly that some people who meet diagnostic criteria for first-episode psychosis can improve substantially without antipsychotics, provided they receive intensive, structured psychosocial care.

Now, that finding doesn’t mean medication-free treatment is appropriate for the majority of young people with first-episode psychosis. What it does suggest is that for a small but meaningful minority, less than 10 percent, it should be presented as a legitimate option, with careful monitoring and a plan to introduce medication promptly if needed. The key is informed choice, safety, and very close clinical attention, which currently and sadly very few services are resourced to provide.

Aftab: Were you surprised by the results? And what can be said about their generalizability?

McGorry: I wasn’t surprised that a carefully selected subgroup could do well without antipsychotics under very specific conditions. That was precisely our hypothesis. But generalizability is always the critical question with findings like these, and I think we need to be quite cautious and precise about the implications.

I also think it’s important to be transparent about investigator perspectives and motivations in this area. Without naming names, there are some researchers studying these questions with a rather dogmatic agenda. They want to demonstrate that antipsychotics are mostly harmful and should be avoided whenever possible. That’s not my position at all, and I want to be clear about that. Psychosis is a very serious condition. Medication is needed by and works for most but not all people, and it remains a central pillar of treatment. New and more diverse medications are also urgently needed.

One of the reasons I moved away from antipsychiatry thinking early in my career is that I witnessed firsthand how beneficial antipsychotics can be, especially when used very precisely, at very low doses, well below the threshold where you’re producing severe extrapyramidal side effects or inducing a “neuroleptic” state that robs people of their vitality. This was known in the 1950s as the “neuroleptic threshold” and this “sweet spot” was validated by brilliant imaging studies in the 1990s in Canada and Sweden. I don’t have any ideological bias against these medications. What I do object to is careless, high-dose, and often coercive prescribing practices that prioritize behavioral control over therapeutic benefit. A much gentler and rational way of managing acute distress, agitation and behavioral disturbance is with short-term use of benzodiazepines, which tend to make the patients feel subjectively better, not worse, when in the grip of acute psychosis.

At the same time, we know from longitudinal data that some people experience a single episode and recover completely; others may need medication for a limited period but not indefinitely. I’ve debated this extensively with John Kane, whose work I deeply respect. His position, roughly speaking, is that because the majority of people with first-episode psychosis will require longer-term treatment to prevent relapse, you should treat everyone uniformly according to that statistical reality. It’s a population-level risk management approach.

My view is different. I believe it’s worth making the effort to identify those individuals who don’t need medication at all, or who don’t need it for very long, even if they represent a minority. That’s what genuine personalization means in medicine, tailoring treatment to the individual rather than applying a one-size-fits-all approach based on group averages. The price of not personalizing is unnecessary exposure to metabolic side effects, neurological risks, and the stigma associated with long-term psychiatric medication for a subset of people who could potentially do well with a different therapeutic pathway. We owe it to patients to try to identify who they are. Currently we struggle to identify them prospectively as a subgroup and hence the one size fits all approach which is overall safer but not optimal.

Aftab: My reading of the DUP literature is that causal inference remains genuinely contested in parts of the academic community. What’s your current assessment? And as psychotherapy and psychosocial interventions are increasingly considered as potential first-line treatments for certain patients, do you think the DUP concept should expand beyond simply “time to first antipsychotic treatment”?

McGorry: Within the early psychosis clinical community, the people actually running services and treating these patients, and I think even in the schizophrenia field generally now I’d say the matter is essentially settled: shortening DUP improves outcomes, at least in the short to medium term, and there’s evidence for longer-term benefits as well.

The researchers who continue to dispute this tend to rely on a relatively narrow set of arguments and studies that, in my view, have significant methodological limitations or don’t adequately account for the full picture. But here’s what I think is crucial: even if you completely set aside the “brain toxicity” hypothesis, the idea that untreated psychosis causes progressive biological injury or neurotoxicity, you don’t need that mechanism to understand why leaving a young person actively psychotic for months or years is profoundly damaging.

Common sense and clinical reality are important here. Who would really like to argue that it is a good idea to advocate for treatment delay once psychosis is established and sustained? That is what we call in Australia “the pub test”—what would the average reasonable person think? If someone is experiencing florid psychosis throughout late adolescence or early adulthood, those critical developmental years, they lose friends, drop out of school or university, withdraw from social networks, fail to achieve key developmental milestones like completing education, forming intimate relationships, or establishing vocational identity. That accumulating social and psychological fallout makes recovery substantially harder, regardless of eventual medication response. Even if you eventually achieve good symptomatic control, the task of rebuilding a life, reestablishing social connections, and catching up developmentally becomes exponentially more difficult the longer psychosis has been allowed to run unchecked.

Research examining the duration of active psychosis after the first episode, looking at relapse duration or time spent symptomatic in longitudinal cohorts, is also broadly consistent with the idea that prolonged time in an actively psychotic state is not benign. It has cumulative costs.

So I genuinely don’t think anyone can be arguing for delaying treatment once psychosis is clearly present and causing distress or functional impairment. Psychiatry has too many fruitless ideological debates, and this strikes me as one of them. The preponderance of evidence, both clinical and empirical, points in one direction.

Now, you raise a genuinely interesting conceptual question: should effective psychosocial treatments count as “treatment” within a DUP framework, rather than defining DUP narrowly as time to first antipsychotic? In principle, yes, absolutely, if those interventions demonstrably reduce distress, diminish symptom intensity, preserve or restore functioning, and prevent the cascading social and developmental losses we’ve been discussing.

Critical Psychiatry

Aftab: You’ve described being influenced by the antipsychiatry movement in the 1960s and 1970s. Over the last two decades, there’s been a resurgence of critical perspectives on psychiatry and a revival of arguments originally made by figures like Thomas Szasz and R.D. Laing. How do you relate intellectually to the earlier antipsychiatry wave versus the contemporary one? What frustrates you about current critiques of psychiatry?

McGorry: I think part of what’s happening reflects broader polarization in society, not just in psychiatry but across many domains. You get increasingly entrenched thesis and antithesis positions, and hopefully something more nuanced and workable eventually emerges from the dialectic. I’ve appreciated the work you’ve done in moving the debates towards a productive synthesis.

I genuinely understand what many critics are reacting to. The concerns that originally motivated me to practice psychiatry from a human rights and humanitarian position were entirely real: patients getting a raw deal, experiencing iatrogenic harm, systematically dehumanizing care in many settings. Those realities resonated very strongly with me then, and they still do. When critics point to coercion, to over-medication, to the dismissal of patients’ subjective experiences, to conflicts of interest with the pharmaceutical industry, those are legitimate concerns that deserve serious engagement.

But I also think that some prominent critics of psychiatry today have become deeply ideological and dogmatic. They will reject this characterization as unfair, but if you look carefully at what they are doing, they frequently start with a predetermined conclusion and then selectively marshal confirming evidence while dismissing or ignoring contrary data. That’s not genuine knowledge-seeking or scientific inquiry. There’s a lack of epistemic humility, a reluctance to genuinely engage with complexity or acknowledge trade-offs.

What these critics often deny or minimize is another set of empirical realities: when antipsychotic medications are used carefully and judiciously, they help people enormously. They prevent suffering, enable recovery, save lives. Without these medications, we would be in a vastly worse situation. I’ve seen that with my own eyes over decades of clinical work. Now, are there valid criticisms of pharmaceutical industry influence? Absolutely. Are there serious problems with careless prescribing practices, with polypharmacy, with using medication primarily for behavioral control? Without question. But acknowledging those real problems doesn’t justify a blunt dismissal of antipsychotics itself.

I don’t have a black-and-white stance on any of this. Frankly, I don’t have a black-and-white stance toward biologically reductionistic psychiatrists either, some of them are far too one-dimensional in the opposite direction. Psychiatry has lurched historically from psychoanalytic reductionism to biological reductionism, and what we desperately need is to find our way back to something genuinely integrative and biopsychosocial, while still demanding real scientific and therapeutic progress.

We need substantially better psychological treatments. CBT for psychosis has shown benefits, but it’s honestly quite limited in what it can do. We need more innovation, perhaps through immersive technologies like virtual reality, through newer forms of psychotherapy, through better integration of peer support and social interventions. But we also desperately need advances in biological treatment. There’s a subset of first-episode patients, roughly 20 to 30 percent, who don’t respond adequately to low-dose dopamine blockade. What do you do for them? We don’t have good answers. One answer we do have is clozapine but the mental health systems around the world are very poor at delivering early access to this life changing and extending medication once treatment non-responsiveness to standard dopamine antagonists is clearly established.

It’s scientifically plausible that glutamatergic agents could help this population, but drug development in this area has been painfully sluggish and frustrating. When you look at what’s happened in oncology over the same time period, the explosion of targeted therapies, immunotherapies, the translation of basic science into clinical benefit, the contrast is striking and frankly dispiriting.

There simply isn’t enough momentum or investment behind the discovery of novel psychiatric agents. We’re also hampered by an excessively rigid regulatory and scientific culture at places like the NIMH in US that insists you must definitively demonstrate the mechanism of action before you can explore clinical efficacy. That stifles innovation. We need more space for intelligently guided empiricism and serendipitous discovery alongside mechanistic neuroscience, the way psychiatric pharmacology actually progressed in its most productive eras.

Clinical staging, transdiagnostic thinking, and “new diagnosis”

Aftab: You’ve worked on clinical staging concepts for decades. How has your thinking about staging developed over that time?

McGorry: We arrived at staging through prospective longitudinal work attempting to define and characterize a subthreshold psychotic state, what eventually became known as the clinical high-risk or ultra-high-risk for psychosis concept. In our early cohort studies in the mid-1990s, transition rates to full-threshold psychosis were quite high, 30 to 40 percent within relatively short follow-up periods.

The fundamental principle underlying staging was this: if you’re going to intervene early, before clear diagnostic thresholds are crossed, you must prioritize safety above all else. “Primum non nocere.” That’s precisely why we argued that psychosocial interventions should be prominent at early stages, while pharmacological approaches should be more conservative and reserved for those who truly need them or who progress despite initial psychosocial treatment.

Over time, as we accumulated longer follow-up data and larger cohorts, the picture became more complex and interesting. The ultra-high-risk group didn’t just transition to psychosis or remain stable, many developed other comorbid or single syndromal outcomes entirely. Some developed severe mood disorders, some anxiety disorders, some substance use problems. That empirical reality pushed us strongly toward a more transdiagnostic conceptual framework. We were clearly dealing with evolving, fluid syndromal pictures in young people, not with discrete disease entities that simply declare themselves over time.

We’ve worked hard to create research infrastructure for studying these developmental pathways, the ebbs and flows of psychopathology as it emerges and transforms in young people. But I have to be honest: I don’t think we’ve pinned down the staging model well enough yet. We need many more high-quality longitudinal studies that carefully track how symptoms cluster, how comorbidity emerges and changes, how functional trajectories diverge… the kind of intensive, long-term cohort work that’s expensive and difficult but absolutely essential. It is already a very good framework for the conduct of clinical trials however.

This all loops back to your fundamental question about ontology: what exactly are we dealing with in psychopathology? If these are syndromes with complex, shifting, multifactorial causal mixtures rather than natural kinds, how do we intelligently connect our classification systems to treatment decisions and biological, psychological, and social interventions?

Aftab: Do you see potential synergy between staging approaches and dimensional classification systems like HiTOP? And what about complex systems approaches, network analysis and related methods?

McGorry: We’ve certainly tried to bring these different theoretical worlds into productive conversation. Just before the pandemic, we organized an international workshop in Amsterdam on what we ambitiously called “new diagnosis.” We invited researchers working on HiTOP, people involved with RDoC, those developing staging models, and others thinking innovatively about psychiatric classification. The goal was to see whether we could build some kind of shared conceptual framework or at least identify areas of convergence. That work was eventually written up and published in Psychological Medicine recently.

To be candid about my own personal view, I think staging has the best chance of achieving real clinical utility in routine practice. What staging does is add an orthogonal temporal dimension, a developmental or longitudinal axis, over the dimensional syndromal space. That combination potentially gives you something useful for clinicians and patients.

With HiTOP, the dimensional structure often makes excellent conceptual sense and fits the psychometric data beautifully. But the critical clinical questions are: how do these dimensions evolve over time in individual patients? How do they guide specific treatment decisions? Network analysis and related complex systems approaches may ultimately capture this kind of dynamic evolution more effectively… if we can generate sufficiently high-quality longitudinal data to feed into these models. Technically, this work is above my pay grade, but conceptually I think that’s where the field needs to move.

There’s also an important practical reality we sometimes overlook: treatment is often inherently transdiagnostic anyway, especially psychosocial interventions. CBT, family work, supported employment, substance use interventions. These don’t neatly map onto diagnostic categories. Even pharmacological treatments are trans-syndromal in their effects but are forced by the FDA and pharma into a procrustean bed of artificially discrete entities.

DSM and attenuated psychosis syndrome

Aftab: When DSM-5 was being developed, there was intense controversy around including attenuated psychosis syndrome or clinical high risk for psychosis in the manual. Allen Frances was particularly vocal in his opposition. How do you reflect on that debate now, more than a decade later?

McGorry: [Laughs] It’s quite tricky, actually. I find myself agreeing with Allen Frances on many things these days. But at the time, I think he misunderstood what we were doing and approached the debate in an unnecessarily heated manner.

His argument was that attenuated psychosis syndrome represented boundary expansion of the kind that had legitimately troubled people with ADHD, autism or pediatric bipolar disorder, that we were pathologizing normal adolescent experiences and creating a new diagnostic category to label people who didn’t genuinely need psychiatric intervention.

But that characterization was not aligned with empirical realities. The data already clearly showed that these young people were actively help-seeking. They weren’t being identified through population screening or dragged into services by worried parents. They had significant functional impairment, elevated rates of distress, and concerning levels of suicidality. They clearly warranted clinical attention and support. The genuine question, the one we were actually trying to answer through rigorous research, was what constituted the right care for this population.

We consistently used staged, sequential or adaptive designs with safety as the paramount concern. The default approach was simpler supportive needs-based psychosocial interventions first, with intensive case management, CBT, family work, with medications held in reserve unless and until someone’s clinical state deteriorated or they developed full-threshold psychosis. Now, we did also explore low-dose antipsychotic treatment as one option in some studies, always with informed consent, because that can be a legitimate clinical choice depending on symptom severity, level of distress, suicide risk, and patient preference. But the entire enterprise got caught up in a politicized battleground over DSM-5 revision politics and broader cultural anxieties about diagnostic inflation and pharmaceutical company influence.

