Amanda Peery-Wolf is a poet, writer, and voice-hearer living in New York City. She is currently at work on a book exploring her experiences hearing voices, a subject she has also written about for the Lancet Psychiatry. Her poetry has appeared in outlets including the North American Review and the Colorado Review, and she is the recipient of the 2020 Iowa Review Award for Poetry.

“Why are you ignoring me?” The voice asks. It’s a blisteringly hot June day, and I’m waiting at a crosswalk in Manhattan, on my way to my local grocery store. Mentally reviewing my grocery list, I don’t respond right away.

“Listen to me!” The voice demands. “You’ve been ignoring me for a thousand years.”

I know no one else can hear the voice. I’m sure of it. And yet, as always, I glance at the people around me, suspicious that someday, someone might hear what I’m hearing. No one looks up. The voice is mine alone. It is a voice in my head.

“I’m not ignoring you,” I respond in my mind. “I’m here.”

“Great,” says the voice. “I’m the tree whose leaves are falling. Battlestruck barbarian. Interesting lizard. I have much to say.”

“Fine,” I say. “But we’ll have to talk later. I’m almost at the store.”

“OK.” The voice falls respectfully silent, then adds, “Don’t forget to inspect the berries. Avoid mold at all costs.” Then, he is quiet. We won’t talk again until evening.

My voice and I have these exchanges at least once a day. Usually benign, often esoteric, sometimes helpful, with an edge of needy recalcitrance. This is how my voice speaks to me.

I started hearing voices about ten years ago. In the time since, I’ve worked with three therapists and seven psychiatrists. These practitioners and I have discussed my voices’ intensity and intrusiveness. We’ve talked about my attitude towards my voices, when and where I hear them, and what I do when they speak to me. We have discussed my diagnosis (shifting over time from Bipolar II to Bipolar I to Bipolar with Psychotic Features to, today, Unspecified Bipolar and Related Disorders). But through these conversations, I found it odd that most of these mental health professionals seemed entirely uninterested in what my voices had to say.

Over the past year, I’ve been reading research on voice hearing, as part of a campaign to understand my own mind, and I’ve noticed the same strange oversight. I’ve read a couple dozen recent books and over a hundred papers, and, with a few noteworthy exceptions, very few researchers seem genuinely interested in, to use the academic term, voice content. I’ve been told that this is especially true in American academia, where quantifiable results are king, and messier phenomenological studies rarely get the funding.

This is a shame. In my own life over the last decade, I’ve clung to the idea that what my voices say is meaningful. This has helped me immensely. Understanding my voices’ messages has been the key to building a better relationship with them. That, in turn, has been crucial to living a full and thriving life as a voice-hearer.

How I Listen to My Voices’ Messages

The first time I heard a voice, I was an undergraduate at Harvard walking across the Yard. As I strode down a neatly groomed path, I suddenly heard something entirely unlike anything I had heard before. It was a deep, clear, male voice that seemed to descend from the sky and, at the same time, arise from somewhere inside my mind. It said: “We who suffer, how we suffer.” I knew no one else could hear it. It was too personal, close, and inhuman. But I was not afraid. The voice was unintrusive and gentle. More importantly, its words were meaningful to me. They felt like commiseration, or comfort. In college, I was, indeed, suffering, experiencing torturous, recurring mood episodes that left me incapacitated for weeks at a time. When the voice spoke, I felt like a distant friend was soothing me. Afterwards, I thought of the experience as a strange but welcome anomaly. I thought of it as a small gift.

So, from my first voice-hearing experience, I felt that the voice’s message was meaningful—not only because it touched my own life, but also simply because it was a message meant for me. If a person turned to speak to me in a crowded room, I would take note of what they said, not just how they said it or the mechanics of their speech. What they said would be, most likely, the most important thing about the interaction. So it was with voices.

By the time I turned 28, I was living with three voices in my head. They arrived one-by-one, a year or two apart. All three appeared as fully formed entities with their own personas, moods, personalities, and, it seemed, inner lives. They had forms I could see clearly in my mind’s eye and very occasionally in the room. One was a raven—the voice that nagged me on the way to the grocery store—one was a queen and a polar bear (both at once), and one was a kind of energy field radiating from my right hip. My relationships with these voices were, and are, complex. They have evolved over time, in a large part due to what my voices have said and how I have understood their messages.

In the beginning, my three voices terrified me. They spoke loudly, repetitively, and intrusively. They were often dark, sometimes bullying. The raven was obsessed with predicting my death and the deaths of people I loved (“You will die by the end of the week;” “Your mom will fall down the stairs. Say goodbye.”) The queen/bear repeated loud opinions about my friends and partners until it was difficult for me to think (“Break up with your boyfriend. Break up. Break up,” etc.). The third one, the energy field, communicated less in words and more in visions and sensations. Sometimes, she (she was a she) caused horrible pain in my right hip that made it difficult to stand up. I was living with three terrifying strangers, and my mind and body were not my own.

Luckily, I had an excellent therapist, one of the three who cared what my voices had to say. She helped me unravel their messages, understanding both literal and non-literal meanings. Adopting some of the Internal Family Systems framework, she encouraged me to see the voices as flawed protectors rather than malicious entities. When the raven told me I would die by the end of the week, maybe he was warning me to be careful that week. Maybe he was reflecting my own anxiety about an upcoming risk I was taking. Or maybe death, to him, was a metaphor—perhaps for transformation or a new beginning. My therapist and I worked through the possibilities. When the queen/bear told me to break up with my long-term partner, maybe she was reflecting tension in my relationship and suggesting I make a change. Her words might be drastic, but the sentiment could be valid. Even the pain caused by the third voice could be a message, for example, about the ways I was treating my body.

By looking closely at my voices’ words and signals, my therapist and I were able to find new, important meanings. The more I understood and engaged with my voices’ messages, the less fear I felt. And as I became less afraid, I began to build better relationships with my voices. I talked to them kindly and listened with an open mind. They, in turn, spoke less often about death, softened their demands, and caused less pain. That’s why, I think, paying close attention to what voices say is important. It can be the first step to helping voice-hearers like me listen differently and live more peacefully with their voices.

For me, the process of learning to listen to my voices was also impacted by antipsychotics. Over the years, I have been prescribed perphenazine, quetiapine, aripiprazole, and lurasidone. All of these drugs muffled my voices, making them at once farther away and more internal. On these medications, I could no longer hear my voices through my ears—they came from farther down, as though I had swallowed them whole. The medications also made my voices more straightforward and less creative with their language, forgoing wordplay and preferring simpler, shorter words and more prosaic sentences. However, the content of my conversations with my voices didn’t change.

Both on and off antipsychotics, my voices and I discuss my life and my relationships and their opinions, predictions, and desires. In both cases, they make bold, odd statements. Both on and off medication, I’m usually able to tease through their messages and understand new meanings. Sometimes, antipsychotics even seem like a useful tool to help me do so. They quiet my voices enough that I have the space and silence to think through what the voices might mean. But at other times—on higher doses—the medications muffle my voices too much, so I can barely understand what they are saying. At those times, I feel at sea in my own mind, unable to make sense of the muffled words I still halfway hear. Today, I try to stay on the lowest possible dose of antipsychotics (while still maintaining a stable brain). Minimizing medication helps me hear and understand my voices better.

What One of My Voices Says—A Miniature Case Study

Recently, I’ve had the chance to observe the exact words one of my voices uses. Six months ago, the energy-field voice—the one who tends to communicate in visions and sensations—was causing terrible pains in my right hip again. She was also causing intrusive emotions, mainly a sudden, destructive rage that descended on me as often as once a week. During these rage episodes, I verbally attacked people close to me. Afterwards, I couldn’t remember what happened. After months of struggling with these agonizing and dissociative symptoms, I struck a deal with my voice. She would stop causing the pain and rage and, in exchange, I would spend thirty minutes a day writing with her. She would dictate what I wrote. For the first time, she would consistently use words. She wanted, she said, to help me understand her.

In February 2026, we began our new arrangement. It quickly evolved into written dialogues: I wrote what I wanted to say to her, then transcribed her responses. Over time, I accumulated notebooks’ worth of conversations. As I did, the pain and rage episodes ebbed away. My mind and body were no longer battlegrounds.

Today, I continue to write with this voice every day. Looking at my notebook pages, I can see how my voice talks to me, and how our conversations have transformed us both.

About half the time, my voice speaks clearly, often in short, repetitive sentences. The other half, she speaks in odd metaphors that I have trouble understanding. We talk about my life: my relationships, my writing, my past, and my recent choices and behaviors. She makes comments and judgments and gives advice. She also tells me about herself. She explains who she is, her relationship to me, and how she got here. She expresses her desires. More than anything, she wants my time and attention, and she wants me to reassure her that I’m not trying to get rid of her.

When I began writing this paper, I thought I would create a taxonomy of what my voice says to me, neatly separating her statements by topics and types. But I found that this did not do justice to the full depth and texture of our conversations, especially when she bends towards metaphor and symbolism. So instead of a high-level overview, I’ll give a few actual examples of what my voice says, drawn directly from my notebooks. These excerpts show the banter, the liveliness, the push and pull, and the frustrating obscurity of our conversations.

Example One

Me (opening the conversation): Windy out.

Her: The wind is a wandering lunatic. Write away, right away. I am an arm and a leg and neither. Bodiless, bawdy. I travel to you. I know what to say. See me during true. This is our forever cousin. This is our dark goodbye.

Me: But what is this?

Her: Our forever cousin, our dark goodbye.

In this excerpt, my voice speaks in a rhythm that feels almost literary, playing with language (”Write away, right away;” “Bodiless, bawdy”). To an outside observer, this might look like disorganized speech, a jumble of meaningless associations. But I believe my voice is doing something meaningful: she is trying to define her own nature. By calling herself “an arm and a leg and neither,” she is acknowledging her strange, dual status as a bodiless presence that nonetheless occupies physical real estate in my life. When I push for clarity, she retreats into cryptic repetition. To me, her cryptic language isn’t a psychotic symptom. It’s how she expresses complex emotions and ideas that can’t be expressed in any other way.

Example Two

Her: I am a being of infinite energy. Rage is my red light.

Me: Do you think rage [episodes] will make things better? If so, why?

Her: I think it will make us safer. Make us cookie cutter soft. Make us run in place a little. Make us not run off.

Me: What do you mean? Some of that seems like the opposite of what rage does.

Her: Rage makes us reticent in our worldview.

Me: To me that seems like the real opposite of rage.

Her: Rage keeps us safe by insulating us…Rage is medicine for every broken heart…

This exchange captures the moment a destructive, terrifying symptom, dissociative rage, is successfully translated into an interpersonal dialogue. Instead of that rage taking over my body and driving me to attack the people I love, it’s safely contained on the page, where the two of us can debate its utility. Here my voice shows herself as—as my therapist suggested—a flawed protector. In her own surreal logic, she believes the rage is a protective armor (”insulating us”) designed to heal a vulnerable core (”medicine for every broken heart”). As I question her logic in real time, I’m able to be an active participant in my own mind. I’m not a passive host to an illness; I’m a partner helping her see that her methods are hurting the very things she wants to protect.

Example Three

Her: I’ll help you achieve your true nature if you let me…One year from today you’ll be huge. One year and you’ll let me use you…

Me: How will you help?

Her: Gentle guidance.

To me, this fragment highlights the shifting power dynamics and the constant negotiation of boundaries between my voice and me. Her initial declaration carries a slightly chilling, invasive edge (“let me use you”). This could easily feel like a slide toward a loss of control. But when I refuse to panic and instead meet my voice with a calm, curious question, “How will you help?”, her posture softens. The ominous promise to “use” me transforms into a promise of “gentle guidance.” My voice is not a static, unyielding script broadcast into my brain. She is a responsive, challenging, thoughtful conversation partner.

It’s important to note that these examples are not cherry-picked for meaningfulness. These are the conversations we have every day, across dozens of notebook pages. My voice reacts to me and I react to her, and through our conversation, we reach new conclusions. I learn to understand the meaning of what she is saying, even when she refuses to clarify, and she learns to understand me, as well. We make meaning together. If I thought my voice was nothing more than random, psychotic noise, then that’s all she ever would have been. She would never have become a companion, an interlocutor, and something (or someone) capable of transformation.

See also:

Share

“Therapy is not easy and it’s particularly not easy when the patient is extremely emotionally unstable because they’ve never had a figure in their lives to help them contain their emotions. So, the whole point of therapy (not only for “borderline” patients but for all patients) is for the therapist to act as a container: they need to remain calm enough, and neutral enough in order to gracefully receive the projections, identify with them “just enough” so that they can understand them, contain them, then metabolize them, and then return them back to the patient in a more palatable and thinkable form. And this is a lot to ask of a person but that’s the job…”

— , in conversation with

In a recent exchange on Miss Apprehension, Zavlis offers a delightfully lucid Bionian picture of psychotherapy. The patient projects onto the therapist, on this reading, to communicate, to regulate, to evacuate an affect they cannot bear on their own. The clinician’s task is to receive it, to identify with it just enough to understand it without being swept into it, to process it, and to return it in a form the patient can tolerate. “This is a lot to ask of a person,” Zavlis writes, “but that’s the job.”

This last bit has been rattling around in my mind. Zavlis is talking about psychotherapists but it applies, in part, to psychiatrists as well since we deal with many of the same problems and the same patients. And yet it seems to me that the psychiatric community has decided that it is not, in fact, our job.1

Many “psychopharmacologists” (as well as nurse practitioners and other advanced practice providers who do a great deal of psychiatric prescribing these days in the US) adopt the attitude that they can be responsible for diagnostic assessments and medication management and do a good job of it while distancing themselves from the emotional lives of their patients. The psychological tangle of ambivalence, frustrations, idealizations, projections, etc., belongs to the therapy hour and to the therapist. The presence of these dynamics in the prescribing room is irksome, met with annoyance and impatience. The prescriber’s remit is narrow and clean. “I’m just here to manage your medications. That sounds like something to bring up with your therapist.”