Aftab: Do you think something like attenuated psychosis syndrome is ready to be formally included in diagnostic classification systems now?

McGorry: I think some form of diagnostic recognition is necessary to make evidence-based treatment accessible and fundable, but we have to be careful about what this syndrome actually represents. It’s pluripotential. It’s a phenotype that clearly warrants clinical care, but the syndromal and developmental outcomes are genuinely heterogenous and extend beyond psychosis alone, even though there is a strong valence for subsequent psychotic illness.

Current data suggest that transition to full-threshold psychosis occurs in roughly 20 percent of these individuals, possibly somewhat higher with extended follow-up, though rates vary considerably depending on how rigorously your sample is ascertained and where you’re recruiting from. But transition to psychosis is only one outcome trajectory among several.

Attenuated psychosis or clinical high risk syndrome is also associated with progression to mood disorders, to substance use disorders, and to persistent subthreshold attenuated symptoms that still cause considerable distress and impairment. In longitudinal studies, only a small minority, perhaps less than 10%, failed to meet criteria for any DSM syndrome over extended periods of time.

So I think it’s most accurately conceptualized as a kind of gateway syndrome, one important pathway into serious mental illness, but not the only one, and not deterministically leading to any single outcome. It identifies a population of young people at elevated risk who need much more than minimal “watchful waiting” but who shouldn’t automatically receive specific antipsychotic pharmacological treatment, especially as first line.

The question of nosological placement is an important one. Placing it exclusively within the psychotic disorders section would be misleading, because it’s emphatically not simply “early schizophrenia” or “prodromal psychosis” in a straightforward sense. But it is a recognizable, clinically meaningful state with characteristic features and predictable risk profiles. It is only in retrospect in the minority who do develop psychotic illness that the term “prodrome” can be applied.

Youth Mental Health

Aftab: You’ve also been a champion of youth mental health system reform and policy initiatives, including the Lancet Commission on youth mental health. Say more about that.

McGorry: After about 10 to 15 years focused intensively on early psychosis, it became increasingly obvious that the issue for mental health reform was much broader: the vast majority of serious mental disorders have their onset in adolescence and young adulthood. We needed to shift from an early psychosis paradigm to a youth mental health paradigm.

The traditional split in mental health services, child and adolescent psychiatry ending at 18, then adult psychiatry beginning at 18, is very problematic developmentally and clinically. What we actually need is a robust, coherent system of care that spans from puberty through the mid-20s, capturing people during the peak incidence period for most mental disorders while being developmentally attuned to the distinctive challenges of the transition to adult roles and responsibilities.

Historically, this has been the weakest, most neglected part of the entire health system. Child and adolescent services were never adequately resourced or conceptually equipped to handle the serious disorders that emerge in late adolescence. Adult services, meanwhile, often only became seriously engaged once chronicity had already developed, essentially waiting for people to fail before offering intensive support. Young people fell through the gap.

So we developed Orygen as a research institute specifically focused on youth mental health, and we advocated persistently with federal and state governments to build a national system of care. In Australia, that eventually resulted in Headspace, a network of youth-friendly primary mental health centers, along with more specialized early intervention services as a “second tier” for those who need more intensive treatment. Other countries have developed variations on this model in different ways, and we tried to synthesize the broader vision and evidence base in the Lancet Commission work.

During the same decades we’ve been building this infrastructure and advocating for reform, the underlying problem appears to have been getting significantly worse. The Lancet Commission devoted considerable attention to assessing whether there’s genuinely a youth mental health crisis unfolding globally, or whether this perception reflects reporting artifacts, increased awareness, or diagnostic boundary expansion.

The data we examined looked disturbingly robust in certain settings, particularly in Australia and Denmark, where high-quality population-level surveillance has been maintained over time. The picture may not be uniform everywhere, and in low- and middle-income countries we often lack adequate epidemiological infrastructure to know with confidence. But where we have reliable data, the trends are deeply concerning.

There’s certainly a “prevalence inflation” phenomenon we have to reckon with, broadening diagnostic criteria over successive DSM editions, self-diagnosis movements facilitated by social media, increased awareness leading to more help-seeking. Some proportion of people who now believe they have a mental disorder genuinely may not meet rigorous diagnostic criteria or have a need for mental health care. That complicates interpretation considerably.

But if you look at hard data from well-designed community epidemiological surveys using consistent methodology, Australia appears to have experienced something on the order of a 50 percent increase in the prevalence of mental disorders among young people over roughly two decades, with the increase particularly concentrated in common mental disorders like anxiety and depression. That’s not an artifact, something real is happening. If prevalence genuinely is rising, you’re forced to think seriously about prevention and about the socioeconomic determinants and upstream causes of mental disorder. It becomes a public health and social policy problem.

Some governments have been eager to pin the youth mental health crisis primarily on social media and smartphone use. There are prominent public intellectuals like Jonathan Haidt pushing that narrative very forcefully. And look, I think it’s plausible that these technologies play some role. But even if that’s a contributing factor, I think broader socioeconomic and cultural megatrends are probably more powerful and more fundamental. Weakening social cohesion and community ties, worsening economic prospects for young people relative to previous generations, housing affordability crises in many developed countries, precarious employment, educational pressure and competition, climate anxiety and existential uncertainty about the future. They create chronic stress, undermine the conditions for healthy development, and erode protective factors.

Mental health is inseparable from social and economic policy. Decisions about education, employment, housing, inequality, and social infrastructure have mental health consequences that dwarf what we can accomplish through downstream clinical intervention alone. I think psychiatry has a genuine responsibility to understand and speak to these broader societal changes, not just to respond clinically after the psychological damage has already been done. We need to be engaging in prevention and advocacy upstream, not just mopping up downstream.

Aftab: Thank you!

McGorry: Thanks Awais, and I want to acknowledge that much of the research I have talked about has been the result of a team effort, with great colleagues at Orygen as well as internationally. It would not have been possible without them and they share the credit.

This Q&A is part of a series featuring interviews and discussions intended to foster a re-examination of philosophical and scientific debates in the psy-sciences. See prior interviews here.

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In “The People v. Insanity,” (The Dispatch, August 6, 2025) examines some uncomfortable questions surrounding mental illness, criminal responsibility, and society’s conflicting responses to the mentally ill, especially those who behave disruptively to a degree that they end up in legal trouble. Rensin’s primary focus is on the insanity plea, however, I am more interested in the non-legal aspects of Rensin’s analysis and the application to our social and clinical lives. Rensin makes a case that our collective discomfort with the insanity defense reflects “an ancient dilemma” that philosophers had recognized and grappled with without much success: “the mad present a problem for our moral intuitions, and we do not know, and perhaps are not even comfortable discussing, what we ought to make of them.”

To illustrate this, Rensin recounts his own psychiatric history. Beginning in adolescence, he experienced escalating psychiatric symptoms, showing signs of mania, paranoia, aggression, and eventually full-blown psychosis. During college, believing a scarf possessed mystical powers, he broke into someone’s apartment to retrieve it, leaving the occupants frightened and terrified. He heard divine commands to crash his car, which he obeyed, nearly killing another driver. Later, convinced he was being poisoned or monitored through hidden cameras, he considered stabbing his roommate preemptively and attempted self-surgery with a bread knife to remove an imagined threat from his neck.

Eventually diagnosed with schizoaffective disorder and treated with medication, Rensin reports he has achieved relative stability over the years. Yet he emphasizes that even stable, he remains “difficult, particularly to those who care about me.” His wife understands that his disorganization and poor executive function result from a psychiatric illness, but…

“Still: It exhausts her. And it frustrates her. And she can’t help getting angry with me because no matter the cause, I am making her life more difficult, and nothing breeds resentment so readily as being hurt and then being told you’re not allowed to hate it, because if you do then you’re a bigot.”

This tension extends to public encounters with the mentally ill. Rensin criticizes activists who respond to public discomfort with homeless mentally ill individuals by “simply lecturing the public about how bad and embarrassing and frankly ableist they are.” This approach, he suggests, “hardens the public’s hearts” and pushes them toward punitive solutions.

Rensin rejects the common therapeutic narrative that mental illness is a “foreign invader” separate from one’s true self. When his therapist suggested forgiving himself because his destructive behavior wasn’t his fault, Rensin calls this “the moral reasoning of a child.” Instead, he insists:

“The real me is a lunatic; the real me is unfit to live among other people. The medicated me, the stable me, is better, but it is artificial, sustained by psychopharmacology and therapeutic intervention.”1

When a friend asked how she could trust he wouldn’t stop medication or relapse, Rensin could only answer honestly: “Well, I guess you can’t.”

The political dimensions are no less uncomfortable. Conservatives advocate mass institutionalization for the severely mentally ill, yet dismiss individual criminal defendants’ insanity claims as malingering. Liberals and leftists, committed to deinstitutionalization and autonomy, respond by “pretending that mental illness never results in antisocial behavior, much less violent crime.” They repeat that the mentally ill are more likely to be victims than perpetrators, which is technically true only because “the mad are victimized so frequently that it dwarfs their more modest propensity toward criminality.” These commentators seem to be engaged in “respectability politics,” an attempt to distance relatively stable people with depression or ADHD from more troubling cases. Severely mad individuals are embarrassing to advocacy efforts aimed at reducing stigma.

The tension Rensin identifies is not with mental illness per se, but rather when mental illness coexists with and contributes to behaviors that strain and exhaust our capacities for sympathy, compassion, and care. States of mania and psychosis leading to violent crime are just one dramatic example because of the harm involved and the fears this generates. But the basic problem of dealing with someone who exhausts others and wears out their emotional capacities plays out at collective, individual, and clinical levels. At each level, we face a version of the uncomfortable truth. There is a tension between recognizing a disturbed person’s compromised agency and seeing them as deserving of compassion and care, while extending to them the roles and responsibilities we reserve for those we trust and rely on. There is a misalignment between being ill and being pro-social. There is a difference between caring for someone and living with them as an equal.

This qualification warrants repetition and elaboration. I am not talking about all or most individuals with mental health problems, psychiatric disorders, mental disabilities, “madness,” or neurodivergence, etc. I am talking about a subset of them, which perhaps is quite small but also quite real, and which finds poor representation in our public narratives in the age of destigmatization. I am also not talking about the distinction between “serious” mental illness vs other sorts of mental illness, or psychotic vs non-psychotic conditions. I am talking instead about what Rensin touches on but doesn’t fully delineate: those with mental disorders who are emotionally difficult to live with, who drive those who care for them to exhaustion and frustration, to the very limits of what they can tolerate and beyond. People with mental illness can be likeable and good-natured. I am not talking about such folks. I am also not talking about people who are perceived by clinicians to be difficult and disagreeable because, say, their problems are poorly responsive to treatment and clinicians are projecting and displacing their own frustration onto the patient. I am not talking about patients who are labelled “difficult” simply because they question or disagree with their doctors, advocate for themselves, or have complex medical needs that are being dismissed. I am talking about the ones that are genuinely challenging and vexing, the interpersonally difficult, the ones who alienate almost everyone close in their lives.

What do we owe to people who, through vagaries of genetics, upbringing, and life choices, are not just mentally ill but also difficult, unlikeable, demanding, needy… insufferable?

To have a genuine partnership requires treating the other person as a moral equal. A healthy relationship between adults presupposes things such as mutual accountability, shared agency, reciprocal vulnerability, and moral standing. When mental illness significantly impairs these capacities, partners can either maintain the fiction of equality, getting angry at behavior they cannot fully control, or adopt what philosopher P.F. Strawson called the “objective stance,” viewing the person as a malfunctioning collection of mechanisms rather than a moral agent. We can suspend our ordinary reactive attitudes toward others, treating them instead as something to be managed, contained, treated, or perhaps avoided. It is a shift from interpersonal engagement to detached clinical engagement. It can work well for some time; this is the classic “sick role,” and it allows for care and recovery. When the illness is discrete and episodic, temporary suspensions of reactive attitudes are often the right answer. But when we are dealing with behaviors that are chronic, when the recovery is partial and unreliable, there is often no good answer.

Holding someone accountable and responsible requires that they have agency, that they could have done otherwise, and that they have the capacity to recognize and respond to moral reasons. Many psychiatric conditions impair these capacities, but often only partially, intermittently, or in specific domains. This demands very difficult calibrations on the part of the loved ones. A partner must simultaneously, for example, hold the person responsible enough to maintain a genuine relationship, make allowances for impairment to avoid cruelty, protect herself from harm from behavioral disruptions and dysregulations, and accept that she cannot predict which version of him she’ll encounter on any particular day.

Paradoxically, her anger and resentment may be the only thing affirming his status as a moral agent, preventing the relationship from degenerating into just a relationship between a sick person and their caregiver. When we consistently excuse someone’s behavior, we implicitly declare them incapable of being held to our moral standards. This is appropriate for small children or people with severe cognitive disabilities but dehumanizing for an adult we are supposed to be in a relatively equal relationship with.

It is not surprising then that such patients often end up isolated and alone. And that may be alright, if they could manage things on their own, but they can’t because they are still ill and impaired. They keep ending up in emergency rooms or being picked up by the police. Anyone who can leave, leaves. The people who can’t leave or are too committed to leave (parents, wives, husbands, children), find themselves resentful and burdened, and they carry on until they can no longer, and the healthcare system or the legal system has to step in.

This is where the focus on autonomy simply sidesteps the problem. The people who just need to be left alone do well by themselves. They build a life for themselves on their own terms. But the genuinely ill and disabled usually cannot.

And then, there are situations when even mental health professionals give up on certain patients.

Psychiatrists fire them. Therapists won’t work with them. Therapy groups block them. Group homes evict them. Community mental health centers treat them with reluctance. These patients often end up in facilities defined by their inability to refuse: emergency rooms, state psychiatric hospitals, and jails. Patients get progressively worse care as they move through systems of care.

What leads even professionals to give up? Often some combination of verbal aggression and threats, sexually and racially inappropriate behaviors, constantly refusing treatment offered or available while constantly demanding help, disruption of treatment environments, and extreme neediness that leads to professional burnout and dread.

This is the uncomfortable truth of clinical practice: some patients are genuinely difficult and disagreeable, sometimes because they are mentally ill, and sometimes because that’s who they are as people and mental illness brings out the worst of them. These patients also genuinely need help, care, and treatment. Their problem is that practically no one can tolerate and put up with them for any extended period.