The trouble is that this is not how prescribing works. (David Mintz’s psychodynamic psychopharmacology is the prime source of wisdom here; see my Q&A with him). The neurochemistry of illness exists in a web of temperament, medications carry meaning and emotional significance, treatment response and resistance are relational as well as pharmacodynamic, and the patient-doctor relationship exists in the graveyard of developmental history.

So affect does not stay politely in the therapist’s office. It shows up wherever it needs to, wherever it must, in whether the patient takes the drug, in how they take the drug, in whether and how they experience its side effects, in the patterns of their exacerbations, in whether they feel heard and seen and how they act out, and in whether they need the treatment to fail. The prescriber who is unable to or refuses to metabolize the emotions finds that the undigested material returns to haunt the therapeutic relationship… as nonadherence, as nocebo, as the slow accretion of polypharmacy, as the “treatment-resistant” patient who is resistant in part because no one in the pharmacological relationship would hold their hesitation and fear and fury long enough to make sense of it.

In some ways, this failure isn’t unique to psychiatry. Under the pressures of time and throughput and an orientation towards disease processes at the cost of the person, medicine has grown steadily less patient with the psychological dimensions of sickness. Patients bring difficult emotions around their illness and treatment to the clinical encounter that, if left unexamined, can corrode their care. When psychiatry is consulted in the hospital, it is at times because the medical and surgical teams are unable to hold and tolerate the affect in the room. They do not have the time, the patience, the attention to deal with it. At some point medicine decided that this is not the job. Or more accurately, the medical bureaucracy decided that clinicians are too highly paid, their time too expensive, for it to be wasted on dealing with this superfluous stuff, and a whole new generation of physicians grew up under the new regime and accepted it as the norm.

Not everyone can do everything, that is true, and specialization is necessary. Most psychiatrists do not need to be psychotherapists (I am not), but they do still need to be attuned to the psychological complexity of the whole person and the relational aspects of psychiatric treatment. Containment is not outsourceable, not fully. The patient ambivalent about a medication needs the prescriber to hold that ambivalence, because the prescriber is the one guiding the pharmacological treatment, and those decisions cannot be made in the therapy room.

Zavlis is right that it is a great deal to ask of anyone. It is a great deal to ask of therapists, who at least have (under ideal circumstances) the training, the supervision and the structure to do the work. Prescribers rarely have anything of the sort. So part of what is needed here is structural. But it begins with relinquishing the fantasy of “pure” medication management. The emotional and relational dynamics are not an intrusion upon the work of prescribing. They are a part of the work itself. Whether you know this or not, whether you accept it or not, that is the job.

See also:

Share

“Why have psychiatrists failed to reach agreement about the diagnosis of schizophrenia? In a nutshell, it is because schizophrenia is an idea without a single defining principle… The problem with schizophrenia is that its intention is ambiguous, and therefore the attempt to reach a consensus on its extension is doomed to frustration. The clarity of Kraepelin’s original idea has been lost, and it now has, not one, but two or even three totally different defining principles.”

I Brockington, Schizophrenia: Yesterday’s Concept (1992)

A little over a century after Bleuler gave us the word, psychiatry cannot agree on what, if anything, to do with “schizophrenia” as a diagnostic construct.

In 2022, Schizophrenia Research devoted a special issue — Re-Inventing Schizophrenia: Updating the Construct — to this question, and the forty or so editorials published in it make for a peculiar reading experience. There is broad agreement on the ways in which the construct of schizophrenia is limited and imperfect, but there is little agreement on what to do about it.

The complaints are by now familiar to most professionals in the mental health field. The category is heterogeneous, in terms of the diversity of clinical profiles and outcomes as well as in terms of likely bundling together many different etiological processes. While there are promising developments in discovering biotypes of psychosis (see B-SNIP biotypes), no biomarker, or even a set of biomarkers, corresponds specifically to “schizophrenia.” There are no points of rarity that separate schizophrenia from its neighbor psychotic disorders; schizophrenia shades into schizoaffective disorder, into bipolar disorder, into psychotic depression, without any natural discontinuity. The risk genes for schizophrenia are shared with bipolar disorder, schizoaffective disorder, and other psychiatric disorders. Its diagnostic thresholds are semi-arbitrary. Pat McGorry argues that the six-month duration criterion in the DSM has “institutionalized the basic flaw” of the concept by hard-coding chronicity into it. The diagnosis has clinical utility, but it is thin, and dimensional approaches to psychosis have plausibly similar or superior practical utility. Interestingly, there is still no agreement on what is even central to the concept. DSM and ICD have enshrined positive symptoms (such as delusions and hallucinations) as central, but the originators of this concept, Kraepelin and Bleuler, had emphasized chronicity, prognosis, cognitive impairment, thought disorder, and negative symptoms. It is well-demonstrated that negative symptoms and cognitive impairment are stronger determinants of long-term outcomes in those diagnosed with schizophrenia than positive symptoms.

Confronted with this list of problems, the field has divided into preservationists, reformers, and discarders when it comes to the “schizophrenia” construct. Do we say that we have nothing demonstrably better yet, so we keep it and iteratively improve? Or do we reform the DSM concept, perhaps to emphasize cognition/prognosis as central? Or do we discard the concept in favor of a psychosis spectrum?

The Epilepsy Comparison

Among the preservationists/reformers, Sophia Frangou offers a defense using an analogy with epilepsy.

The term “epilepsy” is archaic, like “schizophrenia.” It is a Greek term from the fourth century BCE meaning ‘to seize’ or ‘to attack,’ freighted originally with the belief that a seizure was the work of a demon or a god. Epilepsy has historically been subject to tremendous stigma and discrimination and still is today to some extent. And yet there is no movement to rename it; the epilepsy community has put its energy into public education instead.

Both conditions are defined by an obligatory core feature (seizures/psychosis) that persists across highly variable presentations with various companion features. Epilepsy is a disorder of the brain characterized by an enduring disposition toward recurrent seizures, together with the cognitive, psychological, and social sequelae; schizophrenia, on the same model, Frangou suggests, would be an enduring disposition toward recurrent psychotic symptoms with associated dysfunctions.

Just as a single seizure isn’t epilepsy, first-episode psychosis isn’t necessarily schizophrenia. Frangou’s observation is that in medicine these boundaries are set by consensus and revised as understanding improves. Epilepsy draws its line chiefly by recurrence, or by a high risk of recurrence signaled by EEG epileptiform activity or a neuroimaging abnormality. The parallel task in psychosis, on this reading, would be demonstration of recurrence or the presence of robust predictors of psychotic recurrence. (DSM’s 6-month duration requirement for schizophrenia is one way of enriching for chronicity.)

Extending the Epilepsy Comparison

I have also been thinking about a comparison between schizophrenia and epilepsy (and had started doing so before reading the Frangou piece), but my comparison is more along the lines of how classifications of epilepsy can inform classifications of psychosis.

The establishment framework of epilepsy classification comes from the International League Against Epilepsy. The current ILAE system is a multilevel diagnostic scheme: classify the seizure type, then the epilepsy type, then, where possible, the epilepsy syndrome, with a parallel axis for etiology. It is an integrative characterization that relies on the clinical picture, EEG findings, neuroimaging, and genetics, and it is built to be usable by the general neurologist and to guide treatment.

The rival tradition comes from Hans Lüders and his colleagues, first as the Semiological Seizure Classification in the late 1990s and later as a broader four-dimensional scheme (4D-EC). Lüders insists that the description of a seizure (that is, its semiology, what is actually observed to happen) should be kept separate from what we infer about it. This is because the two don’t correspond perfectly; the same seizure semiology can arise from different localization patterns. The semiological classification is deliberately agnostic about the EEG, about localization, about cause; it describes an “automotor” or a “dialeptic” seizure purely as an observable phenomenon. Around that descriptive core the four-dimensional system arranges three further, explicitly independent dimensions: the epileptogenic zone, the etiology, and the associated comorbidities.

Where ILAE would call “focal impaired-awareness seizure with automatisms” (the old complex, partial seizures), 4D-EC would call “automotor” on semiology, without reference to “focal.” Lüders’ objection to the ILAE approach is that its terminology smuggles inference into observation. To call something a “focal motor seizure” based on clinical observation is already to have made a claim about how/where in the brain it originates. The “epileptogenic zone” in 4D-EC is a theoretical, provisional construct. It is operationally the region whose removal renders the patient seizure-free. It can be expected to be revised as work-up proceeds without disturbing the semiology at all. The clinical description is stable; the inferences are revisable.

Epilepsy has an objective anchor that psychosis currently does not. There is an objective correlate of the seizure (the ictal discharge on EEG) and nothing equivalent for psychosis. The lesson for psychiatry, IMO, is in the general philosophy. We need to distinguish what we observe from what we infer; keep the dimensions independent (e.g. not conflate symptomatology, prognosis, and cognition), so that reassessing and revising one does not destabilize the others; and treat the inferential layers as provisional constructs rather than as clinical facts.

Enduring Disposition Towards Recurrent Psychosis

Let’s come back to the idea of schizophrenia, akin to epilepsy, as an enduring disposition toward recurrent psychosis. The current DSM does not define schizophrenia this way. The DSM construct of schizophrenia nor the old Kraepelinian and Bleularian concepts are “a tendency toward recurrent psychosis.” The DSM concept requires a stipulated period of functional decline, symptom duration, and a specified mix of clinical features, the validity of which is all quite unclear. An epilepsy-style definition sweeps those thresholds aside in favor of something closer to recurrent psychosis.

Aside from the recurrence, the second aspect is unprovoked. Isolated seizures with low risk of recurrence are excluded from the diagnosis of epilepsy. A seizure provoked by an acute insult such as a metabolic derangement, a toxin, an acute brain injury is an acute symptomatic seizure, not epilepsy. “Unprovoked psychosis” would be psychosis that is not an acute symptomatic phenomenon: not the psychosis of intoxication, of delirium, of the acute phase of an autoimmune encephalitis, etc. This is basically the primary versus secondary psychosis distinction.

Schizophrenia in this sense would be conceptualized as a primary psychotic disorder defined as an enduring disposition toward recurrent, unprovoked psychosis with associated cognitive, psychological, and social dysfunctions.

Psychosis as Multidimensional Space

What would a Luders-style characterization of psychosis look like? What would the dimensions be? I believe it would look something like below:

1. Symptom dimensions

• a. Positive

• b. Negative

• c. Disorganization

• d. Affective admixture

• e. Catatonia

2. Course and staging

• a. Acute/chronic

• b. First-episode, recurrent, persistent

• c. Onset character (abrupt vs insidious)

• d. Premorbid functioning and prodromal decline

3. Cognitive functioning

• Cognitive profile (processing speed, working memory, verbal learning, executive, social cognition), severity, and trajectory (static vs declining)

4. Functional impairment and disability

5. Etiology

• Primary vs secondary (e.g. secondary to high-penetrance CNVs, 22q11.2, anti-NMDAR and other autoimmune disorders, substance-induced, neurodegenerative, etc, etc).

• Candidate biomarkers for primary psychoses, e.g. B-SNIP biotypes and polygenic risk scores

6. Treatment response

• Responsive/resistant to standard antipsychotics, clozapine-responsive/ultra-resistant

Any particular case of psychosis occupies a particular position in this multidimensional space, and different DSM diagnoses consist of different regions of this space.

Where “Schizophrenia” Sits

The prototypical case of schizophrenia in a textbook carves out a describable region of this space: presence of positive symptoms (hallucinations, delusions, disorganization); a substantial burden of negative and cognitive features; primary rather than secondary etiology; prodromal decline preceding onset; chronic or recurrent course; and high baseline functional impairment.

But move along any one of the axes, away from the center of that region, and there is no sharp boundary to be found. Shorten the course and we enter “schizophreniform” and “brief psychotic disorder” territory without ever stepping over a natural discontinuity. Turn up the affective dial and we slide through schizoaffective disorder into psychotic mood disorder along a gradient. Follow cognition and we will find cases of DSM schizophrenia without cognitive impairment and bipolar psychosis with cognitive impairment. Follow prognosis and we will find cases of good prognosis DSM schizophrenia. Etc.

Schizophrenia exists as a region of multidimensional space but without any natural boundaries separating it from other psychoses.

Agreeing on the Contours

Rajiv Tandon, in his editorial in the issue, is in favor of holding the center, that is, retaining the construct of schizophrenia pragmatically while working collectively toward one shared, clearly bounded definition. The first order of business, in his view, is agreeing on “the contours of schizophrenia.”

I am also in favor of agreeing on the contours, though not quite as he intends. Before we relitigate validity, he says, we should ensure we are all pointing at the same diagnostic construct. I believe that instead of a pragmatic DSM-style schizophrenia category, a multidimensional space characterization of psychosis is a better way for the field to agree on the contours of the problem. A common set of axes is a far more stable shared reference than a diagnostic label that different people operationalize differently or where operationalization relies on arbitrary cut-offs. If we want everyone talking about the same thing, we have to agree on a coordinate system. Furthermore, it’s not just that we want people to agree on “schizophrenia,” we want them to agree on psychosis broadly. For too long we have neglected the spectrum of psychotic experiences and devoted our attention to schizophrenia.

The contours we can come to agree on are the contours of a dimensional space, and “schizophrenia” becomes a fuzzy region within it. That is much closer to William Carpenter’s position of schizophrenia as a clinical syndrome without an essence. We are better off reorganizing the schizophrenia spectrum as primary psychoses and treating the specific psychopathologies present in each individual.

An illustrative precedent of retaining a syndrome within a dimensional classification comes from an unlikely corner… the ICD-11 classification of personality disorders. ICD-11 abolished the categories of personality disorders altogether, and created a rating of severity and a set of trait-domain qualifiers (Negative Affectivity, Detachment, Dissociality, Disinhibition, Anankastia). But the ICD-11 architects kept one of the old categories as an optional “borderline pattern” specifier (added, by most accounts, reluctantly, under pressure from clinicians who weren’t ready to give up their beloved borderline personality disorder category). The borderline pattern specifier is not a categorical diagnosis in the old sense. It is simply a way of pointing towards a fuzzy, heterogenous cluster of dimensional profiles to record that these traits have cohered into a recognizable, clinically familiar shape.

That may very well be the template for future schizophrenia in a classification of primary psychoses. Build a multidimensional space for characterizing psychoses and retain “schizophrenia” as an optional pattern specifier for those who cannot bear to give it up, the ones who think it offers a clinical utility that cannot be replaced by a dimensional characterization.

DSM-5 schizophrenia, however, is an awkward construct that cannot give up chronicity and cognitive impairment but also cannot commit to it. It is arbitrary and unprincipled. Even if we retain a schizophrenia specifier, I do not believe it is wise to adopt the DSM-5 definition.

I think there are two reasonable moves. Either we reconceptualize schizophrenia, epilepsy style, as “recurrent, unprovoked psychosis,” in which case it dissolves into the broader dimensional characterization of primary psychoses and there is no need for schizophrenia specifier at all because schizophrenia simply is primary, recurrent psychosis.

Or, we embrace the textbook schizophrenia prototype and approach schizophrenia as a region of multidimensional space characterized by a prodrome, by cognitive impairment, with a substantial burden of negative symptoms, and with a chronic or recurrent course, in addition to positive symptoms. That is, unlike DSM-5, we incorporate these features into the definition itself.

It is still reasonable for a skeptic to ask, however: why bother? Why hold on to this particular region of psychotic space as something special and distinctive? Is it because we cannot give up the hope yet of finding a unitary disease process behind this profile of clinical features? There is no specific treatment for schizophrenia, compared to other psychotic disorders, no specific biology, and no single defining principle. So what is so special about this yesterday’s concept?

See also:

Share

While most depressed and suicidal people who start an antidepressant experience a reduction in suicidality over the course of treatment as the depression improves, in some cases antidepressants such as SSRIs can lead to suicidal thoughts, suicide attempts, or suicide death. The signal for suicidal ideation is clearer for children and adolescents in clinical trials (hence the FDA black box warning), but the concern is not absent for adults.

SSRI-related suicide deaths in adults at the population level seem to be uncommon enough that observational studies of adults do not show a conclusive link. In RCTs and observational studies, to oversimplify a rather complicated and mixed body of literature, SSRIs seem to neither increase nor decrease suicide rates in adults overall—which could either mean that there is no substantial effect either way or that the two effects are roughly equal in magnitude and cancel out.

In my clinical work, I frequently encounter individuals who tell me that they have experienced suicidal thoughts on antidepressants. This experience is often restricted to a particular antidepressant, and a different one is tolerated well, but not always. In a small number of cases (usually with significant baseline mood dysregulation), all monoaminergic antidepressant medications seem to provoke suicidality.

The scenarios of SSRI-related suicidality I have observed and heard about from patients tend to fall into the following:

• Initiation of antidepressant leads to intense anxiety or dysphoria that produces (or exacerbates existing) suicidality

• Treatment with antidepressant leads to manic or mixed symptoms, which lead to suicidality

• Antidepressants make the person feel emotionally indifferent, and in the context of existing suicidal thoughts, it leads them to act on the suicidal thoughts because the usual emotional aversion to suicidal thoughts gets replaced by, “Eh, so what if I die?”

• Stopping an antidepressant abruptly (in someone who has been on them for a prolonged period) leads to a sudden exacerbation of mood and suicidality (withdrawal-related suicidality)

Such things make physicians uncomfortable, but I’ll restate it clearly: on starting an antidepressant (as well as going off them abruptly), some patients can experience worsening anxiety, agitation, restlessness, irritability, mood lability, or akathisia. These can subsequently induce or exacerbate suicidal thoughts, which in some cases can lead to suicide attempts and, rarely, suicide deaths. In my clinical experience of working with people with complicated mood and anxiety disorders, these issues with antidepressants are common enough that I try to see patients soon after starting an SSRI so that I can address early issues with tolerability. The idea of just starting an antidepressant and seeing them a month (or months) later worries me. As a psychiatrist, I get to see more complicated cases, and my experience doesn’t generalize to primary care, but I do think that even in primary care, it should be anticipated that a substantial number will struggle with SSRI-initiation and that a close follow-up after starting an SSRI is a useful general strategy.

SSRIs perform best, IMO, when the problem is chronic—generalized anxiety, dysthymia, adjustment disorder with high neuroticism—or sufficiently severe, e.g., major depression. Stress-related anxiety or depression that is mild and anticipated to be self-limiting is best addressed via supportive interventions or short-term use of quick-acting medications, such as sedatives. SSRIs can still be reasonable options in such situations, but the risk-benefit considerations are not quite straightforward.

We accept all kinds of risks in our lives. We drive cars on roads, we fly on planes, we drink alcohol socially, we use tobacco and cannabis, we invest our lifesavings in stocks, we undergo general anesthesia for surgical procedures, etc., etc. When my son was an infant, he loved being in a particular bouncer. We used it all the time. This is despite the fact that there was a warning prominently displayed on it. “Fall Hazard: Babies have suffered skull fractures falling while in and from bouncers.” Essentially, we accepted a very small risk of a catastrophic event because of the tremendous everyday convenience the bouncer offered us. Such considerations are ubiquitous in healthcare.

Every time a person uses an antidepressant (or any medication, for that matter), there is a small possibility that their experience may go very badly, sometimes in life-altering ways. Risk is ubiquitous in medicine and in life; the possibility of iatrogenic harm is unavoidable. This will not stop people from using antidepressants and other psychiatric medications. I have worked with many patients who experienced serious adverse effects with an antidepressant in the past but were still interested in trying others because they were desperate for relief.

But being transparent with the public about these risks accomplishes two things.

First, if patients and clinicians are aware of the possibility of harm, they can recognize the problem early and stop the medication before it progresses.

Second, it serves as a reminder that the condition being treated should be distressing enough or severe enough for the person or the benefit of the medication advantageous enough that they are willing to accept the possibility of uncommon but serious adverse events. The threshold for what counts as distressing enough or severe enough or advantageous enough will be different for different people, but what that threshold is in any particular situation for any particular person is worth giving some thought to.

This discussion was originally published as part of a post (Dec 2024) about Thomas Kingston’s death and has been edited to function as a standalone post.

See also:

Share

Sorbie Richner is a renegade independent scholar from the Midwest who writes on her substack, Miss Apprehension.

This essay contains descriptions of self-harm, suicide attempts, and suicides. It also contains spoilers for the film “Harold and Maude” (1971) and the show “The Haunting of Hill House” (2018).

Suicidality has been a main character in my life since I was a little kid. I started covertly making it other people’s problem starting when I was about 9 years old by externalizing it as rage and violence at home and bizarre behavior in school. It overtly became other people’s problem when I was about 11 and I started doing stuff like burning myself with candle wax and slicing open the bottoms of my feet. I was first hospitalized when I was 13, and went on to be hospitalized many more times for almost a decade. The behaviors that led to my (always involuntary) hospitalizations¹ ranged from talking too openly about my desire to die, to very medically significant suicide attempts that landed me in the ICU. I haven’t been hospitalized in many years, I haven’t done what clinicians sometimes call “suicidal gestures” in as long. I’m not really sure what that means about the presence of suicidality in my life today, though. I’m still trying to make sense of what was going on all those years.

Most people who write about suicidality don’t know what the fuck they’re talking about, even clinicians who work closely with the suicidal. I know from reading a lot of books and papers and hearing a lot of Discourse that they know about suicidality in the abstract. They know what it looks like on someone else. I’m not the type to defer epistemically to “lived experience,” or to participate in “stay in your lane” kind of discourse. But even in the era of “mental health” discursive oversaturation, I have not heard that many frank discussions of suicidality by the acutely suicidal, formerly or otherwise. Maybe that’s because a lot of those people are in the psych ward, on the street, or dead. Regardless, those discussions need to be out there, and because they aren’t, we are seriously lacking conceptual, linguistic, and discursive tools to talk about this. So I’m going to be talking about my own experience a lot, because it’s what I know. It’s what I’ve got.

There were times in my life where the suicidality leaked out of me like juice out of trash bag on a hot sidewalk. At such times in my life where it was very public and obvious that something was wrong, a lot of people made misguided attempts to commiserate. “I know how you feel; I have taken prozac for a year.” “I know how you feel; I used to cut my wrists.” “I know how you feel, I have wanted to kill myself before.” These sentiments were counterproductive, because these people didn’t know how I felt. They made me feel like the enormity of the pain was invisible. They made me feel even more alone. In the rare times I did meet someone who knew how I felt (always in psychiatric hospitals and later rich girl rehab), I was so defensive against botched, intrusive attempts at sympathy that I was completely unable to let in genuine emotional resonance, which served to further isolate me. All people need emotional resonance. People who are suffering in ways that are taboo need it even more, because real resonance is all the more scarce. The stakes are high. Isolation with suicidality can kill people. It does kill people. The inverse instinct of inexpert attempts to commiserate is the instinct to send someone to the psych hospital. People who participated in getting me sent to the psych hospital believed they were helping me. They believed they were helping me get to a safe environment where I could stabilize. The psych hospital does not help suicidal people, not really. It further backs them into a corner, it frightens them into submission.

My tone may be coming across as callous to some readers. I think mostly what you’re picking up on is frustration. I’m frustrated that my freedom to talk about this topic was taken from me when I needed it most. It’s frustration in the psychoanalytic sense of the word, it’s the feeling that arises when a desire or need isn’t met over a long, long period of time. I still desire to talk about suicidality, and I still need to. And I needed to hear people talk about it back when suicidality was very active in my experience. I care about the needs of suicidal people. Mincing words and being overly gentle is NOT what suicidal people need. Suicidal people don’t need to be treated like they are ticking time bombs. Acting like you are scared of someone is a surefire way to isolate them and give them feelings of shame.

What is it doing there?

For many years, on and off in my teens and twenties, I was treated by a psychodynamic psychologist. One of the greatest strengths of our work together was that she didn’t fear my suicidality. She believed that suicidality, like any “psychopathology” or “maladaptive” behavior, was a mechanism that served some kind of intrapsychic purpose. She was able to hear me say “I want to die” and instead of immediately carting me to the hospital, she would let it be what it was. She would move closer to it instead of running away from it or rejecting it. Instead of trying to squelch it or exorcise it, she would say, “I don’t want to take away something that you need.” Her primary concern was not the suicidality would do to me, but what it was doing there in the first place.

My life from early childhood to my early twenties was characterized by being alternately idealized and denigrated by the people closest to me. I was a genius, then I was a disabled retard, then I was a genius again. I was beautiful, with refined, classic features, then I was ugly and I didn’t know how to dress myself, then I was beautiful again. My deep, strong emotions were a source of passion and empathic acuity, then they were the scary, dangerous, and volatile products of hysteria, then they were an empathic resource again. I was ruining this family, then I was sick and abject, then I was ruining this family again. This kind of treatment is objectifying, it’s dehumanizing: scapegoating is as objectifying as worship. It’s easy to see why denigration is objectifying; it’s a response to the needs of the person doing the denigrating, not to the reality and fullness of the person being denigrated. Idealization works by the same mechanism. And when the regard of your loved ones seesaws between the negative and positive poles of that mechanism, that makes it very hard to know what role you are supposed to play, especially when such seesawing is occurring during key developmental periods. It makes it impossible to know whether you’re going to be seen as a good object or a bad object on any given day. Nothing I did could possibly be right. Even if I was being good, I was being bad. That led to extreme feelings of helplessness and impotence.

I grew up in a very controlling environment. I don’t mean at home; my parents were actually very permissive (except for sometimes, when without warning and seemingly randomly they decided it was time to punish me, at which point they would rain down their wrath—this was another axis of unpredictability). I mean societally. I grew up on the upper end of the upper middle class in a city of rich liberal strivers. My city is home to a large tier one research university which is slowly subsuming the rest of the town. And let me tell you, that town is a pressure cooker. I estimate that half the girls I grew up with now have some severe form of anxiety disorder (GAD, OCD, you name it), anorexia, or both. Whether they would ever get treatment or diagnosis is another question: only those of us whose pathologies obstructed our productivity and our path to a competitive college got treatment when we were young; an inability to do schoolwork is how you know something is really wrong. Otherwise, extreme anxiety that gives you migraines and makes your hair fall out is just the cost of doing business in the professional managerial class. I was fucked up enough early enough in my life that getting me into an Ivy was out of the question, and I only became more fucked up over time. I had other shit to focus on: regulating my emotions and grasping at sanity was a full-time job; I didn’t have the capacity or desire to do that AND my mind-numbingly repetitive precalc homework AND read To Kill A Mockingbird for the 3rd time AND give a shit about the industrial revolution AND learn about the subjunctive mood in Spanish AND regurgitate information about the goddamn periodic table, let alone try to take AP classes. And yet, you can bet that the shame I felt about not being able to keep up or fit in with the Stanford-bound girls (or even the University-of-Michigan-bound girls) was overwhelming. In PMC world, the baseline for being a worthwhile adolescent is being a member of the National Honors Society, excelling in at least two sports (debate club or theater guild is acceptable, as long as you excel), playing a musical instrument at a high level, and volunteering at the Humane Society or the fancy old folks’ home. Suffice it to say that I was not a worthwhile adolescent by these metrics, and I felt it.

All this made me a terror at home, and it made me really weird outside the home. I struggled to make and keep friends, and the problem only worsened as I got older and weirder. My weirdness and confusing behavior was interpreted by those close to me as simple “cries for attention,” up to and including suicide attempts.

These events and circumstances made me feel crazy, worthless, isolated, alienated, furious, despairing, and above all, trapped. I developed a severe allergy to being confined or told what to do. I developed a chasm-sized need for human connection, and an equally large dearth of the skills I needed to have that connection. I developed a persistent need to get away, and I tried. I ran away from home several times. And I tried to kill myself several times.