These are certainly extreme cases, and it’s not entirely polite or comfortable to talk about them. It is also true that our judgments about who is “likeable” or “difficult” are contaminated by all sorts of prejudice. But pretending they don’t exist only worsens the state of affairs. I remember seeing a patient once as a consult on the medical floor. The internist was convinced that she was psychotic because she had driven the nursing home staff to the end of their ropes. I spent an hour watching a competent, caring nurse trying to change her wound dressings, and this woman burned through every bit of good will. At the end of the hour, the nurse was exhausted and frustrated and done, just done. The woman was not psychotic, she was exasperating. Imagine someone in the 99th percentile of being exasperating. That was her. Unfortunately for everyone involved, she was old, weak and immobile, needed 24/7 nursing care, but no one could stand her and she seemed incapable of recognizing that and changing her behavior. Such patients end up in the long-term care facilities where their needy, irksome nature is balanced only by the deep indifference of the staff.

I think people often underestimate how powerful likeability is as a moderator of the quality of care received. Clinicians want to help people and want to be seen as helpful, and likeable patients make that easy. There is, for example, a dramatic difference in how clinicians treat likeable patients with borderline personality and unlikable patients with borderline personality.

Over the years I’ve had to pay special attention to my own feelings of frustration. Possibly some of the most productive work I’ve done is with patients where I had to recognize and work through my exasperation. That experience also leads me to think that the healthcare system gives up too easily. Healthcare systems are not designed around the prospect of providing care to deeply unlikable and unsympathetic people. They are at times designed to provide care to those perceived to be dangerous. But dangerous and difficult are not the same things, and what works for one doesn’t work for the other.

Patients at the extreme end of exasperating require clinicians at the extreme end of compassionate and tolerant. They require saints. Saints are hard to find, but institutional and structural changes can help make up for that. Current burnout and resource scarcity make the problem worse… clinicians might have more capacity for challenging patients if they weren’t already depleted. I say this jokingly, but only half-jokingly: medicine needs something analogous to SWAT teams or SEAL Team Six, not for handling the dangerous but for handling the demanding and the disagreeable that exceed the capabilities of most clinicians.2

The problem is two-fold; no one wants to really acknowledge that such people exist, and no one really wants to work with them. We run into the limits of the human substrate of medicine. (When it started becoming apparent that AI may be able to provide some forms of clinical care in the future, one of my first thoughts was: this may be a lifeline for those patients whom humans cannot tolerate. LLMs have, at least for now, near-infinite attention and patience.)

Ultimately, issues like the insanity plea and reliable provision of care to those in need are easier to solve because they involve collective responsibility and our ability to figure out how to overcome our emotional limitations to do the right thing. The interpersonal issues at the individual level are a different beast entirely. The best hope we have there is in the development of ways to prune our psyches, to soften our sharp edges enough to allow those who love us to bear with us.3

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There is a peculiar tendency I’ve noticed where people try to understand what ADHD is through the effects of stimulant medications and correspondingly there is an inverse tendency where they try to determine the scope of the appropriate clinical use of stimulants through the boundaries of ADHD as a diagnosis.

The first tendency is particular evident among critics of ADHD who often use evidence of nonspecific psychoactive effects of stimulants to argue against the reality of ADHD as a medical problem, such arguing that individuals with ADHD are just bored individuals trying to medicate their tedium or pursue some misguided ideal of enhancement (“of course you are more focused on Adderall; it’s basically meth, duh.”)

The second tendency is more obvious among clinicians who would only consider formally recognizing a person’s attentional difficulties and prescribing a stimulant if the patient can prove they meet stringent criteria and had diagnosable ADHD as a kid, and among patients who want to make a case that they stand to benefit from stimulants (or want to justify continued use) by proving that they indeed have ADHD.

Given how frequently I encounter this sentiment, it’s worth going into some detail of the mismatch between the “ADHD brain” and the “brain on stimulants.”

ADHD is not a disorder any specific brain network, but stimulants have specific effects on brain networks

A recent blockbuster study in Cell provides a good starting point for this discussion. “Stimulant medications affect arousal and reward, not attention networks” by Benjamin Kay et al. (2025) is a rigorous study showing that stimulants change functional connectivity of brain in networks associated with arousal, in networks associated with salience and reward, but they do not affect canonical attention networks, regardless of whether the person has ADHD.

The first thing to appreciate is the discrepancy between the clinical vs cognitive psychological meaning of “attention.” explains it beautifully in his discussion of the study on his substack, so I’ll just quote him:

“Now onto the second issue: “attention”. This word means different things in different contexts. In ADHD diagnostic criteria, “inattention” means not staying on task, getting distracted, forgetting instructions. These are problems with sustained engagement and persistence. By contrast, in cognitive psychology, attention refers to selective amplification of relevant information, like covertly allocating processing resources to a small patch of visual space (e.g. in a Posner cueing task; see figure below) or selectively increasing focus to one out of several conversation in a crowded room without actually moving your head (the cocktail party problem). That is not what people refer to when they are discussing “attention” in ADHD.

The imaging results therefore line up pretty nicely with the clinical meaning of attention in ADHD, which is about sustained engagement rather than selective processing. Whether stimulants actually help with selective attention in the cognitive psychology sense is not particularly clear because we lack sufficiently high powered studies looking at it from that perspective. That said, it is also unclear whether people with ADHD have selective attention deficits beyond those related to arousal and task engagement. Maybe a subset exists, but that hasn’t been demonstrated empirically as far as I’m aware.”

Let me put it in a different way. Stimulant medications do not directly influence the canonical attention networks (dorsal and ventral attention networks and frontoparietal network), but neither is ADHD a disorder of attention networks. ADHD has no special relationship to attention networks. Or to reward/salience networks, for that matter. In fact, ADHD is not definable as a disorder of any specific brain network at all, even though it involves subtle, distributed connectivity differences across the whole brain.

Take Figure S6 from the Cell paper

This type of diagram is called a connectivity matrix and it shows statistical relationships between brain connections and some variable of interest. The figures here are intended to distinguish acute stimulant effects on brain connectivity from effects of ADHD diagnosis plus any effects of chronic stimulant use.

Panel A represents children prescribed stimulants but who didn’t take them on scan day. The connectivity pattern is mostly noisy and random with no clear structure. There is no clear brain “fingerprint” of brain connectivity in ADHD kids off medication.

Panel B represents children prescribed stimulants and who took their medication on scan day. There is a clear pattern here, particularly a clear blue square in the salience/motor network regions.

Panel C is about ADHD × stimulant interaction, testing whether stimulants affect ADHD brains differently than non-ADHD brains. The pattern is again relatively weak/noisy with no strong structured effects. This means that stimulants produce similar neural effects regardless of ADHD diagnosis, and the therapeutic benefit in ADHD may come from the same brain circuit changes that occur in everyone, but these changes may be more functionally relevant for people with ADHD.

Consider this connectivity matrix from the 2024 paper, “Cumulative Effects of Resting-State Connectivity Across All Brain Networks Significantly Correlate with Attention-Deficit Hyperactivity Disorder Symptoms” in the Journal of Neuroscience:

Figure 3A above shows all brain connections associated with ADHD symptoms, and it shows relatively diffuse, weak patterns with no dramatic focal effects of the sort seen with stimulants. Figure 3B (brain surface map) shows reasonably widespread contribution across multiple networks to the ADHD polygenic risk score, suggesting ADHD is associated with brain-wide connectivity differences. In the same paper, researchers also identify the most predictive connections, which form a distributed pattern across networks.

I am sharing all this to reinforce: ADHD is not a clinical syndrome associated with characteristic alterations in attention networks or salience network or some other specific network. It involves subtle, brain-wide differences in connectivity. It is not yet clear whether there are any distinct subtypes of ADHD that correspond more strongly to specific brain networks.

Stimulants, on the other hand, have a clear pattern of effects on brain circuit connectivity. They change functional connectivity in action regions consistent with arousal, in salience regions consistent with reward, reverse the behavioral and brain effects of sleeping less, but they do not affect canonical attention networks.

Stimulants make boredom tolerable and help undertake unrewarding tasks (the paradoxical calming effect)

Stimulants increase effort, persistence, alertness, and perceived reward, and their beneficial clinical effects seem in part to arise from sustaining engagement with tedious or unrewarding tasks. This also helps explain the paradox that stimulant medications that otherwise increase psychomotor activity reduce hyperactivity in ADHD.

Benjamin Kay and colleagues write in the Cell paper,

“The seemingly paradoxical effect that stimulants can reduce hyperactivity may instead be related to their dopaminergic effects on salience processing. The second largest stimulant-related differences in FC were in SAL/PMN, which together are thought to encode anticipated reward/aversion and thus influence the decision to persist at a task or switch to a more rewarding task. Aspects of ADHD hyperactivity could be associated with searching for more rewarding actions and thus better understood as motivational rather than motoric. We hypothesize that stimulants reduce task-switching and thus appear outwardly to facilitate attention by elevating the perceived salience of mundane tasks (e.g., math homework) through their effect on SAL, boosting persistence and effort without affecting cognitive ability.”

Stimulant medications make boring tasks (like math homework, spreadsheets, laundry) feel more important and worthwhile. This helps people stick with these tasks longer and put in more effort. Mundane tasks feel more worth doing, so people are less likely to abandon them for something more interesting.

This framing can appear to downplay the therapeutic significance of stimulant medications for some readers. It is worth emphasizing that stimulant medications show associations with positive clinical outcomes in the treatment of ADHD that other psychiatric medications can only dream of. In various observational and cohort studies, treatment of ADHD with stimulants reduces accidental injuries, traumatic brain injuries, substance abuse, educational underachievement, bone fractures, sexually transmitted infections, criminal activity, teenage pregnancy, and mortality.

ADHD x Stimulant Clinical Interactions

In the Cell paper, children with ADHD on stimulants demonstrate cognitive performance that is significantly better than their unmedicated ADHD peers and comparable to healthy children. Their school grades improve to match those of children without ADHD, and they show significant improvement on both the NIH Toolbox (a battery of cognitive abilities) and n-back task (a specific working memory test) accuracy measures, reaching the performance level of healthy children. Like all children taking stimulants, they also exhibit faster reaction times on the n-back task. Stimulants also appear to rescue the negative effects of insufficient sleep on academic grades in this group.

Children with ADHD who are not taking stimulants, their cognitive performance is significantly impaired across multiple domains. School grades are substantially worse than their peers, and they score significantly lower on the NIH Toolbox. Their accuracy on the n-back working memory task is also significantly reduced. Their reaction times on the n-back task show no significant difference from healthy children.

Children who are taking stimulants but do not meet stringent criteria for ADHD show the distinctive pattern of brain connectivity changes with stimulant treatment without corresponding cognitive improvement on NIH Toolbox and n-back. Despite stimulant-induced brain changes in arousal and salience/reward networks, their cognitive performance shows no improvement over healthy children not taking stimulants. School grades, NIH Toolbox scores, and n-back accuracy all remain unchanged. The only measurable difference is a faster reaction time of approximately 100ms on the n-back task, an effect shared by all children taking stimulants regardless of ADHD status. This replicates something we already know, stimulants are not cognitive enhancers in healthy individuals.

Healthy children not taking stimulants serve as the baseline reference group, demonstrating “normal” performance across all cognitive measures. Within this group, sleep duration emerges as a significant factor affecting performance. Children who obtain more than 9 hours of sleep per night perform significantly better on school grades, NIH Toolbox scores, and n-back accuracy compared to those with less sleep.

Clinical benefits of stimulants therefore depend on baseline status. For children with ADHD, stimulants have a clear therapeutic effect, “normalizing” their performance to the level of healthy peers across multiple cognitive domains, despite the absence of a normalizing effect seen in brain connectivity patterns. In contrast, non-ADHD children show no cognitive enhancement beyond typical performance levels (stimulants are not “smart drugs”). Stimulants can temporarily compensate for the cognitive effects of inadequate rest, though this should not be viewed as a replacement for proper sleep. All children taking stimulants, regardless of ADHD diagnosis, respond approximately 100ms faster on the n-back task.

Take this 2008 study in Journal of Clinical Psychiatry by Biederman and colleagues. They compared three groups of people on various thinking and attention tasks. People with ADHD not taking stimulant medication. People with ADHD actively taking stimulant medication. People without ADHD (the comparison group).

People with ADHD who weren’t taking medication scored worse than people without ADHD on almost everything tested:

• Overall performance

• Working memory (holding information in your mind)

• Interference control (ignoring distractions)

• Processing speed (how quickly you think)

• Sustained attention (staying focused)

• Verbal learning (remembering words and language)

People with ADHD who were taking stimulants still scored worse than people without ADHD on some things: overall performance, interference control, processing speed.

People with ADHD on medication scored better than those not on medication in two specific areas: sustained attention and verbal learning.

The details vary from study to study, but I think this overall pattern is important: Stimulant medications help people with ADHD improve their ability to stay focused. However, people with ADHD continue to have difficulties in many areas of their cognition that are not remedied by stimulants. There is more to ADHD than is what is addressed by stimulants.

My reading of the literature is that ADHD is heterogeneous in terms of neuropsychological profiles, with executive dysfunction being one important component but not a universal or defining feature of the disorder.

Not all individuals with ADHD show the same pattern or degree of impairment. Some even show no measurable cognitive deficits on standard tests (what’s going on there!). Complex attention tasks (sustained attention, vigilance) and working memory show the most reliable group differences. Traditional executive function tests (set-shifting, planning, inhibition) show inconsistent group differences across studies. Neuropsychological deficits in ADHD overlap substantially with other psychiatric conditions.

This is why clinical consensus is that neuropsychological assessment is neither necessary nor sufficient for ADHD diagnosis, and the “gold standard” for diagnosis remains a clinical assessment based on formal diagnostic criteria rather than neuropsychological testing.

The Anxious Adult with Attention Deficit

It is common for psychiatric clinicians these days to encounter adults who show a clinical picture of generalized anxiety and elevated neuroticism along with focus and attentional difficulties that resemble ADHD. Most of them were never diagnosed with ADHD as children, and often, the retrospective reports of childhood attentional problems aren’t that compelling either. And yet, many of them are genuinely impaired from focus difficulties, the focus difficulties persist despite adequate anxiety and mood treatment, and appear to benefit from stimulant medications.