And what is it, anyway?

Just now, I referred to my “persistent need to get away.” That speaks to an aspect of suicidality, but it doesn’t totally capture it. I find that as I am trying to look directly at it from the vantage of hindsight, it vanishes. So let me approach it by another route and see what I can see.

The distinction is often made between suicidal ideation (I want to kill myself) and suicidal intent (I have procured the weapon and I know when I am going to use it). That’s useful for clinical settings, i.e. deciding if your patient needs to be involuntarily hospitalized. By that metric, though, there are people out there who always have suicidal intent. For the purpose of thinking about my own experiences and writing this essay, I’m going to talk about the acuity of a person’s suicidality, i.e. how close they are to doing it. That’s less cut-and-dry, it’s squishier and more human, and for that reason I like it better for this discussion. Few things are more uniquely human than the self-conscious desire to die.

I also think that of the accounts of suicidality I’ve read in remotely mainstream media, most of those people were not that close to actually doing it—their suicidality was not very acute. This is based on my experience of having had suicidality so acute that I have survived several suicide attempts. It feels different. To one who knows what they’re looking at, it looks different.

People sometimes talk about some suicide attempts as being more “serious” than others. I think that’s true. There are things that everyone knows will kill you if you do them, and there are some that might or might not, and some that might not even hurt you very badly but will look scary. I have done all of those things, and I think each was motivated by something slightly different. I can only see that in retrospect; it is only possible for me to see from this place of temporal remove. From this perspective, I can see that the most acute suicidality is the suicidality of a dead person.

The following delineations can be made along the spectrum of suicidality:

• (not suicidal)

• I wish I weren’t here, I wish the pain would stop

• I wish I were dead

• I want to kill myself

• I am going to kill myself (sometime in the future)

• I am going to kill myself (in x amount of time) and I am going to do it by:
  -a means that might hurt me
  -a means that will likely hurt me
  -a means that is likely to kill me
  -a means that will certainly kill me

• (dead)

On the less acute end of the spectrum lie what clinicians sometimes call “suicidal gestures.” I would draw that line at “I am going to kill myself (in x amount of time) and I am going to do it by a means that might hurt me.” Harold of Harold and Maude (1971) gives us a cartoonish example of the suicidal gesture. (Yes, I really am talking positively about Harold and Maude in my essay about suicide, get at me.) I locate him on the above spectrum between “I wish the pain would stop” and “by a means that might hurt me.” He is straightforwardly making a bid for connection in his staged suicides. His mother writes him off as garishly seeking attention, and she is right. Harold is seeking attention in that he is asking someone to attend to his pain. Harold’s mother’s assessment of the events is correct. The meaning she makes out of it, “my son is acting up again to inconvenience or punish or mock me, and that’s all there is to it,” is not. If a person is “seeking attention,” it’s because they need attention. They need to be attended to.

By contrast, with no preamble and no warning, Maude quietly takes an action that she knows will kill her, and despite Harold’s best attempts to contravene, she dies. The behavior looks different because its motivations are different. Maude, after a long life of directly experiencing the extremes of humans’ will to dominate each other, a life of forcibly living under the terms of others, decides to die on her own terms.

Not to be like “this couldn’t be made today,” but Harold and Maude definitely couldn’t be made today. And yet, Harold and Maude provided some scarce emotional resonance for me when I first saw it some months after my first psychiatric hospitalization at age 13. That movie gets it.

When I was 15 I made a suicide attempt that necessitated the medical hospital (“by a means that might hurt me”) but the psych hospital decided not to admit me because they gauged that I was not in danger of actually killing myself. I had been in Harold mode when I made that attempt. I was in excruciating pain and was completely alone with it; I can see in retrospect that my suicidal gesture was communication more than it was a genuine desire to die. It was an expression of pain that was otherwise inexpressible. Of course, the communication fell on deaf ears. After I came back from my 18-hour hospital stay and getting my drugs rejiggered by my psychiatrist, my mom just made me go to school the next day and no one in my family ever spoke of the incident again.

When I was 20 I made a suicide attempt that almost killed me (“by a means that will certainly kill me”, but the stars didn’t align). I was in excruciating pain, I was completely alone with it, and I had learned by this point that no amount of communicating about it by any means would shift the pain or the aloneness. I had crafted a plan over many months. Because I knew I would die from it, it took me a long time to work up the guts to do it: even when you know that you very badly want to die, taking a human life is a serious act. Luckily for me, several acute stressors suddenly intersected in my life, and I knew it was time. I was in Maude mode when I made that attempt. This attempt was not an attempt at communication. It was an attempt to escape intolerable circumstances and intolerable pain. It was a last-ditch attempt to grasp at agency in a world where I didn’t have any. It was an attempt to do one thing on my terms. This shit is intolerable, and I don’t have to tolerate it.

What followed, because life is not a Hal Ashby film, was some of the most extreme control and domination of my life. The last thing I remember after arriving at the hospital was having my clothes cut off, then I was unconscious for some amount of time (I think it was a few days, but no one ever told me). When I got out of the ICU, I was unable to speak because of having been intubated. I was made to wear special scrubs so that I could be easily identified as a high-risk psychiatric patient, then when a bed opened up, I was moved over to the psych ward. Like at all psych wards, I was under constant surveillence. I was tranqed by injection against my will on several occasions. I was put on a new-to-the-market drug that made me very sick. When I was released, I was shipped back across the country to my parents’ house, where my family was very unhappy to have me there, and I was still drugged out of my mind on the crazy new drug. After about three months, I wound up in a different psych hospital, this time having been taken there in the back of a cop car. And then I was shipped across the country again to residential psychiatric treatment, where I remained for 9 months. The rest is history.

I think probably most people who flirt with suicide are in Harold mode. Goths and emo kids are in Harold mode. I think that most people who kill themselves are in Maude mode, and because of the nature of Maude mode, it’s not really possible to know that someone is in Maude mode until it is too late.

How did it get there?

I remember when I was deep in the throes of it, I would sometimes see in my mind a shadowy figure. (You can see that information as literally or as metaphorically as you need to.) She would be closer or farther. The closer she was, the closer I was to dying. I remember long stretches of time where she was always in the room. She would approach me like a lover, coy and sensual. Sometimes she would stand over me. Sometimes we would breathe each other’s breath. She was so comforting. She wanted me to follow her. She wanted to take me away from the emptiness, loneliness, and profound suffering of my life. She wanted to take me home. She wanted me to join her in death.

I’m reminded of Nell in The Haunting of Hill House (2018). From the time she is a small child, Nell is visited by an apparition she calls “the Bent Neck Lady.” The Bent Neck Lady appears mostly at night. Her neck is twisted at an impossible angle, she has stringy hair and wears a long white nightgown (how original). She appears when Nell is alone and already frightened. Nell and her family are experiencing a lot of upheaval and instability, mostly due to the fact that Nell’s parents are house flippers who have chosen to flip a giant haunted mansion. The Bent Neck Lady begins her visits while the family is living in the haunted mansion. Her first visits also coincide with Nell’s mother’s descent into some kind of mysterious psychospiritual madness; she is possessed by the house and ultimately dies there. Nell and her father and her brothers and sisters flee the house. We don’t get to see what happens in the intervening years, but we learn that Nell continues to be visited by the Bent Neck Lady at night for twenty-odd years. She visits a sleep specialist’s office. She falls in love with the sleep technologist, and over the course of their courting, the Bent Neck Lady, who has now been explained away as simple sleep paralysis, stops visiting. Nell and the sleep tech get married and have a sweet life together, until one night, the Bent Neck Lady pays a visit. The sleep tech husband sits with Nell and gently tries to coax her out of the paralysis, but at that moment, he dies of a freak medical event. Of course, the meaning that Nell makes out of this occurrence is that the Bent Neck Lady killed her husband, the one good thing she had. She tries to cope with her loss by “normal” means (i.e. mediocre-to-bad psychotherapy), but such normal interventions do nothing to shift the magnitude of such abnormal pain. In a state of psychospiritual crisis, Nell eventually drives back to the haunted mansion to contend with the Bent Neck Lady. When she arrives at the haunted mansion, she finds it brightly lit and welcoming her home. We as the viewers can see that the haunted mansion is still dark and haunted, but Nell is in an altered state that makes her see it differently. She enters the house and instead of the Bent Neck Lady, she finds her mother and her late husband. We as the viewers can see that no one is there. Nell dies that night; she hangs herself from some scaffolding in the library. As she falls to her death, her life “flashes before her eyes”: she sees herself as a child in distress and then as an adult in distress. We find out that the Bent Neck Lady that Nell has seen her whole life is in fact herself in the act of dying.

I find it interesting that there are some traditional cultures that know of a suicide spirit. I’m not part of such societies, I don’t know what they know. I know what I directly experienced. In retrospect it is easy to see why a suicide spirit would gain purchase in my life. There weren’t just cracks in my spiritual armor, there were gaping holes. A suicide spirit could easily move in. Whoever was at work in my life, Bent Neck Lady or suicide spirit, she moved into the void where other forces could and should have been at work.

I don’t see that shadowy lady anymore. Sometimes I can feel her somewhere outside my house, somewhere in the neighborhood. But I wouldn’t feel drawn to her even if she showed up on my doorstep. The void that she filled no longer exists, because it is filled with love, meaning, and spiritual richness. I am free, so I don’t need to escape. I don’t need to return home, because I am already home. I don’t need her company, because I am surrounded by people who love me. But because she still shows up in the neighborhood, I am reminded how diligent I have to be in maintaining love, light, and connection to the divine. I don’t want to be tempted to follow her ever again.

This post is an edited version of an essay that was originally published on “Miss Apprehension.” Read the original here.

See also:

Share

In communities organized around antidepressant withdrawal and the broader iatrogenic harm and the deprescribing ecosystem, the term “withdrawal” has acquired an extraordinary breadth and scope. It’s an instance of concept creep on steroids. The term now gets used for a week of brain zaps after stopping paroxetine all the way to years of fatigue and cognitive fog attributed to a drug discontinued long ago. Acute antidepressant withdrawal syndrome is well established at this point; it is more common and more severe than the psychiatric mainstream was willing to admit for an embarrassingly long time. But beyond acute antidepressant withdrawal, there is a lot of confusion and uncertainty, and because after decades of neglect antidepressant withdrawal is finally attracting public attention, there is a strong incentive to stuff more and more forms of medication-related difficulties into this bloated concept.

A taxonomy of post-discontinuation and withdrawal phenomena

The way “withdrawal” is used in iatrogenic harm communities, there appear to be two broad concepts being utilized.

The first is clinical: any clinical difficulty experienced following the discontinuation or dose reduction of a psychiatric medication that isn’t clearly and unequivocally a relapse of the original psychiatric problem. The time duration for “following” ranges from immediately post-discontinuation to several months later.

The second is pharmacological: any clinical difficulty that arises due to the development of neuroadaptation to the presence of a psychiatric medication followed by discontinuation or dose reduction of that medication.

The two concepts aren’t identical, but there is a tendency to assume they are two sides of the same coin. The problem is that clinical difficulties can arise post-discontinuation for a variety of reasons that have little or nothing to do with neuroadaptation, or, in other cases, with just neuroadaptation (e.g. what is experienced is psychopathology altered by neuroadaptation). The causal inference is the tricky part. And we are not yet in a position to directly observe and measure “neuroadaptation.” There are no established and validated biomarkers for this purpose.

Given the very broad nature of these definitions and the difficulties of causal inference, when someone says “withdrawal,” they could be talking about any of the following possibilities. Some of these are extensions of established pharmacology, some are speculative and hypothetical, and some are not withdrawal at all.

Acute withdrawal/discontinuation syndrome is the clearest case. The analogue would be acute alcohol withdrawal. It shows up within days of a dose reduction or discontinuation, brings a recognizable cluster of symptoms (brain zaps, vertigo, nausea, irritability, dysphoria, insomnia, agitation), and is generally self-limiting over days to weeks. Brain zaps in particular are close to pathognomonic when they are present; they don’t show up in depression or anxiety, and you can’t readily explain them away as relapse. Acute withdrawal also tends to respond quickly to resuming the antidepressant at the prior dose.

Symptom rebound is a cousin but conceptually distinct. The amplified, transient return of the original target symptoms past their pre-treatment baseline. Rebound insomnia after stopping a benzodiazepine is the textbook case. By definition it is time-limited; it reflects homeostatic overshoot. For SSRIs, this is usually rebound anxiety and dysphoria. Symptom rebound can possibly occur with or without acute withdrawal syndrome.

Relapse of original psychiatric disorder (e.g. clinical depression or anxiety) triggered by acute discontinuation or rebound. The discontinuation/rebound destabilizes the system to such a degree that a new major depressive episode or generalized anxiety syndrome develops, and requires to be treated as such because it behaves like regular depression or anxiety (it is not transient and doesn’t respond rapidly to restarting the medication)

Protracted withdrawal syndrome covers symptoms persisting for months or years, well past the acute phase. It gets progressively more difficult to say that pharmacological speaking, this is the same sort of thing as acute withdrawal; I will have more to say about it below. The analogue would be post-acute alcohol withdrawal syndrome for alcohol, but that also remains rather poorly characterized with validity issues and remains without formal recognition in diagnostic manuals.

Delayed-onset withdrawal. This is the scenario when symptoms emerge weeks or months after the last dose with no preceding acute phase. Pharmacologically speaking, I find this to be the most puzzling. It requires a mechanism that produces no symptoms during and shortly after the period when the drug is actually leaving the body and occupancy is actually changing, and intense symptoms appear weeks later that are neither relapse nor, proponents allege, better explained by a different psychopathological process.

Several other things routinely get folded into the category of “withdrawal.”