This is related to what some folks call “anxious ADHD,” a hypothesized subset of individuals with a form of ADHD where anxiety is the primary subjective experience because executive dysfunction creates chronic stress and a perceived inability to cope.

The anxious adults with attention deficit who improve on a stimulant may genuinely have a profile of neuropsychological deficits with childhood onset but they could also just have attentional symptoms that respond to nonspecific motivational and arousal effects regardless of neurodevelopmental history. Stimulants improve alertness, motivation, and engagement in most people regardless of ADHD (although objective improvements on neuropsychological testing seem to be restricted to ADHD folks; most of the time, we are not testing that in the clinic, we are relying on perceived improvement). So a positive response to stimulants doesn’t confirm “ADHD,” but genuine clinical benefit from stimulants also cannot be dismissed just because the problem didn’t originate in childhood.

A situation like this represents several possibilities:

• Our current diagnostic criteria poorly capture the genuine diversity of ADHD presentations.

• There are transdiagnostic attentional deficit syndromes with or without neurodevelopmental onset.

• Neurotypical people, or neurodevelopmentally intact individuals, can genuinely experience impairment from increased attentional demands that respond favorably to stimulants, and right now we don’t have a way of talking about them diagnostically.

• Anxiety, mood, or memory symptoms are being misrepresented, misinterpreted, or misdiagnosed as primarily attentional symptoms.

I have suspected each of these possibilities at one time or another in different patients.

The Adult ADHD Perplexity

In the famous Moffitt et al. (2015) Dunedin study, most adults with ADHD at age 38 did not have diagnosed childhood ADHD. Adult-onset group showed significant functional impairment, but adult-onset group did not have neuropsychological deficits on testing.

In words of the authors,

“As expected, childhood ADHD had a prevalence of 6% (predominantly male) and was associated with childhood comorbid disorders, neurocognitive deficits, polygenic risk, and residual adult life impairment. Also as expected, adult ADHD had a prevalence of 3% (gender balanced) and was associated with adult substance dependence, adult life impairment, and treatment contact. Unexpectedly, the childhood ADHD and adult ADHD groups comprised virtually nonoverlapping sets; 90% of adult ADHD cases lacked a history of childhood ADHD. Also unexpectedly, the adult ADHD group did not show tested neuropsychological deficits in childhood or adulthood, nor did they show polygenic risk for childhood ADHD.”

Similar pattern has been found in other studies. Majority of ADHD adults do not have childhood diagnoses but they show comparable impairment to ADHD adults with childhood diagnosis.

Critics of the idea that adult ADHD can genuinely have an onset in adult tend to argue that “late-onset” cases may represent childhood subthreshold ADHD that progresses to full syndrome subsequently, many individuals in the late-onset group do show some ADHD symptoms in childhood, and that higher IQ and supportive environments can mask symptoms in childhood, with decompensation occurring with demands of adulthood.

So the psychiatric community is divided along 3 camps, so to speak.

• Childhood-onset ADHD and adult-onset ADHD are distinct syndromes, and only the former is neurodevelopmental in origin.

• Most late-onset ADHD cases are instances of delayed expression of subthreshold childhood ADHD or delayed recognition of childhood-onset ADHD.

• Age of onset criterion is unreliable and of uncertain clinical significance anyway. Clinicians should focus on current symptoms and impairment. Treat what’s clinically present.

DSM doesn’t currently recognize adult-onset ADHD, so clinicians who want to diagnose by the book either have to ignore the attentional impairment and continue treating anxiety and mood, or they have to look really hard for and overinterpret evidence in support of childhood ADHD.

I am partial to the third view, the pragmatic clinician camp, while acknowledging that the true relationship between adulthood ADHD and childhood ADHD is a matter for science to clarify. Adults who show ADHD symptoms without clear-cut childhood onset are still impaired, and stand to benefit from treatment. I do not think we should let patients suffer while our formal classification systems play catch-up with clinical realities.

The Venn diagram of ADHD and stimulant use is not a circle

Stimulant medications have therapeutic effects that go beyond ADHD. Some of these therapeutic uses are already formally recognized. Stimulant medications are used in sleep disorders such as narcolepsy. They can be useful in geriatric depression as well as depression with residual fatigue/anergia. They can be useful in various neuropsychiatric disorders with prominent apathy, fatigue, or focus difficulties.

There are situations where clinical use of stimulants is clearly inappropriate, but neurodevelopmentally intact people experiencing genuine impairment from excessive and inescapable attentional demands also constitute a clinical grey area that the profession seems hesitant to talk about. It brings its own ethical challenges… what to do about situations where people are overwhelmed by the requirements of work in the post-Fordist era? What to do about “Mother’s Little Helper” type scenarios? What about people trying to survive in time-pressured work environments? Or those trying to use stimulants to cope with chronic sleep deprivation? Or those so depleted by anxiety and stress that they have no motivation left for unrewarding tasks on which their survival depends? And yet, amidst all these clinical dilemmas, we also show a certain hypocrisy: we do not withhold SSRIs from people who experience impairment from increased emotional demands. The diagnostic criteria for depression are oblivious to context.

My allegiance is not to diagnostic manuals; it is to my patients. I am not doing my job well if I refuse to recognize distress and impairment that can be addressed via appropriate clinical interventions. But what I do not want to do is provide that help under false pretenses. I don’t want to say someone has a neurodevelopmental disorder when they don’t so that they can access a medication that they can benefit from.

The Venn diagram of ADHD and stimulant therapeutic effects is two overlapping circles. And yet there is tremendous pressure in clinical practice to treat those circles as coinciding.

The clinical use of stimulants beyond ADHD (and a handful of other diagnoses) is an uncharted territory from the vantage of “evidence-based medicine.” There is little we can say with confidence or certainty. And yet, countless clinicians and patients have been operating in this territory for a long time while having to pretend they are still in the charted ADHD territory. Because of our ridiculous moralism around stimulant medications and diagnostic conservatism about attentional problems, we have become unable and unwilling to recognize clinically significant distress and impairment in all its shapes and forms.

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Dr. Robert Haim Belmaker is an Israeli psychiatrist and was the Hoffer-Vickar Professor of Psychiatry at Ben-Gurion University of the Negev, Beersheva Israel (holding the first named Chair of Psychiatry in Israel) until his retirement and is now Emeritus. He opened a public Bipolar Disorders clinic 40 years ago and continues to see patients at his private practice in Modiin, Israel. He has received numerous awards and honors over the course of his career, including the National Alliance for Research on Schizophrenia and Depression Lifetime Achievement Falcone Award for research in mood disorders (2000). He was the President of the CINP 2008-2010 (International College of Neuropsychopharmacology). He is the author, with Pesach Lichtenberg, of the 2023 volume “Psychopharmacology Reconsidered - A Concise Guide Exploring the Limits of Diagnosis and Treatment” (Springer).

A wave of critical psychiatry in its moderate and thoughtful form, epitomized by Awais Aftab’s column, has engaged with many entrenched myths of the profession, whether these are ideas of neurotransmitter deficiencies or simplistic notions that decoding the human genome would uncover the essences of psychiatric illness. One of the still-remaining and rarely touched psychiatric shibboleths has been my personal anguish in recent years, the idea that lithium is the “gold standard” treatment for bipolar disorder. In 2025, I wrote about this issue in detail in an academic paper for a special issue of Pharmaceuticals celebrating the 75^th anniversary of lithium as psychiatric therapy, and I write now to share my perspective with the readers of Psychiatry at the Margins.

I participated in one of the first groups to use lithium in the United States in 1971 while a medical student at Duke University Medical School, where my teachers had an Investigational New Drug (IND) application for the as-yet unapproved use of lithium. In 1972 I went to NIMH as a psychiatric clinical associate. The environment was full of excitement about the promise of neurochemistry in psychiatry and I rapidly became enthusiastic and optimistic. I acquired training in clinical trials and the belief that controlled clinical trials were the only key to any real knowledge of psychopharmacologic treatment. I also acquired neurochemical laboratory skills in a lab affiliated with Nobel Prize-winning Julius Axelrod who made famous discoveries about monoamines. Lithium and bipolar disorder were one of the key interests of the enthusiastic NIMH psychiatrists because it is a simple ion that has a profound effect in bipolar disorder. The ethos was that if we could understand the neurochemistry of lithium we would unravel the neurochemistry of bipolar disorder. Bipolar disorder at the time had been diagnosed in the US much less frequently than schizophrenia whereas in Kraepelinian Europe the ratio was the other way around. Fred Goodwin at NIMH did studies of lithium in highly psychotic manic patients and found that many of them responded to lithium. He promoted the concept that affective symptoms, when present with a remitting clinical course, were a reliable predictor of lithium response, even in highly psychotic patients. His work influenced subsequent revision of DSM to widen the diagnosis of bipolar disorder and to increase enthusiasm for the new drug lithium that was approved for use in the US in the ensuing years.

On coming to Jerusalem in 1974, I fully embraced the NIMH model of working both in a clinical research unit and an adjacent psychopharmacology lab. My collaborator Richard Ebstein, a Yale-trained neurochemist, gave our work considerable gravitas. I inherited a lithium clinic that had been founded by Elliot Gershon who later went onto a career in American psychiatric genetics. For ten years in Jerusalem and for twenty-five years thereafter in Beersheba, I maintained a personal weekly Lithium Clinic maintaining hundreds of patients. We came upon an idea that lithium might work by inhibiting adenylate cyclase, the enzyme that converts ATP into cyclic AMP. Cyclic AMP had recently been found to be the second messenger system for many neurotransmitters. Lithium has been reported obscurely to inhibit this enzyme and we thought that this could fit a monoamine-based theory of mania. It worked and we followed up the leads from this exciting finding for almost a decade.

Meanwhile, in our clinical research I was eager to test Fred Goodwin’s idea that lithium response could define manic depressive illness (which is what we then called bipolar disorder). Collaborating with Joeseph Biederman who went on to become a distinguished Harvard professor of child psychiatry in later years in Boston, we treated all acute psychiatric admissions with standard antipsychotic (haloperidol) treatment. In addition, they received in a randomized fashion either placebo tablets or lithium tablets. Blood lithium was measured weekly and the results reported to a technician who made up false lithium levels for those who were taking placebo. The results were contrary to our hypothesis and were published in the Archives of General Psychiatry in 1979. Lithium added benefit across the whole range of acute psychoses as an additive to dopamine blocking antipsychotic medication. There was no clear boundary between excited schizophrenia, schizoaffective mania, psychotic manias with mood incongruent symptoms, psychotic manias with mood congruent symptoms, and non-psychotic manias. The first seeds of doubt for me were planted about the idea that lithium was specific to bipolar disorder.

In the lab doubts also arose about whether lithium could really be acting on adenylate cyclase as its mechanism of action. Adenylate cyclase is ubiquitous in the body and its inhibition should affect almost every conceivable neuroendocrine and neurotransmitter process. We tried to find whether some adenylate cyclases were more sensitive to lithium but made little progress. In the early 1980s Sir Michael Berridge from Oxford received the Wolf Prize in Jerusalem for his findings that lithium inhibits an entirely different enzyme, inositol monophosphatase and lowers the concentration of an important second messenger precursor in the brain, inositol. I was invited to the ceremony at the Knesset and was deeply impressed. By coincidence, an important contributor to the inositol and lithium field was Bill Sherman, Professor in the Psychiatry Department at Washington University in St. Louis, where my wife’s parents lived. I was able to do a two-month sabbatical with Bill Sherman and tooled myself up for studying this new theory of lithium action, the inositol depletion hypothesis.

By this time I had become Professor and Chairman of Psychiatry at Ben Gurion University of the Negev in Beersheva. I continued to maintain a weekly personal lithium clinic seeing patients who had been hospitalized at least once for bipolar disorder and who were being followed up for lithium prophylaxis. When I first started in Jerusalem in 1974 I had the flame spectrometer in its most primitive version in my own office and I took blood and measured lithium levels myself getting a result with the patient still in the room. My patients were almost all on lithium monotherapy. By 1982 I organized the International College of Neuropharmacology (CINP) meetings in Jerusalem. I met there Hinderk Emerich, a German psychiatrist who had serendipitously noticed that valproate, which had been used as an antiepileptic and sedative, was also effective in bipolar disorder. Charles Bowden in the USA took up this idea after Abbott Pharmaceuticals achieved a patent for the derivative divalproex sodium. (Divalproex sodium dissolves in the stomach into valproate and in blood is measured as valproate and has no conceivable scientific advantage over valproate). Bowden conducted a large commercial multi-center clinical controlled trial with a lithium arm, a valproate arm and a placebo arm. He did studies both in acute mania and in prophylaxis. Valproate was at least as good as lithium. It was then reported that Okuma in Japan (in Japanese) that a controlled trial of carbamazepine, another antiepileptic, was effective in the prophylaxis of bipolar disorder. His results were rapidly taken up by Bob Post at NIMH and carbamazepine was studied and introduced for bipolar disorder in most countries. While I was reluctant at first to abandon my belief in lithium as monotherapy, clinical needs pushed me to reality: Many of my patients had relapses on lithium and did better when valproate or carbamazepine was added. Some patients developed intolerable lithium side effects and we found that we could manage their bipolar disorder by switching to valproate or carbamazepine. Some patients did not want to start on lithium treatment because they did not want frequent blood testing and we started them on valproate or carbamazepine instead because the anti-epileptics required less frequent blood testing. Many patients seemed to do as well as the patients on lithium or as well as they themselves had done on lithium. In 2010 we reluctantly published our results, called the New Lithium Clinic, where only about a third of patients were taking lithium monotherapy. Many were taking valproate or carbamazepine monotherapy, but even more were taking lithium/valproate combination, lithium/carbamazepine combination therapy or even lithium/carbamazepine/valproate triple therapy. Bob Post dignified this by calling it rational polypharmacy. This gave us some comfort as we did not want to be confused with the sloppy polypharmacy that we had criticized so much at the beginning of the psychopharmacological revolution.

Back to the lab we rushed to see if we could find any biochemical common denominators of lithium, carbamazepine and valproate. If they were all mood stabilizers in bipolar disorder, Occam’s Razor would suggest that we could find their mechanism of action by finding some common mechanism. Inspired by Husseini Manji, whom I met at NIMH on a visit in 1983 and who led this field, we spent some effort on enzymes like protein kinase C which might have been affected by all three compounds. However, nothing specific emerged. Valproate and carbamazepine had no effects of the kind that lithium had on the phosphatidylinositol system. In 1995 Manji participated in a conference I organized in Jerusalem on the mechanism of antibipolar drugs. Husseini went on to become Global Head of Neuroscience Research at Johnson & Johnson. A conclusive common mechanism of action of these three mood stabilizers has yet to emerge.

In the clinical treatment of bipolar patients, the rug was pulled out from under the lithium monotherapy clinic by the development of second-generation antipsychotics. I had become active in the International College of Neuropsychopharmacology beginning in 1978 and joined the council after the 1982 meetings in Jerusalem and was President 2008-2010. This position allowed me to visit many countries outside of the US and Israel. Lithium was rarely available in Asian, Latin American, African countries or Soviet bloc countries because of the absence of access to frequent blood monitoring. First generation antipsychotics, especially in injectable long-lasting form, were the mainline treatment for all recurrent psychoses including those who were clearly affective and even bipolar. I assumed (mea culpa) that results were poor or that side effects were intolerable and that Western standards of course were superior. No textbook of psychiatry mentioned first generation antipsychotics as options for bipolar disorder prophylaxis. When I corresponded about this with several textbook editors, I was told that the question was uninteresting because tardive dyskinesia would in any case prevent a trial of such compounds. When second generation antipsychotics became available after clozapine showed the way, our center participated in some of the early commercially sponsored multi-center trials of risperidone and olanzapine in one or more than one of the phases of bipolar disorder. Second generation antipsychotics rapidly proved themselves to be effective treatments for all phases of bipolar disorder. While all these compounds called second generation antipsychotics have complex pharmacologies, all block dopamine receptors. Moreover, a few small but convincing studies have gone back to show that first generation injectable long-acting antipsychotics are also prophylactic in bipolar disorder as well as being clearly anti-manic as monotherapy. Second generation antipsychotics were rapidly added to our armamentarium in the “New Lithium Clinic” and are now routinely used either on a continuous basis together with lithium, valproate and carbamazepine for prophylaxis for bipolar disorder or as immediate supplementations upon the appearance of manic or depressive symptomatology in a bipolar or schizoaffective patient taking lithium or an anti-epileptic mood stabilizer.

In the lab we had spent an exhilarating decade studying the inositol depletion hypothesis but came to a dead end. In light of this failure, we shifted to a new theory of lithium action first proposed by Klein and Melton in 1996 and called the glycogen synthase kinase 3 beta theory of lithium action. Like adenylate cyclase and inositol monophosphatase, GSK3b is a ubiquitous enzyme in the body but its inhibition by lithium seemed exciting and promising. We shifted our resources in the lab to studying this new enzyme. Some of the published findings we simply could not replicate. This could be part of a well-known phenomenon and the subject of many recent books and articles dealing with the difficulty of non-replication in biological sciences, psychological sciences and particularly in neurochemistry and neuropharmacological systems. More relevant to our story here is the fact that lithium inhibition of GSK3b rapidly became just one of the effects of psychiatric drugs on GSK3b. GSK3b is also affected by antipsychotic drugs and many drugs in different ways, places and time courses. It is not, to my knowledge, affected by valproate and carbamazepine; so it is not the Occam’s Razor that we were looking for that could be a common mechanism of action for all mood stabilizers. (GSK-3beta is also important in cancer research).

As the complexities of treatment of bipolar disorder increased, I feel more and more effective as a clinical psychiatrist in treating bipolar disorder. I have many tools, not just one: lithium. I could offer patients choices. I could offer patients who failed lithium many choices. I could offer patients who respond to lithium but who had milder relapses than they had before lithium a polypharmacy approach. I began to have experiences with patients who were referred to me after the treatment of a manic episode in hospital with risperidone or olanzapine and who did not want to go onto lithium with its blood tests. These patients have often done very well even on small maintenance doses of 2.5 mg olanzapine or 1-3 mg of risperidone. I also noticed that the exact DSM diagnosis did not predict response to lithium vs. carbamazepine vs. valproate vs. second generation antipsychotic in my practice. Some patients reached me with a diagnosis of schizoaffective disorder or SSRI-resistant depression and responded well to lithium.

I was thus taken aback to see in 2023 an editorial in Bipolar Disorders declaring that lithium is still the gold standard in the treatment of bipolar disorder. It encouraged me to reread the literature that I thought I had been reading. I could not find a single study or meta-analysis finding lithium superior to valproate or carbamazepine in bipolar disorder. One could evaluate quality of evidence, or perhaps decide that there are more studies of lithium than the others, but that is an odd kind of epistemology in my opinion. The strongest statement of our literature, in my opinion, are the network meta-analyses of Kishi et al (2021; 2022). A meta-analysis allows researchers to combine the results of many controlled trials, say of lithium vs. valproate, that use different measuring instruments and different sample sizes into one overall measure. In our field there are meta-analyses that compare lithium to valproate, and those that compare lithium to second generation antipsychotics etc. However, a network meta-analysis allows the researcher to combine studies that compared A to B with those that compared B to C with those that compared C to D with those that compared D to F. The meta-analysis then allows the researcher to compare A to F, even if there were few or no studies directly comparing A to F head-to-head. These meta-analyses show absolutely no overall superiority of lithium to any of the other treatments of bipolar disorder aforementioned. This does not rule out the possibility that there are some individuals who only respond to lithium. This is clearly true. However, there are some bipolar disorder patients who respond only to valproate or only to carbamazepine and, heaven forbid, there are some clearly bipolar disorder patients who do absolutely best on olanzapine, risperidone or another second-generation antipsychotics.

Several large observational and nationwide cohort studies have found that people with bipolar disorder taking lithium have lower rates of rehospitalization. However, the picture isn’t entirely clear-cut in my assessment. The advantage over other medications tends to be weak and of uncertain clinical significance, and in many cases, lithium doesn’t statistically separate from other mood stabilizers or antipsychotics when you look at the data. Plus, this benefit isn’t unique to lithium, we see similar results with other treatments, like long-acting injectable antipsychotics.

There’s also ongoing debate about lithium’s relationship with suicide risk. Some research suggests fewer suicide attempts and deaths among lithium users, but it’s not certain this is directly due to the medication itself. It’s possible that what we’re seeing is partly a side effect of the regular blood tests lithium requires, these frequent check-ins mean patients on lithium get more consistent medical monitoring, which could be protective in its own right, or that the blood test requirements self-select for certain sorts of patients. I have no problem with suicidality risk being a positive consideration in the choice of lithium treatment in patients if clinical use of lithium is otherwise indicated. But the hype around this has led to the misguided use of lithium in the population of chronically suicidal patients and patients whose suicidality is related to personality disorders, substance use, and chronic pain.

Why is it then that there seems to be a movement in academic psychiatry to reaffirm the concept, in my own view long dead, that lithium is the gold standard specific treatment for bipolar disorder?

The answer is not pharmaceutical company backing. Lithium is not patentable and no company has funded large clinical trials or paid for promotion of lithium as a treatment (an exception might be some delayed release formulations of lithium). Pharmaceutical companies have sometimes benefited indirectly from lithium’s academic halo by funding symposia at academic psychiatry meetings focused on their own new antibipolar compounds, be it Abbott’s Divalproex or Lilly’s olanzapine. They include a lecturer on lithium as an academic proof of the seriousness of their compound even if the symposium is completely oriented in a commercial way to the new compound. What then could be the reason why so many papers have been published in the last decade lamenting the declining use of lithium and claiming that lithium is still the gold standard for the treatment of a DSM-definable illness called “bipolar disorder”? It seems that these authors have not realized that bipolar disorder itself is a highly heterogenous concept whether looked at genetically, phenomenologically or prognostically. The effect of these declarations of the gold standard is to make the clinical psychiatrist in the field and the resident in the emergency room confused and feel inferior. It is a kind of town-gown conflict of the old times when I studied at Harvard College 1963-1967 where the students of the elite university looked down on the residents of the city. Academics who deal with data analysis, laboratory research summaries and meta-analyses love lithium. The resident in the emergency room has a much more difficult choice to refer a patient to lithium without taking many economic and logistical issues into account. Highly psychotic, violent, overactive manic patients in the inpatient service are almost never treatable with lithium in today’s short stay reality and short-staffed psychiatry wards. Injectable antipsychotics are a frequent necessity. When the patient is discharged and prophylaxis is considered, sometimes it is easiest to remain on the same second-generation antipsychotic that the patient started in his inpatient mania. Lithium should certainly be considered in some patients who have poor prophylaxis or side effects from antipsychotics: valproate and carbamazepine should also be considered.

The academic hubris mentioned above is complicated in those academic psychiatrists who also do biochemical research. We have held our flag up for 75 years that we have a simple compound that can fix a complicated illness. We have erred. This may be a simple chemical element but it is hugely complicated in its biochemical effects, as complicated as valproate, carbamazepine and olanzapine. Moreover, it has serious long term side effects on the kidney and the parathyroid, side effects that are no less serious than the tardive dyskinesia of the first-generation antipsychotics or the metabolic side effects of second-generation antipsychotics. Lithium is one of our tools but has no special status. The search for a specific biochemical effect of lithium that could then unravel the cause of bipolar disorder has been a fruitless search. So far, the Occam’s Razor approach of finding a common denominator of the antibipolar armamentarium has also led us nowhere. Apparently, mental illness is highly heterogenous, highly complex and we need a more trial-and-error empirical relationship to find the right treatment for the right patient. This approach de-emphasizes the role of specific clinical trials that recruit specific DSM diagnoses with a monotherapy treatment. Such trials are demanded by the FDA but they produce knowledge that is not relevant for most clinical work or at least not entirely adequate for clinical work. The true clinical work goes on in a doctor/patient relationship where a doctor sees a patient over time and can compare the clinical results with one treatment and then another treatment and then a combination of treatments and find thereby the right treatment for the right patient. Precision medicine, where perfect treatments can be predicted in advance, would be wonderful but so far there are far many more articles written on the subject than patients who have been helped by it. We must accept that there is an imperfect relationship between diagnosis and treatment in psychiatry. Examples: antidepressants are useful for anxiety and OCD as well as depression and can sometimes help depressive symptoms in schizophrenia. Lithium in bipolar disorder is no exception to this heterogeneity and non-specific approach. The continued halo has misled our field into a great excess of articles with titles like “Lithium in immortalized white blood cells affects gene transcription of gene x.” Such papers make big waves but should never be accepted without a comparison group of valproate, carbamazepine and olanzapine which may do the same thing in at least one or two other genes which may be experiencing the same effect. In 2004 in the New England Journal of Medicine I proposed a theory of the history of lithium research. I found that in 1970s when monoamines were all the rage in neurochemistry, scientists reported lithium effects on monoamines; on the 1980s when second messengers were all the rage, scientists reported lithium effects on second messengers; in the 1990s when third messengers were all the rage, scientists reported lithium effects on third messengers; in 2000s when neuroprotection was all the rage, scientists reported lithium effects on neuroprotection. These reports were barely replicable by other laboratories. If they were replicated, they never led to further mechanistic understanding. Some of the effects were never disproved but merely abandoned when scientists went on to the new framework of the day.

Lithium will always be an important tool in the armamentarium of the clinical psychiatrist. The percentage of patients taking lithium is not and should not be equal to the percentage of the population diagnosed with bipolar disorder but will vary according to the alternative medicines available, the socioeconomic framework of medical care in particular countries, cities and settings and the preferences of individual patients for different potential side effects of the different drugs. It is time for academic leadership in psychiatry to learn from what’s going on in the field rather than only criticizing it.

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What should we make of the idea that a psychiatric crisis can save someone’s life? Depression immobilized Tyler Alterman for over a year, leaving him barely able to get off his mattress. A decade later, he describes feeling “regularly grateful” for that period of severe depression, claiming it saved his life. Jazmine Russell experienced a terrifying psychotic episode in 2015 that she also later credits with saving her life. Both are powerful stories and testimonies. Both challenge conventional psychiatric thinking about mental illness as unambiguously bad events; both raise difficult questions of how we interpret psychiatric crises and their role in people’s lives.

I came across Tyler Alterman’s story on X/Twitter (Oct 24, 2025, discovered thanks to Cooper Davis). I am not reproducing the entire post here, but you should read his story in his own eloquent words. Alterman describes pushing himself into “a life that was terrible for me, like a person smashing themselves into a wall.” He reports that his “self” sent escalating warnings, first a sense of wrongness, then exhaustion, all of which he ignored. When healthy habits like exercise, meditation, and therapy only provided “energy to smash myself against the wall again,” his depression progressed to complete immobilization.

For over a year, he could barely leave his mattress. At the time, believing his only value came from his ability to contribute, he experienced suicidal ideation. He now reinterprets this as “a desire for the self-harming version of myself to die.” His depression eventually lifted without psychiatric intervention, and he credits the immobilization as a necessary step that prevented continued self-destruction and enabled the incredible life he has today.

Alterman distinguishes between depression that responds to lifestyle interventions and depression that resists them because “these healthy habits will only give a person more energy to throw themselves back into an unhealthy job, relationship, identity.” He cautions against judging people for “not wanting to get better,” suggesting their resistance may actually be self-protective.

is a mental health educator, host of the Depth Work Podcast, and a co-editor of the 2024 volume Mad Studies Reader. She describes her story in this substack post (Nov 5,2025). Working as a crisis counselor while carrying unprocessed childhood sexual abuse trauma, Russell was chronically ill, sleep-deprived, and overworked. Standing on the Williamsburg Bridge on her birthday, she begged the universe to “get this darkness out of me... at any cost.”

Weeks later, she experienced acute psychosis with hallucinations of shadow figures and delusions requiring ritualistic responses. Despite knowing she was hallucinating, she couldn’t prevent herself from trying to bury herself in her backyard or performing cleansing rituals in the shower.

Russell frames her psychosis as a revelation rather than a breakdown: “it was not my mind, but rather the life that I was living that was fractured and broken.” She describes psychosis as “a sharp clear looking glass, through which I could see all that was already destroyed.” The experience became what she calls “the final warning; keep going like this and you’ll die.”

Russell credits three factors for her survival: avoiding psychiatric hospitalization (which would have stripped her of “the right to own your story”), having a robust community of friends and healers providing alternatives, and receiving appropriate medical investigation that identified autoimmune disease rather than just psychiatric diagnosis. She identifies five converging roots of her psychosis: interpersonal trauma, intergenerational trauma, autoimmunity, structural inequity, and spiritual crisis.