Hypothesized receptor “supersensitivity” syndromes. This is by analogy to tardive dyskinesia, where chronic receptor modulation leaves lasting changes that outlast the drug. Dyskinesias related to dopaminergic supersensitivity are well-established; the extrapolation to serotonergic systems is entirely hypothetical at this point.

Post-SSRI sexual dysfunction (PSSD). Cases of persistent genital anesthesia, anorgasmia, loss of libido continuing for months or years have also been reported to emerge after stopping the SSRI (the more usual case is emergence during treatment). Because of some reported cases of emergence post-discontinuation, it sometimes gets discussed under the withdrawal umbrella, but if these post-discontinuation reports are genuine, they are really a sort of persistent medication-induced adverse effect, not withdrawal in any traditional sense.

Persistent neurocognitive or neurological changes, claims of lasting cognitive impairment or emotional blunting long after discontinuation. The analogue would be lasting cognitive impairment from severe and prolonged alcohol use. Again, to the extent this happens (I’m not sure), this isn’t technically withdrawal, it’s medication-related injury.

Discontinuation-triggered psychiatric syndromes different from the original psychiatric diagnosis. This would include things like new-onset mania, or psychosis, or panic attacks precipitated by stopping the medication without any prior history of these problems. Discontinuation-related mania is among the better-evidenced post-discontinuation phenomena, documented in a few careful case series, but we know very little beyond that. This is a situation where the perturbation of discontinuation leads to a new psychiatric syndrome and the usual stress-diathesis considerations would apply.

Relapse or return of the original condition (without significant rebound and without withdrawal precipitating it). For episodic conditions like episodic major depression, the odds of this happening in the first few weeks of discontinuation are low, but for chronic conditions like dysthymia and generalized anxiety, symptoms can return with original intensity soon after discontinuation (similar to how controlled chronic pain would reemerge soon after stopping analgesics).

And then there is the category of things that may simply be misattributed to medication discontinuation or may have an indirect relationship to medication discontinuation. This would include functional neurological and psychosomatic symptom presentations; nocebo responses; ordinary somatic and psychological variation reinterpreted through a withdrawal lens by people primed to do exactly that, and the coincidental development of conditions like post-viral syndromes or chronic fatigue syndrome, etc.

Finally, “withdrawal” sometimes isn’t simply a clinical description anymore but also an identity. “Being in withdrawal” becomes a standing condition rather than a time-limited state, a mark of membership in the iatrogenic harm community, which is categorically unlike how the word functions in pharmacology or addiction medicine, where you go through withdrawal and come out the other side.

“Withdrawal” has been stretched from a reasonably precise pharmacological concept (neuroadaptive rebound after removal of a substance) into a catch-all, wastebasket of speculative inferences for a wide range of problems that follow any encounter with a psychiatric drug.

The withdrawal intellectuals

At this stage, let’s briefly examine how some prominent figures associated with the withdrawal discourse have approached these issues. I’m thinking of Guy and Virginie-Anne Chouinard, Giovanni Fava, Mark Horowitz, David Healy, and Adele Framer.

The Chouinards offer the most formally differentiated and defensible scheme. Their 2015 classification creates three diagnostically distinct categories, with proposed (not yet validated) criteria: new withdrawal symptoms (novel to the patient, self-limiting), rebound symptoms (the original symptoms at greater intensity, also self-limiting), and persistent post-withdrawal disorders (lasting syndromes that may reflect, hypothetically, receptor supersensitivity).

Fava embeds withdrawal in a larger framework he calls “oppositional tolerance.” On this view, withdrawal is just one expression of a complicated underlying process, i.e. the body’s compensatory adaptation to chronic antidepressant/medication exposure, pushing back against the drug’s intended effect. This creates a whole family of oppositional phenomena, e.g. loss of efficacy over time, paradoxical worsening with treatment, bipolar switching during treatment, withdrawal on stopping, persistent post-withdrawal disorders, refractoriness on reinstatement.

Horowitz (with Taylor) gives a mechanistic specific grounded in receptor occupancy. Because the relationship between dose and serotonin transporter occupancy is hyperbolic, conventional linear dose reductions produce disproportionately large perturbations at the low end. Hence proportional tapering, cut by a percentage of the current dose rather than a fixed amount.

What the occupancy curve story has not done, though, is tell us clearly what “withdrawal” means in a way that would make it reliably separable from the competing explanations. What Horowitz offers (most systematically in the 2022 paper with David Taylor in BJPsych Advancesv) is a set of heuristic distinguishing features, such as onset soon after a reduction (but not always), psychological symptoms co-occurring with distinctive physical ones like brain zaps (but not always), a prompt response to reinstatement (but not always), a “wave” pattern of onset-peak-resolution (but, you guessed it, not always). Some of these are useful pattern-recognition tools, but withdrawal is being defined negatively (by its contrast with relapse) rather than positively, with its own diagnostic criteria. The working definition reduces to something like: symptoms after dose reduction that aren’t relapse. And the criteria for “not relapse” are themselves soft and probabilistic, and inclusive of things like symptom rebound and discontinuation-triggered-relapse.

Once you grant that withdrawal can onset immediately or weeks later, can last days or years, can present with distinctive neurological signs or with symptoms indistinguishable from the previous psychiatric disorder, and can be confirmed by reinstatement response but also might not respond to reinstatement, at that point you have described a category that is far too flexible to do meaningful discriminatory work. That is not necessarily wrong; biological phenomena really can be heterogeneous, but it is diagnostically slippery and scientifically underdeveloped. Validated criteria for the differentiation simply do not exist at present.

Healy, from what I can tell, has been walking away from the “withdrawal” in favor of characterizations like “iatrogenic dysregulation.” The term “withdrawal” imports connotations from the substance abuse world; SSRIs act extensively on peripheral serotonin systems, so a neuroadaptive story centered on brain receptor recalibration may be incomplete in a fundamental way; and conditions like PSSD are not “withdrawal” but drug-induced injuries. The existence of these dysregulations and injuries, neurologically speaking, is speculative, but the move from “withdrawal” to “dysregulation” is a telling one.

Framer, who founded Surviving Antidepressants, seems to work with the organizing idea of nervous system destabilization or dysregulation, that withdrawal symptoms “indicate the nervous system is becoming destabilized,” and this destabilization is what accounts for the variety and variability of symptoms across body systems. Her description takes in acute symptoms, protracted symptoms, delayed-onset symptoms, and symptoms during tapering, all reflective of a destabilization of some sort.

What do we really know?

Once we get past acute discontinuation syndrome, the empirical evidence becomes progressively thin and causal attributions more and more speculative, and this is true no matter which side of the debate one is on.

Acute withdrawal syndrome is fairly well-established as a clinically significant phenomenon. The argument here is largely about the range of incidence and severity, not existence.

Symptom rebound is pharmacologically grounded and often clinically observed, but because few separate it from acute withdrawal, we have no clear idea of its incidence separate from aggregate withdrawal statistics. The same goes for relapse of the original psychiatric disorder (e.g. clinical depression or anxiety) triggered by acute discontinuation or rebound.

Discontinuation-related mania and other psychiatric syndromes have been reported in case series (Goldstein et al. 1999 for discontinuation-related mania, for example) and at least, based on reported cases, seem to be rare.

PSSD remains without a reliable estimate, and we know even less about PSSD onset post-discontinuation.

Protracted withdrawal syndrome… the evidence base consists of the Hengartner et al. 2020 analysis of 69 Surviving Antidepressants narratives, community surveys, and clinical observation from a handful of specialized deprescribing clinicians. There is no prospective, controlled study documenting protracted withdrawal. Nobody has followed a cohort of discontinuers for 6–12+ months with baseline assessments and a comparison group and shown that protracted withdrawal occurs at a rate above what we’d expect from chance and coincidence and other diagnostic possibilities.

We can say with reasonable confidence that some patients have persistent distressing symptoms after discontinuation that are not explained by return of the original psychiatric condition. The label “protracted withdrawal syndrome,” however, smuggles in the presupposition that it is “withdrawal” in some meaningful sense of the word “withdrawal” and a supposition of mechanistic unity that has not yet been demonstrated.

Delayed-onset withdrawal has the basic pharmacological problem I flagged earlier. What produces no symptoms during the window when the drug is clearing and occupancy is shifting, and then produces symptoms later, once the perturbation is over? It’s not impossible (something, something, cascading downstream effects), but the evidence is almost entirely retrospective self-report with uncertain causal attributions.

Does medicine offer any clean precedent for genuinely delayed withdrawal… physiological dependence where the clinical syndrome shows up well after the drug has cleared? Chronic exogenous corticosteroids suppress the HPA axis and, through prolonged ACTH suppression, cause physical atrophy of the adrenal glands. Stop the steroids and the adrenals can’t immediately resume adequate cortisol output. But the crisis (adrenal insufficiency) need not manifest with clinical symptoms right away. It may appear days to weeks later, often when some physiological stressor arrives that the atrophied glands can’t handle.

Perhaps something similar happens in the case of delayed SSRI withdrawal? The serotonergic system experiences some sort of functional loss. It is able to handle functional demands in the period after discontinuation but fails weeks or months later from the accumulated stress. What we are talking about in this sort of situation is a reduced or impaired physiological capacity secondary to prolonged drug exposure, akin to adrenal atrophy; it is conceptually distinct from classic withdrawal. As should be apparent, this is entirely speculative, and we have no idea what an analogue of adrenal atrophy would be like for the serotonin system and whether it even exists.

The basic problem underneath all this uncertainty is depressing as well as simple. The research infrastructure to study these discontinuation-related iatrogenic phenomena was never built and never funded. The studies that would settle these questions, large prospective cohorts with validated instruments and proper comparison groups, do not exist. Until they do, everyone is forced to rely on clinical observations, self-reports, extrapolations of established pharmacological principles, and unrestrained speculations.

The implausibility problem

When someone says they have been “in withdrawal” for three years, they might mean they have been tapering for three years, or they might mean the last dose was three years ago and they still have symptoms they believe to be caused by stopping the drug. The first isn’t technically withdrawal, and the second strikes most people as implausible.

“Withdrawal,” in pharmacology, is a function of neuroadaptation. When a substance is removed, there is neuroadaptive rebound; adjusted set points based on the continued presence of the substance produce dysfunction until the system readapts with new set points. This runs on timescales of days to weeks for occupancy changes, weeks to maybe months for receptor density normalization.

So what could be driving persistent symptoms years later? If the symptoms are a direct physiological consequence of medication exposure and discontinuation, the situation is that of a (hypothetical) persistent drug toxicity of some sort akin to alcohol-related cognitive deficits or some sort of (hypothetical) super-sensitivity akin to tardive dyskinesia or some sort of (hypothetical) post-viral syndrome-like picture, except it’s post-medication. These possibilities are not instances of “withdrawal” and it’s a misnomer to call them so.

And then there’s the possibility that what is happening at three years is not causally tied to the discontinued drug in the way the person believes. It is a post-viral syndrome or chronic fatigue syndrome that coincidentally developed in the weeks following antidepressant discontinuation. (Given the base rates of these conditions and antidepressant use, when we are looking at large populations, such coincidences are bound to happen.) It can also very well be some form of functional neurological or psychosomatic disorder. Or something else entirely not causally tied to the medication.

The dogmas and unknowns of hyperbolic tapering

PET studies showing hyperbolic SERT occupancy curves are well-established. The trouble is the inferential gap between the occupancy curves and the clinical symptomatology and tapering recommendations. Withdrawal symptoms are not direct consequences of changes in transporter occupancy. They are consequences of downstream intracellular and network-level changes such as altered postsynaptic receptor sensitivity, second-messenger modifications, gene expression shifts, neurogenesis effects, etc. The relationship between an occupancy change and these downstream adaptations need not be hyperbolic at all. If the downstream systems carry their own nonlinear dynamics, then the optimal taper shape is a function of some complicated composite of the occupancy curve and the downstream dose-response relationships, not of the occupancy curve by itself.

Let’s consider the asymmetry between starting a medication and stopping it. When we start a patient on 20 mg of fluoxetine, we take a brain at 0% SERT occupancy and jump it to 70-80% in a very short period of time. The brain adapts over a few weeks… nobody proposes hyperbolically titrating upward in 10% increments over months. Yet the framework implies that on the way down, a reduction from, say, 40% occupancy to 20% is a dangerously large perturbation. But 40% occupancy is pharmacologically subtherapeutic on the way up. So if the serotonergic system can absorb partial transporter blockade without meaningful functional consequence when the drug is being started (much as Parkinson’s produces no motor symptoms until 60–80% of dopaminergic neurons are gone), why would restoring the system toward its native state produce severe symptoms on the way down?

The therapeutic-threshold tells us something about the system’s functional sensitivity. If we need 70-80% occupancy to get a clinically meaningful antidepressant effect, then the system has substantial buffering capacity. It can absorb a lot of transporter blockade before the downstream signal changes in a therapeutically relevant way. Going from 0% to 50% apparently doesn’t do much of consequence.

Neuroadaptation should be proportional to the degree of functional perturbation from baseline, and if subtherapeutic occupancy produces minimal functional perturbation going up, the adaptations laid down at those occupancy levels should be correspondingly minimal.

The standard answer is that a drug-adapted brain is not a drug-naive brain. True, but for the hyperbolic logic to work, it would have to mean that the relationship between occupancy and neuroadaptation is itself nonlinear in a way that does not track the therapeutic dose-response curve. Meaning the system adapts substantially even at subtherapeutic occupancy, and the buffering capacity seen under usual circumstances is no longer present (why though?), and withdrawal is driven by a different unknown and unspecified downstream process than the one producing benefit.

And here is a further wrinkle: if the system has been re-adapting at every step, which is the whole premise of slow hyperbolic tapering, then by the time one reaches 40% occupancy after months of stepwise reduction, the downstream systems should have substantially readjusted, and the acute perturbation at each remaining step should be small. But people in the withdrawal communities routinely say that going down from something like 3 mg of escitalopram to 2 mg of escitalopram produces agonizing withdrawal, which makes little sense in light of the buffering capacity seen under usual circumstances and given the fact that the brain has supposedly re-adapted to the 3 mg dose.