Ten years later, having never experienced another episode, Russell describes her body as refusing to “let me get away with anything other than full integrity of body mind and spirit.” While not calling psychosis itself a gift, she values what she frames as her body’s protective intervention.

Both stories share a basic theme: psychiatric symptoms as protective interventions that forced necessary life changes. Alterman’s “self” sends increasingly urgent warnings. Russell’s “body-mind” reveals truths she had avoided. Both frame their symptoms as emergency measures preventing continued self-destruction.

Justin Garson’s philosophical work distinguishes between “madness-as-dysfunction” (symptoms as broken systems) and “madness-as-design” (symptoms as manifestations of mechanisms doing what they are supposed to do or designed to do). The latter perspective assumes that at least some conditions we call mental disorders represent adaptive, functional, meaningful, goal-directed, or naturally selected responses rather than mechanism failures.

This line of thinking is familiar to folks working in the area of evolutionary psychiatry. It is hypothesized by and others that some instances of depressed mood and related behavioral features (withdrawal, loss of motivation, behavioral inhibition) may represent the human mind doing what it is designed by evolution to do in lose-lose unwinnable situations, where low mood can prevent wasted effort. In this view, Alterman’s depressive immobilization could represent the presence of an intact mechanism that prevents continued investment in harmful pursuits.

In Good Reasons for Bad Feelings (2019), Randy Nesse describes the memorable case of a young man of a working-class background who presented with classic depressive symptoms while struggling to stay in school. His primary motivation was to maintain a relationship with his “beautiful and brilliant” girlfriend, who, he was convinced, would leave him if he dropped out of college; the girlfriend was also headed to Vassar in a few months, and the patient was committed to trying to make it work. Despite antidepressant treatment and cognitive behavioral therapy leading to no improvement, months later he was “transformed” after quitting school to work with his father and ending the relationship with his high-status girlfriend for someone who “likes to do all the same kind of things I do.” Nesse believed that his depression lifted primarily because he moved out of an untenable social situation rather than trying to make it work. As a clinician, I’ve had my fair share of patients in similar situations.

Bleuler—who coined the term schizophrenia—was of the view that delusions and hallucinations were responses recruited to help an individual with a malfunctioning brain navigate the world. Anne Harrington described it in Mind Fixers, “There was no point, Bleuler said, in trying to find a biological cause for those symptoms, because they were not caused by brains gone wrong. They were instead caused by patients’ use of psychological mechanisms (especially the kinds identified by Freud) to defend themselves against a world that they experienced through brains that didn’t work right.” At the very origin of our modern concept of schizophrenia is this complex interplay between function and dysfunction. For contemporary versions of such ideas, consider the hypothesis that delusions are a “doxastic shear pin,” a mechanism that errs so as to prevent the destruction of the machine (brain) and permit continued function (in an attenuated capacity) (Fineberg & Corlett, 2016).

Psychodynamic theory has long maintained that psychiatric symptoms carry unconscious meaning and serve psychological purposes. Even when the pathological nature of psychosis is clearer, it is common to observe thematic links between the content of delusions and hallucinations and various conscious-unconscious aspects of their psychological lives, links that can be productively explored in clinical settings and that can serve as sources of psychological insight.

Both Alterman and Russell describe their symptoms as communications from disavowed parts of the psyche. Alterman’s narrative suggests a split between a conscious, striving self pursuing a particular life course and an unconscious, protective self that recognized the path’s destructiveness. The depression represented not a random malfunction but a desperate, albeit maladaptive, solution to an intolerable situation. Russell frames her psychosis as her body “revealing what had made me sick, trapped, and withering away in the first place.” The symbolic content of her hallucinations seemed to connect to her trauma history.

Whether or not symptoms literally “communicate,” constructing such narratives seems to have therapeutic value. They transform seemingly senseless suffering into comprehensible, even purposeful experience. This value cannot be easily discounted.

The Mad Studies perspective, emerging in part from psychiatric survivor movements, also takes the view that “mental illness” often contains elements of meaningful response to oppressive circumstances, identity transformation, or spiritual development. This is the Laingian idea that madness need not be all breakdown, it may also be breakthrough. Russell’s psychosis wasn’t merely a state of impairment but “a necessary process” of death and rebirth. Alterman’s depression enabled the death of his “self-harming version.” The Mad Studies framework also validates resistance to conventional recovery narratives. Both Alterman and Russell warn against pressuring people toward normative functioning (returning to work, maintaining productivity) without questioning whether that functioning serves genuine well-being.

Consider a different scenario: A person is stressed, overworked, sleep-deprived, and developing an alcohol problem. One day while driving home, they get into a serious car accident due to their impaired state. The car is totaled. They end up hospitalized, needing major surgery. While recovering, they see the accident as a wake-up call that their life has become unsustainable. They quit their job, prioritize sleep and exercise, minimize alcohol use, and ultimately have a good life. They say the accident saved their life.

In one sense, this is true; the accident catalyzed necessary changes. But it would be an error to conclude that:

• Car accidents are, in some situations, adaptive protective responses to unsustainable lifestyles

• The person’s body wisely caused the accident to save them

• The accident was “trying to tell them something”

• Preventing car accidents might also prevent necessary transformation

The accident was purely “dysfunctional” in mechanism: impaired judgment, substance effects, random chance, and thermodynamics. Nothing about the accident’s mechanism was adaptive, functional, or protective. The crash didn’t occur in order to save the person’s life.

Yet the accident had adaptive consequences: it forced interruption of destructive patterns, created undeniable evidence of unsustainability, provided time for reflection, and generated a crisis point enabling life change.

Or consider someone who receives a cancer diagnosis and successfully recovers but in the process finds a renewed sense of meaning and a renewed engagement with life. The cancer did not occur in order to improve this person’s life or give them a sense of meaning. It merely served as an accidental catalyst for that change.

This distinction between a mechanism that is adaptive in design versus a mechanism that has adaptive consequences but may itself just be pure breakdown seems to me to be missing from Alterman and Russell’s self-narratives.

The car accident analogy also reveals problems with assuming the severity that occurred was necessary or optimal. The person got lucky surviving a major accident. A lesser accident might also have worked as a “wake up” call. A fatal accident would have achieved nothing. The fact that a particular severity achieved change doesn’t mean that severity was optimal.

Alterman and Russell experienced psychiatric crises that seriously jeopardized their well-being. It may be tempting to consider the severity (“dose”) they survived as the dose that was needed, but we can imagine alternatives where they reached transformation without going through a crisis. The crisis wasn’t the best route to change, maybe just the route that actually happened to catalyze it.

There is fundamental uncertainty about such interpretations. We don’t know the counterfactuals. What would have happened with different choices? Would Alterman have changed his life without becoming immobilized? Would Russell have addressed her trauma without psychotic decompensation?

Retrospective narratives exhibit coherence bias, survivorship bias, and outcome-dependent interpretations. The narrative is shaped by knowing the ending, making the path seem more intentional or necessary than it was. These biases don’t automatically make the narratives false or unhelpful, but they should temper confidence in them to some degree.

I can’t help but wonder: Would Alterman have been receptive to his current interpretation while he was acutely depressed? There are reasons to suspect that he may not have been.

Depressed Alterman, lying drained on his mattress, likely couldn’t have entertained the complex metacognitive interpretation that post-depression Alterman articulates. The interpretation requires distance and an existential awareness that is often threatened by severe depression. In the middle of that state, he may have experienced the depression as pure suicidal torment without redemptive meaning.

I also wonder about how the interpretation is offered, by whom, and under what conditions. Coming from a dismissive clinician, the interpretation of symptoms as purposeful could even have been seen as invalidating (“You don’t need medical treatment; nothing is wrong with you; you need to change your whole life”). Maybe Alterman and Russell needed to construct these narratives themselves for them to have the value that they do.

In the process of a psychiatric evaluation, it is important to ask, in addition to symptom severity, duration, and functional impairment: what is this person’s life actually like? What might their symptoms be responding to? Work satisfaction and meaning, relationship quality and authenticity, alignment between stated values and lived choices, chronic stressors or impossible situations the patient feels trapped within.

Alterman’s distinction between depression that responds well over time to healthy habits and depression is a potentially significant one. Some depressed patients need behavioral activation as a priority. Some depressed patients may need a reassessment and reorientation of their goals. As a clinician, however, I fully recognize that this is easier said than done. Real-life presentations are just too tangled and complicated. Still, it is worth asking patients: when you imagine feeling better and having more energy, what would you do with it and what significance does that have for you? I have worked with many patients with inadequate responses to treatments who have been focused on getting well to return to a marriage or a job or a life that even they recognize at some level is unhealthy for them and not sustainable.

We need more clinical space for reflection. The clinician’s goal should be to facilitate the process while avoiding imposing interpretive frameworks. Clinicians can present various interpretive possibilities without demanding patients accept any particular one. Sometimes simply opening up the space of possibilities itself is beneficial.

Kemtrup raised the point on X/Twitter once that sometimes the purpose of psychoanalytic interpretations in psychotherapy contexts is not to demonstrate their absolute truth but to facilitate a pluralistic understanding of oneself:

“Sometimes the pt and analyst/therapist explore things similar to what gets described in science as “underdetermination of theory by evidence” wherein two or more explanations equally fit with the available case history, facts about the pt. And the pt can BENEFIT from understanding that he can be understood in more than one way, and humility is felt as a virtue, which opens up possibilities for new ways of thinking, acting, and feeling. Often, a sign of health in a patient is that they start to understand themselves pluralistically, through multiple lenses. “I suppose one way to think about what I did is this, but another is this. I don’t really know which is true at the moment.”

When patients construct redemptive narratives like Alterman and Russell’s, I am of the view that clinicians should generally respect these without claiming to be in a position to determine their objective accuracy. “It sounds like you’ve found a way of understanding your experience that feels meaningful and has helped your recovery. That’s valuable.” A narrative of recovery can have utility without being true. We should honor the patient’s meaning-making while being mindful of its fallibility.

Even if depression or psychosis might serve protective functions in some situations, these experiences remain distressing, disabling, and disruptive. We should reduce the harms involved without nullifying the prospect for any future adaptive consequences. There are moments as a clinician when I find myself juggling: “What you are experiencing is serious, and we need to address it and ensure your well-being. And we should explore what might be happening in your life that this may be a response to. And it’s possible this difficult period could ultimately lead somewhere important, even if we can’t see that yet.”

When Russell says, “it was not my mind, but rather the life that I was living that was fractured and broken,” I wonder, why couldn’t it be both? Could the fractured and broken life have led to a (transiently) fractured and broken mind?

Just as clinical judgments of “dysfunction” in the DSM sense do not necessarily correspond to dysfunctions in an evolutionary sense, or biostatistical sense, or neurobiological sense, etc., first-person perceptions of an illness experience “saving” one’s life from “self-destruction” also need not correspond to the existence of functional, adaptive mechanisms.

Recall the distinction between a mechanism that is adaptive in design versus a mechanism that has adaptive consequences but may itself just be pure breakdown. (Nesse characterizes two serious errors often made by those looking for evolutionary explanations in medicine: Viewing Symptoms as Diseases and Viewing Diseases as Adaptations.)

Psychiatric crises are dangerous inflection points that can lead to deterioration as well as transformation, perhaps depending on factors such as available support, treatment quality, resources, resilience, timing, insight, and chance. I don’t know if the machinery of any particular crisis inherently contains elements that are adaptive, but transformation is nonetheless possible, and patients may legitimately perceive the episode as putting their life on a better trajectory. Sometimes madness does stop and immobilize, whether by design or by accident, people who are on a self-destructive or unsustainable path. Alterman and Russell found their ways through to meaningful lives. I want to help others find theirs, and I want to encourage people to explore the relationships between their symptoms and their lives, without deciding for them what story they use to make sense of what went wrong and what went right.

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• in What’s the point of words? offers the best commentary on the analytic vs continental philosophy debate that swept Substack a few weeks back:

Once you’ve established that language is not a perfectly transparent vehicle for the neutral description of facts, you can’t then attempt to just neutrally describe that situation… You have to engage with the system of words on their own terms.

So: language has betrayed us. Now what? What can language do, besides simulate reality? There are the various perlocutionary acts, persuading, forbidding, seducing, offending, and so on. Language mediates social games and forms the structure of subjectivity. It throws up its own internal problems that can be solved or expanded for fun and profit. It has a shibboleth function, which allows you to distinguish between friend and enemy based on whether they use words like hegemony or not. Some of these intersubjective functions are not always particularly positive, and definitely not useful to philosophy. But others are. We can still use language to access objective reality, as long as we’re prepared to let it take a more active role than straightforward description. Language, and especially philosophical language, changes how the world discloses itself to us.

The only remnant of the grand analytic experiment is the vague sense that it would be nice if language could clearly account for reality, and it’s virtuous to keep on pretending as much as possible that it can, even though it can’t. But there is also a ritual. Every so often, the survivors from the shipwreck of analytic philosophy all gather round to shriek at Judith Butler’s terrible, terrible sentence. Sure, all our attempts to clearly express the world in language ended in failure—but get a load of these guys! It’s like they’re not even trying.

• tackles some difficult questions about AI neurosis with his characteristic sophistication. The age of neurotic AI is here. Or: how a LLM having a panic attack taught me to love myself

Chater’s argument is that introspection is always improvisation: we generate explanations in real time and then experience them as if they were read-outs from depth. The mind’s apparent interior behaves like a narrator producing plausible continuations rather than an instrument panel that actually displays anything corresponding to the underlying mechanisms. We interpret our physiological states and we construct a plausible narrative to explain them. Introspection is fully illusory, for us as much as for LLMs.

If that picture has any truth, it changes how this Gemini transcript should be read and the distinction between “real” and “simulated” neurosis collapses. The text can be socially meaningful but still remain a poor guide to the underlying generative dynamics that produced it. But is it causally potent? I’m not sure that question has ever mattered as much as we think it does. Human rumination already occupies this awkward - and causally fairly uncertain - space.

See also: Pollack’s thought experiment: What shape is your mind?

• , An open mea culpa to Marsha Linehan

Also, I hate to say this, but I think some of your devotees made your modality stupid. My personal conviction, based on observation of various gurus and modalities, is that whatever wisdom is in a given modality is actually mostly in the practitioner. I believe that you have helped patients, I believe that Otto Kernberg has helped patients, I believe Janina Fisher has helped patients, to name a few. I don’t believe that many of their trainees help patients with anything like the frequency or degree of efficacy that the teachers did. (I once had a therapist who was trained by Janina Fisher herself who did some of the stupidest therapy on me that I’ve ever received, and I’ve received plenty. You get the point.) Most people who say they do DBT don’t do the real thing, and this would be true even if DBT to fidelity weren’t so intensive and difficult to practice—something here about maps and terrain. DBT seems, based on the pedestrian knowledge that I have, to be a wise modality based not only on Scientific Evidence, but on your own experience surmounting the insurmountable. Good luck putting that in a manual and having it withstand MSWs who have never really suffered.

• has done exceptional work on this year. My favorite is: Why I’m Trying Psych Meds Again, and how I’ve changed my mind about their critics

Reading these thinkers caused me to view scientific studies through this lens, and it made me cynical as hell. It was intellectually limiting — I was no longer curious about studies of the brain and its chemicals, but immediately trying to find fault with them so I could retain my worldview.

This meant that my ideas couldn’t evolve, which is what has happened to Timimi and Moncrieff — they’ve made the same arguments, over and over for decades now, never updating or adjusting, but doubling down no matter what. I don’t want to be that kind of thinker, or person in general.

Probably the most influential factor in changing my mind, though, was developing a genuinely therapeutic relationship with a doctor. One who is honest with me about drugs, including their limitations and their risks, who does not answer the phone in my face, or get annoyed when I ask a lot of questions, or roll her eyes and sigh when I bring up what I’ve been reading, but is actually, genuinely interested, and even directs me to good research papers.

Jesse’s review of Sami Timimi’s book is also a delight. Are We All Just Having ‘Understandable Human Reactions’? Sami Timimi’s new book paints neurodivergent and trans people as dupes of neoliberalism

After reading [Timimi’s] new book, though, I have realized: critical for me means, let’s ask more questions about who gets to call the shots. Critical for Timimi means, if there’s not a specific biomarker that correlates with a specific diagnosis, then you’re all just having a collective hallucination!

• , The missing heritability question is now (mostly) answered: Not with a bang but with a whimper

twin studies produce a ~2x inflated estimate of narrow-sense heritability when compared to molecular estimates that are free of environmental confounding. The mystery of twin heritability comes to an ignoble end: no massive tranche of rare variants, no phantom interactions, just inflation.

• writes about psychoanalytic considerations around sibling dynamics. On Siblings:

Sibling dynamics can show up in interesting ways in the transference, of course. There is the anguish of realizing the therapist (mother or father) has other children (patients) and the subsequent felt hatred towards the “competition.” I’ve found there is often a desire for patients to be the preferred sibling, in some way. The wish to know that they are, in fact, special, and not just another “mouth to feed.”

But perhaps less talked about in psychoanalytic literature is sibling transference. A patient who is around the same age may unconsciously see us as their rival. I wonder if this is sometimes confused as vertical/Oedipal, when really it’s a reliving of something on the lateral axis.

In the end, as with most developmental phenomena, we are perhaps left to sit with something unresolved. I may always, unconsciously, fear that I murdered my brother. There were moments I wanted him gone, after all, when I was little. And now he is gone, forever.

• , Insanity: What it really feels like to live on the edge of madness

It is shameful to admit that I don’t want to give up being borderline. But I want to want it. I know that sounds absurd, but once I truly give it up I’ll cease to exist. I’ve spent so long as two halves that I’ve never truly been whole. The woman that is Autumn without insanity has to destroy the old self. I was right when I told my other self that it could die. But really, we both had to die.

I know what it’s like to live in constant, benumbing pain. I don’t know what it’d be like to live without it. The thing I have to become is alien to me. Who would I be when I’m no longer victim and monster, innocent and terror? Who would I be without the constant self deception and sabotage, the rage and the dark?

• discusses the recent neuroimaging study that reported that stimulant medications primarily affect arousal and reward processing networks instead of attention networks in the brain.

Now onto the second issue: “attention”. This word means different things in different contexts. In ADHD diagnostic criteria, “inattention” means not staying on task, getting distracted, forgetting instructions. These are problems with sustained engagement and persistence. By contrast, in cognitive psychology, attention refers to selective amplification of relevant information, like covertly allocating processing resources to a small patch of visual space (e.g. in a Posner cueing task; see figure below) or selectively increasing focus to one out of several conversation in a crowded room without actually moving your head (the cocktail party problem). That is not what people refer to when they are discussing “attention” in ADHD. The imaging results therefore line up pretty nicely with the clinical meaning of attention in ADHD, which is about sustained engagement rather than selective processing.

• , Alternate Lives: Critical Junctures in Psychiatric Illness

I question the role of psychiatry and psychotherapy in finding these moments of plasticity in someone’s life. My revelation in Alaska, where I was inundated with the feeling of being helpful, mattering, being liked, was so profound because it was spontaneous. No one could have planned or prescribed that experience, no hospital could have simulated it- it just had to happen.

What we can do as clinicians is to recognize the importance of these moments, and remain curious about the possibilities for healing the world might provide.

• in The Mel Jar, “Kill Your Darlings”: analysis, diagnosis, countertransference, and the Imaginary

In my opinion, it would be best if we all learn to do this — to question our own framings. To develop the skill and insight to see them as incomplete, or in need of total revision. To understand that no matter how clear, thorough, or “objective” we have consistently attempted to be, that everything is indeed a construct, a narrative of convenience, a “just so” story of the Imaginary.

No matter how artful or elegant, no matter how much clinical utility is has, no matter if we like it very much, and our patients like it very much, and if we have become publicly identified with it — maybe written a bunch on it, won awards off of it, gotten famous off of it, built a whole career off of it — all of it is a conjecture, a hypothesis, and/or a “theory,” not “fact.”

• unpacks the argument that personality disorder is not about personality traits, because traits are about all psychopathology.

We can therefore see that even when we categorise most psychopathologies in terms of personality, we still end up with the following non-personality categories: the emotional disorders (neuroticism), the impulse disorders (disinhibition), the cognitive-perceptual disorders (psychoticism), and the relational disorders (antagonism and detachment). Astute readers may, at this point, have noticed that this organisation matches the well-known organisation from the hierarchical taxonomy of psychopathology (HiTOP)…

This equivalence suggests that there is nothing unique about the association between personality traits and the putative disorders of ‘personality’. Instead, all psychopathologies are invariably associated with personality traits that match their underlying pathologies. In that sense, all psychopathologies both are and are not personality pathologies.

• ’s analysis of overfitting and cultural stagnation. Our Overfitted Century: Cultural stagnation is because we’re stuck in-distribution

Overall, I think the switch from an editorial room with conscious human oversight to algorithmic feeds (which plenty of others pinpoint as a possible cause for cultural stagnation) likely was a major factor in the 21st century becoming overfitted. And also, again, the efficiency of financing, capital markets (and now prediction markets), and so on, all conspire toward this.

People get riled up if you use the word “capitalism” as an explanation for things, and everyone squares off for a political debate. But, while I’m mostly avoiding that debate here, I can’t help but wonder if some of the complaints about “late-stage capitalism” actually break down into something like “this system has gotten oppressively efficient and therefore overfitted, and overfitted systems suck to live in.”

• , Mostly Harmless? Understanding the Adverse Effects of Psychotherapy

Psychotherapy operates by modifying patterns of thought, emotion, and behavior through guided reflection, practice, and interpersonal feedback. The same processes that facilitate recovery can, depending on patient characteristics or therapeutic context, also contribute to distress or symptom worsening. Almost half of treatments result in an unwanted effect. Severe effects occur in about one out of ten cases.

• on how psychotherapy has become a “status symbol” in India. Therapy was co-opted to serve as a signal of emotional intelligence, and now there’s a backlash brewing.

For every status symbol, there is a counter-symbol. For every mainstream culture piece, there is a counterculture that develops in opposition to it… The same thing happened to therapy, too. It’s actually happening right now.

“Therapy? That’s just something the rich kids need. There’s nothing a night out with friends cannot fix.”

Everything seems better and cheaper than therapy if you scroll through social media.

“Ice cream is cheaper than therapy.”

“Shopping is my therapy.”

“Who needs therapy when we have the mountains?”

These sentences may seem like a simple misunderstanding of the therapeutic process, but they reveal a sense of rebellion — a rebellion against the status symbol that is therapy. A mini-resistance against the world telling you to visit a therapist.

• , Anatomy of a kvetch

The frustration that I have, with most of these critics [of capitalism], is that if you gave them a menu of feasible options for organizing a complex economy and asked them to pick one, the vast majority, after a bit of foot-dragging, would choose some form of suitably regulated market economy with a generous welfare state. So then what is the point of all the bluster about capitalism, if you don’t intend to do anything about it? It just seems like an idle complaint. More specifically, it seems like kvetching…

• presents the curriculum details of a hypothetical psychiatry fellowship, The Inpatient Psychiatry Fellowship I Wish I’d Had in Residency

I find it odd that psychiatry does not have an established fellowship for treating our sickest patients, regardless of which diagnostic silo they happen to fall under (this would be vaguely analogous to not having ICU/Critical Care fellowships for internal medicine residents)… As an inpatient psychiatrist my bias may be showing, but I am convinced the greatest social demand for our profession right now is in treating the severely and chronically mentally ill. It is a national problem and the cards are stacked against us. For one thing, we lack institutional support for anything resembling serious treatment, including long-term and asylum care (much touted “community treatment” only works if there’s a decently functioning community for the patient to go back to). To make matters worse, since the downsizing and closing of most long-term psychiatric hospitals we have lost inestimable knowledge accrued over the generations by those who spent their lives treating these patients.

• shares a list of 45 things he believes, What I believe in Medicine.

9. I will bet you two espressos that quality improvement initiatives reduce quality.

30. When in doubt, go see the patient.

40. Nearly every treatment recommendation in modern medicine is preference sensitive. Never say someone “needs” anything. People need food and water. Almost everything else is sensitive to patient preferences.

• , Calling out grape culture

I wonder if perhaps these euphemisms are nothing more or less than manifestations of trauma-brain: synonymous with pathological (if understandable) attempts to control and police the external in an attempt to soothe the chaotic rage, fear and sadness within. The world must change, because I’m scared I can’t.

The loss of trust in self, others, and the world so often found in trauma, packaged up in emoji form.

After all, what is trauma but profound inability to bear and process the knowledge of what happened to you? What is recovery but having the words to say it, making a picture from the fragments, piecing yourself together, and being able to look at what you find and realise you survived?

• and in . Evolutionary Mismatch and Modern Motherhood: Elena Bridgers on alloparenting, postpartum mental health, and what research on hunter-gatherers reveals (and much more)

Bridgers: “At the risk of sounding a bit corny or new-agey, I feel like studying hunter-gatherer societies has been a kind of awakening for me. It has totally changed my paradigm, not just the way I think about motherhood, but about the way I think about all of Western society, and about what I value. We are very individualistic in our culture, and I don’t think it’s healthy. We pathologize any kind of interdependence, but humans are a social and interdependent species. Hunter-gatherer societies are incredibly care-oriented relative to Western society, where we tend to view care as a burden. Studying these societies has helped me lean into motherhood more, lean into my relationships more, and let go (at least a little bit) of the achievement/productivity focus that drove most of my young adult life.”

• , The Decline of Deviance. Where has all the weirdness gone?

Whenever I read biographies of famous scientists, I notice that a) they’re all pretty weird, and b) I don’t know anyone like them today, at least not in academia. I’ve met some odd people at universities, to be sure, but most of them end up leaving, a phenomenon the biologist Ruxandra Teslo calls “the flight of the Weird Nerd from academia”. The people who remain may be super smart, but they’re unlikely to rock the boat.

• , The curious case of broken theorems: Mathematics shouldn’t survive logical errors—yet it does

Meaningless formal systems should break down like Prince Rupert’s drops, these toughened glass beads that are unbelievably resistant, until you snap them at the right place and they explode into powder.

By contrast, real-world mathematics breaks down like pottery. As a whole, the mathematical corpus is a giant, collaborative work of kintsugi, the Japanese art of pottery-fixing. The whole thing started off as unstructured clay and was made hard by our very hand.

• , Is autoimmune psychosis a thing?

In my mind there are two ways to resolve whether the autoantibodies found in first episode psychosis patients are indeed pathological. The first is to screen large numbers of patients using lumbar puncture to obtain cerebrospinal fluid. This has been advocated by Belinda and Tom but it would require a change in clinical practice and is a logistical challenge. Most patients I see who are acutely psychotic would lack capacity to consent from a somewhat invasive procedure with uncertain benefits. The second is to do what we always do to resolve clinical equipoise, a randomised trial.

• , Should All Depressed Patients Be On Adjunctive Mirtazapine?

A detailed discussion of a 2022 meta-analysis by Henssler et al. that also serves as an excellent primer on heterogeneity, tau, and random-effects models in meta-analyses.

We should now understand that random-effects models will heavily downplay the effects of large, precise studies and amplify the effects of small, imprecise studies with large effect sizes.

• , When the Real Reason for Therapy Finally Surfaces

In psychotherapy, the real reason a person comes is not always clear—not to us, not even to them. They may have no words for it, only a diffuse sense that something is wrong. It may take months to surface, often in what seems like a sudden revelation. But that moment is the culmination of months of work.

• , Behind The Rise of Psychiatric Diagnosis

(Carl’s response to my Asterisk magazine article on the DSM)

Simply put, DSM-III gave psychiatry a common language that made its categories useful to insurers, researchers, epidemiologists, regulators, and pharmaceutical companies—and, soon enough, seemingly, to the rest of humanity. Once diagnosis became the shared language of research, clinical practice, and marketing, it naturally filtered into popular culture. That alignment of powerful forces—science, policy, commerce—is what made diagnosis culturally significant. Without that, the DSM is just a bunch of definitions in a book that few people bother to read. With it, DSM-III is instrumental in research, insurance coverage, public policy, law, self-understanding, and the day-to-day practice of medicine.

• , Defending Dissensus as a Democratic Principle

Seen through this lens, the persistent debates and disagreements in psychiatry are not failures to be eradicated but opportunities to practice agonistic pluralism. In Mouffe’s sense, pluralism is not about diluting differences in pursuit of consensus; it is about institutionalizing spaces where dissent is legitimate, and disagreement is recognized as a driver of critical thought and democratic vitality. By accepting the legitimacy of multiple perspectives—whether naturalistic, phenomenological, hermeneutic, or social—psychiatry can move toward a culture where differences are negotiated, not suppressed, and where patients, clinicians, and researchers can engage in ongoing, respectful struggle over meaning, evidence, and values.