There is also an open question of whether the specific “hyperbolic” shape of tapering is mechanistically relevant, or whether a slow taper of some semi-linear shape of equivalent duration accompanied by equivalent clinical support would do just as well.

Does hyperbolic tapering “work” through the passage of time? If it takes 2 years to taper, a lot would have and could have changed in those 2 years.

Does hyperbolic tapering work for psychological reasons that have nothing to do with pharmacokinetics? A structured protocol provides reassurance, a locus of control, a plan for when symptoms are prominent, and graduated confidence building at each small step. All of which are therapeutic mechanisms. If the active ingredient is structure and reassurance, not hyperbolic shape, then the same support for a slow linear taper of equivalent duration should perform identically.

Is there any evidence that hyperbolic tapering prevents protracted or delayed withdrawal? Not really. And if protracted symptoms reflect some sort of neurological injury (again, hypothetical), then the rate of tapering might make no difference at all, just as the persistence of alcohol-related cognitive deficits doesn’t depend on how fast you taper off alcohol.

Can very long tapers keep people “stuck”? The notion that one’s nervous system is fragile and must be handled with exquisite care can keep the medication the central organizing fact of one’s life in a multi-year taper. Every little fluctuation is filtered through the lens of withdrawal.

Some predictions, frankly speculative

What follows is educated guesswork and a series of personal bets about where the field of antidepressant withdrawal (and withdrawal from other psychiatric medications) goes over the next decade. These predictions are conditional on withdrawal receiving more attention from the medical research community and on the collection of high-quality data through funded research. I don’t know the future. I likely will be shown wrong on at least some predictions. Nobody really knows right now since there is no meaningful data on most of these questions. I’m laying out these predictions anyway, to stimulate further discussion along these lines and to outline my own thinking about these complicated matters.

“Withdrawal” as a broad iatrogenic concept is going to be problematized. As more people become interested in scientifically studying reports of withdrawal, the heterogeneity hiding under the term “withdrawal” will become impossible to ignore, and researchers will start calling for differentiated and more precise characterizations, à la Chouinards. The politics of iatrogenic harm communities will slow it down, because conceptual unity under the banner of withdrawal has been strategically useful for advocacy, and disaggregation opens the door to minimization of some groups with iatrogenic concerns. But the science will force the issue eventually.

Hyperbolic tapering will show modest or no superiority over slow quasi-linear tapering under blinded and randomized conditions. If the shape of the dose reduction matters less than the duration of taper, clinical framing, and the patient’s psychological relationship to the taper, then a slow quasi-linear taper of equivalent duration should perform comparably under controlled conditions. A Cohen’s d under 0.3 is my best guess. By quasi-linear I’m envisioning something like linear dose reduction down to the last standard dose (e.g. 5 mg of escitalopram) and then going down by half or quarter tablet intervals (e.g. by 2.5 mg or by 1.25 mg).

“Hyperbolic” will come to mean “nonlinear” rather than a specific geometric shape following the receptor occupancy curve. In practice I feel this is already underway. The precise matching of SERT occupancy curves will turn out to be unsupported, I suspect, and it will give way to a general principle of gradual, nonlinear (but not strictly hyperbolic) tapering, and research may turn up nonlinear shapes that predict symptom severity or guide tapering better than the exact shape of the receptor occupancy curve.

Hyperbolic tapering will show no advantage for relapse prevention over slow quasi-linear tapering, and both will show higher relapse rates than maintenance treatment. I do believe hyperbolic tapering is superior to a rapid linear taper for relapse prevention, but I doubt the superiority will hold once time duration and expectancy effects are taken into account.

A meaningful minority of people with years-long “withdrawal” will turn out to have something like ME/CFS, POTS, or post-viral syndromes, and no clear causal relationship to antidepressant discontinuation will be established. My estimate is that this will be applicable to something like 10–20% of patients with self-described protracted withdrawal.

Another meaningful minority of individuals in self-described protracted withdrawal will be good candidates for a functional neurological or somatization-related diagnosis. Again, maybe 10–20%. There is conceptual work to be done before this can be stated with confidence. The extension of FND to iatrogenic states needs better characterization.

Tapering outcomes will turn out to depend heavily on expectancy and placebo/nocebo. People who expect severe, protracted withdrawal will have longer, more symptom-laden tapers, even after we control for everything else. Expectancy and nocebo will not explain everything, but they will emerge as powerful predictors of variance. Something on the order of 30-40% of variance will be explained by expectancy and nocebo.

Outcomes will also track personality characteristics, in the way David Mintz’s psychodynamic psychopharmacology describes for pharmacological outcomes generally. Attachment style, distress tolerance, health anxiety, neuroticism, etc, I expect these to emerge as moderators.

The study of withdrawal will move toward a “biopsychosocial” model. In addition to the physiological aspects, the experience of withdrawal will turn out to be modulated by a variety of psychological factors, and the trajectory will be shaped by social context such as community membership, information environment, the therapeutic relationship with the deprescriber, etc, etc. The exclusive focus on receptor occupancy curves will come to be regarded as naïve and reductionistic.

Adjunctive medications will get studied for facilitating withdrawal. Lamotrigine comes to mind as a plausible candidate. Other mood-stabilizing and anxiolytic medications as well. It is also possible that the first agents shown to help will be the ones addressing symptoms like anxiety, insomnia, somatic hyperarousal (e.g. gabapentin, propranolol, clonidine) rather than ones selected by receptor-level reasoning. These medications will be resisted by old-school folks belonging to iatrogenic harm communities, but new patients with no ideological commitments, looking simply for relief, will welcome them from their physicians.

In other domains of substance dependence, the standard approach includes pharmacological management of the withdrawal state. Alcohol withdrawal is treated with benzodiazepines or phenobarbital. Opioid withdrawal is managed with buprenorphine. There is an ideological current in the current antidepressant withdrawal community that is suspicious of pharmacological solutions on principle. Proposing another drug to manage the withdrawal feels like doubling down on the original sin.

Iatrogenic harm identity will get recognized the way illness identity already is. Somebody is eventually going to write about this community in the vein of Rachel Aviv’s Strangers to Ourselves.1 Within a decade I expect one or two high-profile cases of people who lived “in withdrawal” for years publicly reconceptualizing the experience (for a glimpse of this sort of thing, see Lisa Wallace’s story).

Share

There has been a quiet transformation in how we understand the biology of psychotic disorders like schizophrenia and bipolar with psychosis, and I am surprised more people in the mental health field aren’t talking about it. Genome-wide association studies and neuroimaging methods have attracted a lot more attention and have generally under-delivered, but a large-scale, sustained, methodical effort to characterize cognition and brain electrophysiology across the spectrum of psychotic disorders has been fruitful.

I am talking here about the Bipolar-Schizophrenia Network for Intermediate Phenotypes, known as B-SNIP, a multi-site North American research consortium, established in 2007, that set out to find biological markers of psychosis and to understand the role of cognition and brain functioning across psychotic disorders. They have been investigating whether biological patterns emerge that offer mechanistic clues and suggest treatments (they do) and whether they respect our diagnostic boundaries (they don’t).

There are two headline results:

1. Demonstration of a neurocognitive severity continuum that loosely aligns with the schizophrenia-bipolar psychosis spectrum, and

2. Three biologically defined subgroups of psychosis, i.e., “biotypes,” with distinctive cognitive and neurophysiological profiles.

The B-SNIP biotypes have been recognized by the Future DSM committee as among the most promising candidate biomarkers we currently possess.

This post is about how B-SNIP biotypes were discovered, what they appear to show, and how I make sense of them.

The B-SNIP Project

Three methodological choices are key to B-SNIP.

The first is large, transdiagnostic samples, consisting of the diagnosis of schizophrenia, schizoaffective disorder, and bipolar disorder with psychosis (diagnoses were based on DSM-IV). Over thirteen years the consortium recruited more than 700 people with schizophrenia, over 500 with schizoaffective disorder, more than 700 with bipolar disorder with psychosis, and more than 900 healthy community members. This was done as two separate samples of more than ~900 people each, collected years apart, so that any finding in the first sample could be tested for replication in the second.

The second was dense, multi-level measurement. Each participant was assessed across cognition, brain electrophysiology, structural and functional brain imaging, molecular and inflammatory markers, and clinical and social functioning. The core battery that defined the biotypes drew on the following:

• Brief Assessment of Cognition in Schizophrenia (BACS) for general cognitive performance;

• Stop Signal Task for motor inhibition;

• Pro- and antisaccade eye-movement tasks for visual orienting and inhibitory control; and

• Two auditory EEG paradigms (paired-stimuli and oddball tasks) that measure how strongly and how cleanly the brain responds to sound.

These tasks are what researchers call “endophenotypes,” or “intermediate phenotypes,” measurements that sit partway between genes and clinical symptoms.

The third choice was the use of “bio-factors,” groups of biological measurements, rather than single measures. A bio-factor is a statistical composite that combines several related individual measures. For example, antisaccade response latency and prosaccade response latency both index the speed of visual orienting, so they are merged into a single visual-orienting bio-factor. This is done through principal component analysis, a statistical method that allows for such aggregation. In the end, 44 individual biomarker variables were collected into 9 bio-factors.

The biotypes themselves were created by feeding those 9 bio-factors into a clustering algorithm called k-means, run only on the psychosis cases. K-means looks for groupings in the data, sorting cases so that people within a group are as similar to one another as possible. The number of clusters was not chosen in advance; the researchers used formal statistical procedures to ask how many groups the data actually supported, and the answer, in every analysis, was three.

Researchers then sought to validate these clusters. The k-means solution was obtained separately in the original sample and the replication sample, and the resulting bio-factor patterns were almost identical between them, with an intraclass correlation of 0.95. The ICC of 0.95 compares the group-level profiles, the pattern of bio-factor means across the three biotypes. It asks: if you line up the nine bio-factor averages for biotype 1 in B-SNIP first sample against the nine bio-factor averages for biotype 1 in the replication sample, and do the same for biotypes 2 and 3, how similar are those profiles? An ICC of 0.95 means the shapes of the profiles are nearly identical.

When the researchers took the clustering rule derived in one sample and applied it to the other, cases were sorted into the same groups roughly 89 percent of the time. Here the researchers took the actual k-means decision boundaries learned from one sample and applied them to the raw bio-factor scores of every individual in the other sample, then checked whether each person landed in the same biotype they’d been assigned by the independent clustering of their own sample. The fact that roughly 11% of cases were classified differently tells us something about the fuzziness of boundary regions. There’s a meaningful minority of individuals whose bio-factor profiles sit close enough to the borders between clusters that small differences in where those borders fall can tip them one way or the other.

The three-cluster structure is not a statistical fluke of one dataset. It shows up again, in more or less the same way, in an entirely separate group of patients collected years later.

B-SNIP and DSM Diagnoses

As expected, the DSM categories did not correspond to distinct biological entities. Instead, they lined up along a continuum of severity that appears across multiple bio-factor domains. On cognition, all four groups were significantly differentiated: schizophrenia performed worst, then schizoaffective disorder, then bipolar disorder with psychosis, then healthy participants.

Several neurophysiological measures showed the same gradient but in coarser form. The N100 and P300 brain responses followed the pattern but could not separate the two schizophrenia-spectrum diagnoses from each other. Antisaccade performance could not distinguish schizoaffective from bipolar cases. The paired-stimuli brain response could not separate bipolar cases from healthy participants. The stop signal task separated psychosis cases from healthy people but could not distinguish the three psychosis diagnoses from each other. Saccade latency and ongoing high-frequency brain activity showed no significant differences between the DSM diagnoses.

The differences between the diagnoses were also small in magnitude. On cognition, schizophrenia and bipolar psychosis cases differed by less than half a standard deviation. Even when the researchers combined all nine bio-factors at once to maximize the separation, the gap between the two extreme groups reached only about 0.9 standard deviations. And no biomarker or biofactor deviation was specific to any one DSM diagnosis.

While this neurocognitive continuum spans multiple measurement domains, it is dominated by cognition. When the B-SNIP group asked formally whether all their measures could be captured by a single underlying function, 95.5% of structural MRI variables and 65% of neuropsychology-psychophysiology variables fit one cognition-anchored dimension.

So the DSM psychosis diagnoses, analyzed biologically and cognitively, look less like separate entities and more like different points on a shared gradient of neurocognitive severity.

B-SNIP Biotypes

When the B-SNIP researchers set aside DSM diagnoses and let statistics sort the biological variables into clusters, the three biotypes that emerged did not simply recreate the severity continuum in the same way as DSM categories. They showed different profiles of brain activity.

Biotype 1 (B-SNIP1 n=263, replication n=277): Marked cognitive deficit on the BACS, combined with globally diminished neural response magnitudes (low N100, low P300, low paired-stimuli S2 response), reduced ongoing neural activity, and slowed saccade latencies. The defining signature is a dampened brain that under-responds to stimuli.

Biotype 2 (B-SNIP1 n=222, replication n=208): Cognitive deficit comparable to BT1, but a different neurophysiological profile. Ongoing neural activity is accentuated (not diminished), the P200 ERP is exaggerated, and performance on tasks requiring motor inhibition (antisaccade, SST) is the worst of any group. The defining signature is excessive background neural activity with poor inhibitory control.

Biotype 3 (B-SNIP1 n=226, replication n=232): Near-normal on most bio-factors, with modest deviations on cognition and the P200 ERP. Despite carrying a clinical psychosis diagnosis, these cases resemble healthy participants across the biomarker panel.

The canonical discriminant analysis for biotypes yielded two significant functions, unlike the single function for DSM diagnoses. The first function captured “Neural Response Magnitude” (BT1 at the deficit extreme), and the second captured “Neural Disinhibition” (BT2 at the extreme of overactivity and poor inhibition). The resulting centroid separations in two-dimensional space ranged from 2.07 to 2.64 standard deviations… substantially larger than anything achievable with DSM diagnoses.

Biotypes 1 and 2 share severely impaired cognition but seem to arrive there through opposite physiological routes. One brain under-responds; the other is struggling with its own background noise.

From my perspective, we can also visualize this as a 2x2 diagram:

It is notable here that the biotypes do not map onto DSM diagnoses. All three diagnoses appear in all three biotypes. About a third of schizophrenia and schizoaffective cases lack the cognitive impairment usually thought to define them, and a substantial number of bipolar cases carry cognitive deficits as severe as anyone’s.

BT1 was predominantly schizophrenia (40.7%) and schizoaffective (42.3%). BT2 was largely schizophrenia (36.9%) but also contained substantial schizoaffective (21.8%) and bipolar (21.8%) fractions. BT3 was heavily bipolar (48.6%) but still included over 50% schizophrenia and schizoaffective cases.

External Validation

A clustering algorithm will always find clusters if you ask it to, so the real test is whether the biotypes differ on measures that were not used to build them. Reassuringly, they do. The biotypes differ on structural and functional brain imaging, on white matter microstructure, on inflammatory markers, and on clinical and social functioning, none of which went into the original clustering.

The strongest evidence for the reality of biotypes came from measures not used in their construction. Two independent measures were deployed:

Intrinsic EEG Activity: Background EEG recorded during the 9–10 second inter-pair intervals of the paired-stimuli task, when no stimuli were presented and subjects had no task. All empirically derived frequency bands significantly differentiated biotypes (BT1 low, BT2 high) but failed to differentiate DSM diagnoses. This directly confirmed the core physiological distinction between biotypes 1 and 2.

Auditory Steady State Response (40 Hz): In a subset of 437 participants, prolonged 40-Hz stimulation of auditory cortex replicated all three key findings. The N100 onset response was diminished in BT1 (consistent with dampened neural responding). The P200 was accentuated in BT2 (consistent with excessive neural activity). And the sustained 40-Hz oscillatory power during stimulation was low in BT1 and high in BT2, mirroring the intrinsic activity pattern exactly.

Stability Over Time, and the Signal in Relatives

B-SNIP re-measured participants at baseline, six months, and twelve months. The bio-factors were highly stable across that year, with reliability coefficients ranging from 0.76 to 0.95, and the cognition bio-factor was the most stable of all at 0.95. These are trait-like measures.

The researchers also showed that medications could not account for the group differences; across hundreds of analyses, drug use explained almost none of the variance in the biomarkers.

There is also a familial signal. In the original B-SNIP sample, every psychosis case had at least one first-degree biological relative enrolled, and those relatives showed the same bio-factor patterns as the patients they were related to. When cognition is plotted against brain structure and physiology, patients, their relatives, and healthy people all fall along the same underlying function. Bio-factors appear to be tapping into something heritable rather than something produced by the illness itself.

Clinical Recognition of Biotypes

The full B-SNIP biomarker battery is inaccessible in the vast majority of clinical settings, so the consortium developed an algorithm, called ADEPT, that estimates a person’s biotype from a much smaller set of measurements available in a clinical setting.

The first version, ADEPT-CLIN, uses only clinical ratings, the kind any clinician can gather from an interview. With just 10 to 11 such ratings, it assigns biotypes with an accuracy (area under the curve) of about 0.80. The top clinical discriminators, in order of importance, are difficulty in abstract thinking, social functioning (including occupational involvement and prosocial behavior), conceptual disorganization, severity of hallucinations, stereotyped thinking, suspiciousness, unusual thought content, lack of spontaneous speech, and severity of delusions.

How do these features differ across the three biotypes? On these items, biotypes 1 and 2 score more abnormally than biotype 3, and biotype 2 is marginally the most clinically deviant of the three. For instance, on PANSS difficulty in abstract thinking (scored on a 1-to-7 scale), Biotype 2 averages 3.25, Biotype 1 averages 3.04, and Biotype 3 averages 2.46. On conceptual disorganization: BT2 scores 2.38, BT1 scores 2.16, BT3 scores 1.77. On suspiciousness: BT2 scores 3.23, BT1 scores 2.93, BT3 scores 2.65.

The BT1-to-BT2 gap on these clinical features is small, usually just 0.1 to 0.3 points on a 7-point scale. The BT1/BT2-to-BT3 gap is much larger. So the clinical interview mainly separates the cognitively impaired biotypes from the near-normal one. Yet those two biotypes, as the investigators point out, “apparently come by their clinical pictures via different physiologies.” The second version of the algorithm, ADEPT-COG, adds a handful of cognitive tests and pushes accuracy up to about 0.95 for distinguishing one biotype from the rest. That is a large gain, and it makes biotype estimation feasible in real clinical and research settings.

These clinical features are not the same as the ones that best distinguish DSM diagnoses. The top DSM discriminators are indicators of physiological dysregulation (reduced need for sleep, excitement, anxiety, somatic complaints, lassitude), not the cognition-and-social-functioning cluster that separates the biotypes. The algorithm is adaptive: the items assessed, and the order in which they are assessed, are unique to each individual case.

Treatment Implications

Consider the idea of signal-to-noise ratio. The brain has to generate a clear response to meaningful events against a background of ongoing activity. Biotype 1 has a weak signal against a quiet background; the brain under-reacts to the world. Biotype 2 has an adequate signal that is drowned out by excessive background noise. Both end up with poor signal-to-noise, but for different reasons; this would be suggest that one needs interventions to boost the signal in biotype 1 and to quiet the background noise in biotype 2. A sensory training program has shown early, preliminary evidence of enhancing brain responses in biotype 1 cases and could perhaps adapted for reducing background noise as well.

The clearest example of potential clinical application involves clozapine, the most effective antipsychotic but one that is severely underused because of its side effects and monitoring requirements. Clozapine uniquely increases alpha and theta EEG power, the frequencies that are deficient in biotype 1. In cross-sectional data, biotype 1 cases taking clozapine had intrinsic activity comparable to normal, healthy levels, whereas biotype 2 and 3 cases on clozapine were driven further from normal. This raises the possibility that biotype 1 may respond particularly well to clozapine, a question that is now being tested in a clinical trial.

An Analogy: Kidney Function and Insulin Resistance

How should we make sense of what these biotypes are? Here I think an analogy from general medicine would be useful. The analogy is far from perfect but hopefully close enough to be illustrative. (If you can think of a better analogy, let me know!)

Imagine having a large sample of people with a mix of urinary and metabolic problems and plotting two continuous biological dimensions against each other. On one axis, kidney filtration, measured by eGFR, running from normal to low. On the other axis, insulin resistance, running from normal sensitivity to high resistance. This produces four regions on a 2x2 table.

People with normal kidney function and normal insulin sensitivity are, roughly, “healthy.” They may have urinary symptoms but these symptoms are unrelated to eGFR and insulin sensitivity. People with high insulin resistance but preserved kidney function have something like metabolic syndrome or pre-diabetes. People with low eGFR but normal insulin sensitivity have non-diabetic chronic kidney disease, with many separate causes (hypertensive nephrosclerosis, IgA nephropathy, ANCA vasculitis, polycystic kidney disease, reflux nephropathy, etc, etc).

There is a corner where eGFR is low and insulin resistance is high. The dominant story there is diabetic kidney disease, that is, type 2 diabetes leading to diabetic nephropathy. But that corner is not pure. It also contains people with kidney disease from other causes who happen to also have metabolic syndrome.

In this analogy, biotype 3 will correspond to the “normal eGFR, normal insulin sensitivity” cluster. Both have clinical symptoms but for reasons unrelated to these particular biological dimensions.

So what is “low eGFR plus high insulin resistance” cluster? It is a biological region defined by the intersection of two dimensions. It shows real, non-accidental clustering of cases, and it has fuzzy boundaries. It is heterogeneous enough that no single causal story explains every case in it. And yet it contains a dominant etiology, diabetic kidney disease, coherent enough that studying and treating that region is genuinely productive.

My suspicion is that B-SNIP biotypes 1 and 2 are, conceptually, the same kind of thing as the “low eGFR plus high insulin resistance” cluster. They are biological regions defined by the intersection of multiple dimensions. They show non-accidental clustering and fuzzy boundaries. They are very likely heterogeneous enough that no single causal story will explain all the cases in any one biotype. But they may well have enough etiological coherence within the clusters that research and treatment can be productive.

Let’s say it’s 2036 and the B-SNIP biotypes have scientifically “flopped.”

What could have led to this sort of outcome? In my mind, there are 2 major possibilities.

One. It may be the case that for various methodological reasons that are above my pay grade, we have over-interpreted the clusters arising from the intersection between “Neural Response Magnitude” and “Neural Disinhibition,” and in reality, there is just a single continuum of cognitive and neurophysiological severity. Maybe. But even if that turns out to be the case, the neurocognitive spectrum still provides a stable neuroscientific foundation not provided to us by clinical categories, and not all would be lost. We can still meaningfully characterize patients across the psychosis spectrum based on their cognitive and neurophysiological profiles. The neurobiological architecture would be dimensional rather than taxonic but there would still be an architecture to work with.

Two. It may turn out that the biotypes are robust and highly replicable biological clusters but sadly they do not correspond to anything clinically useful. The clozapine-biotype 1 hypothesis fails. Sensory training goes nowhere. That would be disappointing, and these things are hard to predict. Who can say. Still, once we have discovered a stable architecture beneath psychosis, even if it doesn’t lend itself to clinical application in the near future, perhaps because we don’t have the right tools or the right interventions, there is always the possibility that somewhere down the road, unexpected utility may emerge. In 2050, e.g., a hypothetical new treatment developed for psychosis and undergoing RCTs could be found to be effective along BSNIP biotypic lines.

Even granting the reality of B-SNIP biotypes, there is still a lot we don’t know. We are very far from a scientific theory of how psychotic symptoms emerge or how they relate to the neurophysiological and cognitive features. We do not know how trauma, social adversity, cannabis use, infectious exposures, personality functioning, etc, relate to biotypes. We have not “solved” the neuroscience of psychotic disorder, any more than recognizing the “low eGFR plus high insulin resistance” cluster provides us with an etiology of diabetic kidney disease. I am personally hopeful that the “signal-to-noise” ratio framing of biotypes provides a productive link to computational models of psychosis.

It is clear to me that B-SNIP are not disease entities akin to measles or Hungtington’s disease. But we may be a bit closer to something like chest pain with or without ST elevation on EKG (with or without the clinical utility!). It is a start. It is stable rocky ground in a desert of shifting sands.

The two key reference papers for my discussion are:

• Clementz, B. A., Parker, D. A., Trotti, R. L., McDowell, J. E., Keedy, S. K., Keshavan, M. S., ... & Tamminga, C. A. (2022). Psychosis biotypes: replication and validation from the B-SNIP consortium. Schizophrenia Bulletin, 48(1), 56-68.

• Clementz, B. A., Assaf, M., Sweeney, J. A., Gershon, E. S., Keedy, S. K., Hill, S. K., ... & Pearlson, G. D. (2024). Categorical and dimensional approaches for psychiatric classification and treatment targeting: considerations from psychosis biotypes. Neurophysiologic Biomarkers in Neuropsychiatric Disorders: Etiologic and Treatment Considerations, 685-723.

This post is dedicated to Dr. Godfrey Pearlson, who, during my trip to the Institute of Living (Hartford, CT), helped me see the significance of B-SNIP biotypes in a way I had not appreciated before.

Share

See also:

“Mixed Bag” is a series where I ask a guest to select 5 items to explore a particular topic: a book, a concept, a person, an article, and a surprise item (at the expert’s discretion). For each item, they have to explain why they selected it and what it signifies. — Awais Aftab

Darby Saxbe, PhD is a professor of psychology and neuroscience at the University of Southern California. She runs the Neuroendocrinology of Social Ties lab at USC, which studies the neurobiological adaptations that accompany the human transition to parenthood. She is the author of the new book Dad Brain: The New Science of Fatherhood and How it Shapes Men’s Lives (Flatiron Books, June 9, 2026). You can learn more about her here and find her on Substack, Instagram, LinkedIn, X, and Bluesky.

Book: Dad Brain

I’ll get the self-promotional part out of the way first and tell you about my new book, Dad Brain, which is about the science of fatherhood and how it changes men’s neurobiology, health, relationships, and identity. I drew on research I’ve conducted in my lab over the last fifteen years, following first-time parents from pregnancy across the first year postpartum. But it’s not just about my work; it’s about the evolutionary biology of fatherhood and about how men’s fathering roles have changed in contemporary societies and the implications for workplaces and societies. I interviewed dozens of fathers who shared their stories in the book.

As someone who was trained as an academic and has written mostly scientific journal articles, writing a popular science book was really fun. It felt like a sneaky vacation from my “day job”: I get to tell stories and even joke around a little? I’m proud of the book, and antsy and eager to get it out into the world. In the rest of this Mixed Bag, I’ll share some of the concepts, people, and articles that had the biggest influences on me while I was writing it.

Concept: Facultative adaptation

One of the most fascinating aspects of fatherhood is its variability. Some men are hands-on primary caregivers of children, whereas other men have absolutely nothing to do with their own offspring. Fatherhood is shaped in part by our biology—that’s a major theme of my book—but it’s also shaped by our culture and by the demands of our local social worlds. Why would we evolve to have such a wide range of behaviors from a genetically related parent? I find the concept of facultative adaptation to be a useful way to think about fatherhood.

In evolutionary biology and psychology, adaptations can be either obligate or facultative. An obligate adaptation could be called “hardwired”: it develops the same way regardless of environmental conditions. A facultative adaptation, by contrast, depends on the environment. We have the capacity for a range of responses, but the specific response is triggered by a particular cue. In the book, I used the analogy of facultative bipedalism. Humans and birds are obligate bipeds, who will walk on two legs in almost any situation. But other species can switch from four to two legs when conditions change. If lizards need to run at top speed, they’ll rise up onto their hind legs. If great apes need to reach for fruit or carry a stash of nuts, it’s very useful to use their front legs as arms and walk on two legs. Human fatherhood is a little like those bonus arms, allowing human children to receive more care when they need it. Since we are born immature, in need of round-the-clock care, fathers frequently play an important role in helping offspring thrive. But children can and do survive without fathers in the picture. Different societies have different models of “good” fatherhood—whether a father ought to focus solely on the provider role, the protector role, or engage in hands-on care—and contemporary society’s expectations of fathers have been changing quickly, within just the past few decades.