As a little treat for scrolling all the way to the end, here are some personal media favorites from 2025.

• Music album: “Lux” by Rosalía. Pop music with a touch of the divine, unlike anything I’ve heard before.

• Fiction: “There Is No Antimemetics Division” by qntm. An unforgettable sci-fi horror about an organization that combats “antimemes,” phenomena that resist being remembered and recorded.

• Non-Fiction: “Elusive Cures” by Nicole C. Rust, on how neuroscience is responding to failures of the bench-to-bed pipeline (see my review here), and “Shamanism” by Manvir Singh, a fascinating exploration of shamanism throughout human history.

• TV shows: “Pluribus” (Apple TV), innovative story with strong performances; “Andor,” season two (Disney), a solid final season that seals Andor’s track record as an exceptional show; and “The Pitt” (HBO Max), one of the best medical shows ever.

• Film: “Train Dreams” (directed by Clint Bentley), an elegant meditation on life and loss

The 6 most popular posts from 2025 on Psychiatry at the Margins

Per the Substack algorithm (which appears to use some combination of likes, views, and shares)

• Autism’s Confusing Cousins

• Confessions of an Ambivalent Psychiatrist, guest post by

• Schizophrenia Is the Price We Pay for Minds Poised Near the Edge of a Cliff

• Rich Girl Rehab, guest post by

• Groundbreaking Analysis Upends Our Understanding of Psychiatric Holds

• The “Overdiagnosis” Confusion

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Dan J. Stein

Professor Dan Stein was a psychiatrist’s psychiatrist, a world-renowned and distinguished South African psychiatrist with doctoral degrees in neuroscience and philosophy, chair of the department of psychiatry at the University of Cape Town, with contributions to wide-ranging areas such as psychopharmacology, psychiatric neuroscience, psychiatric classification, anxiety disorders and obsessive-compulsive disorders, epidemiology, philosophy of psychiatry, and evolutionary psychiatry. He was also warm, kind, wise, and a good friend. Stein passed away on Dec 6, 2025; he was only 63. It was an unexpected death, we had emailed only two weeks prior.

You can see formal obituaries from the University of Cape Town and the International College of Neuropsychopharmacology with details about his life and career.

On Nov 6, 2020, Dan had sent me an email that started with, “Dear Dr Aftab. I have very much enjoyed reading your columns in Psychiatric Times; many congratulations!”

That email was the beginning of a rich five-year intellectual friendship…

I knew of Dan Stein prior to that but had never had an opportunity to approach him myself. I was a young pup, barely out of psychiatric training, trying to figure out the intellectual landscape of psychiatry and scratching the surface of complicated philosophical and scientific debates. He was really gracious to me.

Our friendship resulted in several collaborations, including his interview in my Conversations in Critical Psychiatry series, our 2022 paper on psychopharmacology and explanatory pluralism in JAMA Psychiatry, and the 2024 forum article on philosophy of psychiatry in World Psychiatry. We also presented together in October 2023 at the ECNP meeting in Barcelona.

Stein’s central philosophical contribution was his classic-critical-integrative framework, which he applied to questions in psychopharmacology, psychopathology, and neuroscience. In his telling, the classic position holds that mental disorders are natural kinds, with an objective, biological essence, and they are real, discoverable entities governed by scientific laws. The critical position argues that mental disorders are socially constructed human kinds, that psychiatric nosology is value-laden through and through, and that understanding mental illness requires hermeneutic (interpretive) approaches rather than scientific ones. The “integrative position” was Stein’s preferred approach, which attempted to transcend this binary.

He held that psychiatric disorders have both biologically grounded and socially mediated aspects, that they are better understood as “soft natural kinds” rather than strict natural kinds or pure human kinds. Psychiatric science is theory-laden and value-bound, like all science, and can make genuine progress. Psychiatric understanding requires integrating both mechanisms as outlined by cognitive-affective neurosciences as well as meanings derived from subjective experience. Biological and social perspectives are necessary and complementary.

“Philosophy of Psychopharmacology” (2008) applied this framework to fundamental questions about psychopharmacology, including whether it’s good to treat psychiatric disorders and the ethics of “cosmetic psychopharmacology.”

“Problems of Living” (2021) later extended the integrative framework to broader philosophical questions, drawing on critical realism, pragmatic realism, embodied cognition, moral naturalism, and engaging with developments in cognitive-affective neuroscience. Stein approached the brain-mind as “wetware,” a dynamic, interactive system that is embodied and embedded. Stein explored the promise and limitations of neuroscience in addressing the “big questions” of existence.

Stein was also interested in what evolutionary perspectives have to tell us about psychopathology and psychopharmacology. Randy Nesse, a pioneer in evolutionary medicine and evolutionary psychiatry, was another one of his collaborators and friends, and they did some wonderful work together on papers such as “Towards a genuinely medical model for psychiatric nosology” (2012), “How evolutionary psychiatry can advance psychopharmacology” (2019), and “Tacit Creationism Encourages Oversimplified Views of Functions and Dysfunctions” (2025).

Stein’s philosophy was characterized by methodological pluralism, soft naturalism, anti-reductionism, pragmatism, and integration over polarization. As he described himself, he was “a fox, not a hedgehog,” someone who knew many things rather than one big thing, and he did this really well.

As I write all this, I am struck once again by his humility and warmth, the kindness and generosity he extended to others, and the attention he offered to colleagues. He nurtured friendships wherever he went. I hope he knew how much he meant to me, and so many others across the world.

Lisa Wallace

Lisa Wallace died on Dec 2, 2025. She was an artist and a writer, and she wrote on her blog, “Travels Through Psychiatry,” about her “45 years in and out of psychiatric treatment.”

I do not exactly remember when Lisa Wallace reached out to me on Twitter, but it was around 4 years ago at a point in her life when she was beginning to reconsider her self-image as a “harmed ex-patient,” and she was curious about better understanding psychiatry and had found my posts and writings helpful in that regard. The more I got to know her, the more impressed I was by her character and her spirit.

When I started Psychiatry at the Margins in late 2022, the first person I invited to write a guest post for this substack was Lisa Wallace. And she wrote something wonderfully raw, candid, ambivalent, and hopeful, “A Psychiatric Survivor Comes to a Place of Understanding,” in which she explored why she had left psychiatric care and why she may one day return. A little more than a year later, she wrote a powerful follow-up post, “Finding My Way Out of Anti-Psychiatry.”

She was deeply honest and ethically grounded. She was concerned about protecting others, refusing to exploit her story, worrying about generalizing her experience to others, and calling out rhetoric that might harm vulnerable people in crisis. She was wounded but resilient. She continued working toward a better emotional existence through psychotherapy, carefully considered medication, creative expression, and honest self-examination.

Lisa’s ethical integrity is particularly evident in her last blog post, “I Guess I’m Still Shrunk” (August 02, 2025),

“I will stand by my need for treatment, no matter what I stumble into. I’m firm in this.

The very thought of turning aspects of my mental illness, and how psychiatrists and therapists dealt with me, into an enterprise against the idea of mental illness itself hits as an attack on not only me, but anyone with mental illness.

How could I assert with tremendous confidence that my experiences are everyone’s and that I have the knowledge, as if I’ve been to the mountaintop, to formulate a new way forward that rejects psychiatry and ignores all progress in the field. I won’t casually glance at psychiatry’s inherent self-criticism and say I don’t see it. I won’t lay claim to innovations that aren’t mine and that already existed long before I noticed them.

I won’t take part in the industries springing up that encourage hatred of mentally ill people with insinuations of weakness…

I’m not going to corrupt who I am, where I’ve been and the value in coming to terms just to seek retribution, constantly plunging a knife into a ghostly entity of psychiatry, demanding that it take the blame.”

In the last years of her life, Lisa had, with some luck, found an empathetic, collaborative psychiatrist to provide clinical treatment, and this therapeutic relationship was transformative for her. She would often reach out to me and share updates on how she was doing, and a frequent sentiment she expressed was one of gratitude for the psychiatric care she was receiving.

This image below is Lisa’s summary of her travels through psychiatric treatment in her own words.

The following is a painting Lisa made about her history of mental health treatment, titled Hard Stories to Tell.

Lisa, I will miss you. Thank you for making me a part of your life.

The phrase “The all of thine that cannot die” in the title of the post comes from the poem And Thou art Dead, as Young and Fair by Lord Byron.

[Comments are open]

One of the most memorable essays I’ve ever read is “Scott And Scurvy” (2010) by Maciej Cegłowski about how the cure for scurvy was lost.

In 1911, a British expedition to Antarctica included a doctor who lectured confidently about scurvy, yet his understanding of the disease was completely wrong. This seems baffling because scurvy had supposedly been “cured” over 150 years earlier. In 1747, Scottish physician James Lind demonstrated that citrus fruits could treat the disease, and by 1799, the Royal Navy required daily lemon juice for sailors. Scurvy had virtually disappeared from British ships following that intervention.

“Somehow a highly-trained group of scientists at the start of the 20th century knew less about scurvy than the average sea captain in Napoleonic times… in the second half of the nineteenth century, the cure for scurvy was lost. The story of how this happened is a striking demonstration of the problem of induction, and how progress in one field of study can lead to unintended steps backward in another.”

Scurvy is a serious and potentially fatal disease caused by vitamin C deficiency. Gums become swollen and purple, teeth loosen, old wounds reopen, and limbs swell and blacken. Death eventually follows. Fresh fruits, vegetables, and even fresh meat contain vitamin C, and restoring it to the diet quickly cures the disease. Eighteenth-century doctors understood this in terms of the curative powers of citrus fruit, in particular lemon juice, without having any knowledge of the existence of vitamin C. The citrus cure worked spectacularly and scurvy became very rare in the British Royal Navy after citrus requirements were implemented. Several factors worked in combination to cast the citrus cure into doubt.

First, steam-powered ships shortened voyages so substantially that sailors rarely spent enough time without fresh food to develop scurvy. The disease became rare, which meant fewer people witnessed citrus cures working.

Second, the navy quietly substituted an ineffective remedy for an effective one. In 1860, they switched from Mediterranean lemons to West Indian limes, a substitution based on colonial trade convenience that seemed harmless since both were citrus fruits. “Moreover, as there was a widespread belief that the antiscorbutic properties of lemons were due to their acidity, it made sense that the more acidic Caribbean limes would be even better at fighting the disease.”

But limes contain only a quarter of the vitamin C that lemons do. Worse, the lime juice was stored in copper-lined containers and left exposed to air, which destroyed what little vitamin C remained. By the 1870s, sailors were drinking something essentially useless while believing they were protected.

Third, medical theory evolved in ways that obscured the truth. Bacteria had recently been discovered as the cause of diseases like tuberculosis and cholera. The germ theory of disease was revolutionary science. Doctors began wondering whether scurvy, too, might be a bacterial disease rather than a nutritional one. A theory emerged that scurvy came from “ptomaines,” hypothetical toxic substances produced by bacteria in preserved meat. Fresh food prevented scurvy not because it contained some vital nutrient, but because it wasn’t contaminated.

This theory actually made sense given the evidence available. Fresh meat did prevent scurvy (organ meats are rich in vitamin C), while preserved meats didn’t, while citrus fruit in the form of West Indian limes seemed an unreliable preventative and curative treatment. The theory correctly predicted what foods would help, even though its explanation was completely wrong.

“This pattern of fresh meat preventing scurvy would be a consistent one in Arctic exploration. It defied the common understanding of scurvy as a deficiency in vegetable matter. Somehow men could live for years on a meat-only diet and remain healthy, provided that the meat was fresh. This is a good example of how the very ubiquity of vitamin C made it hard to identify. Though scurvy was always associated with a lack of greens, fresh meat contains adequate amounts of vitamin C, with particularly high concentrations in the organ meats… But unless you already understand and believe in the vitamin model of nutrition, the notion of a trace substance that exists both in fresh limes and bear kidneys, but is absent from a cask of lime juice because you happened to prepare it in a copper vessel, begins to sound pretty contrived.”

These mistaken ideas shaped how polar expeditions prepared for long journeys across the ice, with at times disastrous results. I will refer you to the Cegłowski essay for those details, especially expeditions by Robert Scott.

The actual cause of scurvy was found again through pure luck. Scientists studying beriberi (another deficiency disease) in pigeons decided to switch to guinea pigs. They happened to choose one of the only animals besides humans and monkeys that cannot make its own vitamin C. When fed a grain-only diet, the guinea pigs developed scurvy, and researchers were able to create an animal model of scurvy for the first time. By 1932, vitamin C was definitively identified.

Cegłowski notes that throughout these centuries of confusion, doctors rarely admitted ignorance. Scurvy could be explained by whatever theory was fashionable, imbalanced humors, bad air, acidified blood, bacterial infection. Physicians always sounded confident, even when they were wrong.

The evidence by itself didn’t point clearly to the truth. Without the concept of a “vitamin,” the same observations could support multiple theories. Fresh meat preventing scurvy seemed to confirm the ptomaine theory just as easily as it confirmed the deficiency theory. Knowing which results to trust and which to explain away required concepts that didn’t yet exist.

“Now that we understand scurvy as a deficiency disease, we can explain away the anomalous results that seem to contradict that theory (the failure of lime juice on polar expeditions, for example). But the evidence on its own did not point clearly at any solution. It was not clear which results were the anomalous ones that needed explaining away. The ptomaine theory made correct predictions (fresh meat will prevent scurvy) even though it was completely wrong.”

“It was not clear which results were the anomalous ones that needed explaining away” is an important sentence that bears repetition.

Steam power made voyages safer but allowed the switch to ineffective lime juice to go unnoticed for quite some time. Pasteurization protected infants from bacterial infection but destroyed the vitamin C in their milk, causing outbreaks of infantile scurvy among wealthy families who could afford the “best” processed foods.

We assume knowledge, once gained, stays with us. But holding onto truth requires constant effort. A disease that killed millions, with an unambiguous cure known for centuries, still managed to confound humanity for decades.

Let’s reflect on some parallels between the history of scurvy and its cure and the current ignorance about the causes of mental disorders and the messy, inconsistent literature on when and how treatments for mental disorders help people. Like physicians treating scurvy in the late 19th century, psychiatry’s current situation is also one of profound ignorance and trial and error.

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