Person: Sarah Hrdy

Hrdy is an anthropologist and primatologist who wrote the books Mother Nature, Mothers and Others, and, most recently, Father Time. Her work grapples with the evolution of parenting behavior, and she popularized the term alloparenting. We humans are alloparents, or cooperative breeders: we raise our children in a community. Because our infants are born immature and in need of intensive care, we rely on multiple caregivers who can pitch in and share in the work of childrearing. We develop big social brains in part so we can monitor who needs care and who can be trusted to provide care.

Not only have Hrdy’s ideas informed my own work, but I am also inspired by her career arc. She was part of a generation of women who fought to be taken seriously within academia. As a graduate student at Harvard in the 1960s, she encountered colleagues who thought motherhood was a frivolous or uninteresting topic. The field’s sexist biases meant that there was little understanding of how female agency might shape reproductive decision-making until she published her observations. She raised kids of her own at a time when mothers were not encouraged to pursue faculty careers. In addition to her academic research, she has written popular science books that are funny and interesting. She also runs a commercial walnut farm with her husband in Northern California that produces sustainably grown walnuts—how cool is that?

Article: Rilling, J. K. (2013). The neural and hormonal bases of human parental care. Neuropsychologia, 51(4), 731-747.

It was difficult to settle on just one article. I thought about citing foundational work by Ruth Feldman, Lee Gettler, Michael Numan, and many others. Ultimately I picked this paper by Jim Rilling, an anthropologist and neuroscientist based at Emory University, because it was published right around the time I was starting to map out my longitudinal transition-to-parenthood study, and it influenced my data collection plan. It’s a review of both the hormone and brain characteristics that undergird sensitive and nurturing parenting. Rilling covers oxytocin, vasopressin, prolactin, and testosterone, and talks about both cortical and subcortical brain systems that are implicated in parental behavior.

Surprise item: The prairie vole

Most male mammals do not engage in hands-on (paws-on?) parenthood. Biparental mammals are interesting to study since they provide closer analogues to our own style of shared care. The prairie vole is a cute, furry critter known for forming long-term, monogamous pair-bonds and for providing both maternal and paternal care. Prairie voles like to cuddle with each other, and they seem to show empathy and helping behaviors, as well as parental care. Bonded pairs even show neural synchrony. Many of these prosocial behaviors seem to be motivated by the oxytocin system, and research on prairie voles has informed our understanding of mating and parenting within male-female couples. Plus, they’re very cute!

See previous posts in the “Mixed Bag” series.

Psychiatry at the Margins is a reader-supported publication. Subscribe here.

Share

My friend and collaborator Alan Levinovitz recently posed a question to me that, slightly paraphrased, goes something like this… It’s relatively easy to argue against the hyperbolic view that mental illness doesn’t exist. What’s much harder is defining “disorder” in a way that draws clear boundaries around the scope of medical and psychiatric expertise; it’s hard enough in general medicine, significantly harder in mental health. The strongest version of the critique isn’t the claim that there’s no such thing as mental illness but rather something along the lines of: Mental health professionals have no good way to define the scope of their expertise, and so they have expanded that scope, along with the domain of “disorder,” in ways that amount to the over-medicalization of suffering and invite skepticism about this claimed authority.

I think Alan is right that this is the more important argument. It’s also an argument that cannot be answered by pointing to brain scans, genetic studies, or DSM criteria. It requires a different kind of answer altogether, and I believe, in the process of answering it, we have to relinquish certain comforting illusions about what grounds the authority of clinicians.

Here is the core of what I want to say: There is no objective or a priori way of determining the authority of medicine and clinical disciplines, and the scope of these disciplines is pragmatic and institutional in nature. It is historically contingent, pluralistic, uncertain, open-ended, subject to revision, and sensitive to the presence of other viable institutional alternatives.

While this may sound deflating to some, I myself find it liberating as well as a more honest and more defensible answer.

Getting the Order of Things Right

The standard move when defending the legitimacy of psychiatry is to argue that psychiatric disorders are real… that they are, in some sense, natural kinds or at least track genuine dysfunctions in the organism. The implicit logic is: disorders exist in nature → medicine is the discipline that treats disorders → therefore psychiatry is legitimate because it treats real disorders.

I believe that this gets the order of things backwards. The attempt to fix medicine’s legitimacy with reference to “disorder” as a fact of nature, to anchor the scope of clinical authority in an objective demarcation between the normal and the pathological, has not succeeded. The philosophical complexity surrounding “dysfunction” and “disorder” is, at this point, well-documented, and I won’t rehearse the debate here. I take it for granted that the project of defining the authority of medicine and clinical disciplines in terms of disorder concepts on the basis of objective, value-free facts has failed. We need a different account of what grounds clinical legitimacy.

Clinical and Pragmatic Justification

So if “disorder” doesn’t do the foundational work, what does? The legitimacy of medicine rests on a constellation of pragmatic and institutional considerations: the presence of suffering, impairment, and harm that exceed our ordinary capacities and the ordinary personal and social resources available to us; the illness experience, which constitutes a call to action for the healing professions; medicine’s ability to accurately understand the nature of, and effectively treat, instances of vulnerability and suffering, and to undertake research where understanding and treatment are lacking; medicine’s accountability to science and society, and the social and scientific standing of its professional training.

In other words, we don’t first define “disorder” and then determine the scope of medicine. Rather, people suffer in various ways, and that suffering arrives at the doorsteps of various institutions (medicine, psychology, social work, education, law, religion…) and the question arises: which institutions have something meaningful to offer, and under what circumstances?

Let’s bypass the philosophical labyrinth of “dysfunction” and consider the matter practically. Experiences and behaviors become problematic in a particular context, and then these problems are brought to clinical attention.

Why do some experiences and behaviors emerge as “problems”? Typically because they are distressing, disabling, or disruptive, and because they are understood (usually on the basis of largely common-sensical, folk-psychological judgments) to be excessive, disproportionate to the circumstances, unintelligible, lacking meaningful connections to the person’s situation, persisting beyond sociocultural expectations, and so on.

Why do some problems come to clinical attention? Because ordinary personal and social resources available to us have failed to address them, and we have reasons to think that healthcare clinicians can do something about them in a way that other social institutions cannot.

This is a thoroughly pragmatic and institutional picture. And when these processes of problem recognition and clinical attention occur transparently, scientifically, democratically, and with good intentions, they go reasonably well.

The Scope of Institutions

It’s worth pausing here to notice that the question about the scope of authority is a question that can be asked of any social institution, and the answer is rarely clean and circumscribed.

What is the scope of Law? There is no essence of “the legal” that determines, in advance and for all time, which human conflicts and behaviors fall within the jurisdiction of legal institutions and which do not. The boundaries of law have shifted enormously across history: marital rape was once outside the law’s concern; blasphemy was once firmly within it. We do not think this historical contingency makes law illegitimate. We understand, implicitly, that the scope of legal authority is negotiated through democratic processes, responsive to social values, shaped by the availability of alternative dispute-resolution mechanisms, and revisable as circumstances change.

What is the scope of Education? There is no natural fact that tells us whether sex education, financial literacy, or civic responsibility are “really” educational matters or matters for families and communities to address outside of formal educational institutions. The answer varies by era, by culture, by political climate, based on reasons that can be good or bad, with advantages and disadvantages. The scope of educational institutes is determined by a society’s collective and pragmatic judgment about what schools can usefully accomplish and what other institutions are available to accomplish the rest.

What is the scope of Counseling and Psychotherapy? This question has been live and contentious for over a century now. The boundaries between psychotherapy, pastoral care, life coaching, peer support, and self-help have been unstable. Clinical psychology has an uncomfortable relationship with medicine; many clinical psychologists work in hospitals, hold appointments in medical departments, serve on multidisciplinary medical teams, but many psychologists also can’t really stop bashing what they understand to be the “medical model” and feel strongly that psychology shouldn’t emulate medicine. Spitzer’s initial proposed definition for DSM-III defined “mental illness” as a subset of “medical illness,” and American psychologists objected strenuously, arguing that conditions acquired through learning experiences and lacking demonstrated organic etiology had no justification for a medical label. The DSM-III task force yielded and created the more agnostic definition of “mental disorder” that we’ve inherited. Rather than an empirical clarification about the boundaries of medicine, it was a negotiation between professional communities.

The scope of these institutions, all institutions, is determined pragmatically, historically, and in negotiation with other institutions that serve overlapping but not identical functions. The question “What is the scope of medicine?” is not categorically different. It only feels different because medicine, more than law or education, has invested its self-understanding in the idea that its jurisdiction is carved at the joints of nature by the concept of “disease” or “disorder.”

Contingency Without Catastrophe

The scope of medicine is contingent, and so is the scope of things like clinical psychology and social work. Tim Thornton captures this well when he writes that “it can seem a contingent matter that a number of conditions have come to be classed as illnesses. That is, it is conceivable that they might not have done.”

We can choose to draw the boundaries differently, and that we can, in principle, choose not to employ medical concepts at all for certain forms of human suffering, but these choices are (or at least should be) informed by relevant facts at hand and the reasons in favor or against these choices can be examined and supported or disputed. Contingency is not the same as arbitrariness, because it is contingency within the space of reasons and within the historical evolution of institutions.

Consider a peculiar but illustrative example. After Ivan Illich, the author of Medical Nemesis, was diagnosed with cancer in 1983, he refused all treatment. As the tumor on his cheek grew, he reportedly declared: “I am not ill, it’s not an illness. It is something completely different—a very complicated relationship.” (source) Illich could accept the physiological reality of the tumor, the reality of the uncontrolled cellular proliferation, while denying the conceptual characterization of it as an “illness,” because of his unique and extreme embrace of the art of suffering.

This is an attitude that is not shared by the vast majority of people, which is why the characterization of malignancy as illness is, for all practical purposes, basically uncontested. In the realm of psychiatry, however, there are fewer facts at hand to constrain possible disagreements, and there is much more diversity in the values that people hold. This is what makes the boundaries of psychiatric authority contested in ways that the boundaries of oncology are not.

Communities as Justification

I find it helpful to draw on the pragmatist tradition and the insight that communities play a constitutive role in establishing norms and reasons. As Jules Gleeson writes in the context of discussing Robert Brandom’s philosophy: “We are obliged to make sense of the world, and have no ‘given’ that we can depend on across every context. But we are never left attempting this alone. Reasons both arise from communities and are appeals to them.”

Along similar lines, we are obliged to make sense of the domain of distress, disability, risk, and harm that comes to clinical attention. We have no universal “givens” to fall back on, no foundational truths in the form of pristine “disorder” concepts. But there are legitimate reasons for medicine (and psychology, and social work, and service users…) to tackle this domain with the tools it has at its disposal. These reasons arise from and are justified by the norms of the medical community, what it has to offer, the particular history in which it exists, and the relationships it has with other communities.

In this sense, over-medicalization is a question about institutional and social relationships and the negotiation of boundaries.

Pluralism

Something can be within the domain of mental health disciplines and yet not be exclusively within the domain of healthcare. A “medical problem” is not just a medical problem, because this characterization is not something intrinsic to it. The same condition can also be an interpersonal problem, an existential problem, a problem of living, a spiritual problem, one that may be addressed successfully by non-clinical interventions. The medical perspective is simply one way of conceptualizing a condition, and it is not always or not necessarily the best way to view or help every problem.

This raises the obvious question: When should the characterization of a condition as a medical or clinical problem dominate over other forms of characterization? And how should competing conceptualizations coexist?

My answer is that these are questions that cannot be settled a priori. They are settled, provisionally, imperfectly, revisably, through ongoing negotiation between institutions, informed by empirical evidence, constrained by values, and responsive to the experiences and preferences of the people these institutions serve.

Clinical conceptualizations and treatments are not universally helpful. For some people they will be useless, and for some harmful. Some people are better off trying to understand and manage their suffering through non-clinical approaches: self-help, spiritual practices, lifestyle changes, coaching, political engagement, financial support, existential reflection, peer support, and so on. The problem is that we don’t have a good way of knowing in advance who will benefit from the clinical approach and who will not, so we clinicians end up casting and people end up accepting a wide net, albeit with some ambivalence and resistance.

If clinical diagnosis and treatment are understood as one way of conceptualizing and helping a condition, and not necessarily the only way, and not automatically the best way of helping to achieve all or indeed any desired outcomes, then this necessitates a robust pluralism of conceptualization and intervention. Diagnosis is a partial perspective on a person’s challenges. The clinical lens is appealing because it offers a useful hermeneutic framework through which to look at our problems. But it remains one hermeneutic framework among many that can address individual distress in different contexts. Recognizing this plurality does not negate the value of medical thinking, which remains essential. But to reduce this plurality of perspectives to a single dominant narrative, whatever that may be, is to impoverish our existence and to deprive us of the tools we need to make sense of ourselves in relation to our worlds.

Where Things Go Wrong

Because these processes of problem recognition and clinical categorization are value-laden, socioculturally dependent, and susceptible to various biases, they can be distorted. When the guiding values are corrupted, when clinical services are wielded by the state for confinement and control or when benign states of distress are encouraged to be conceptualized as diseases requiring medications by pharmaceutical companies, we get the clearest perversions of the process. But subtler forms of distortion are all present: when guild interests shape diagnostic boundaries or psychotherapy is recommended as the default response to all life distress, or when the absence of viable or accessible non-medical alternatives creates a vacuum.

The answer to these problems, though, is not to search for an incorruptible, naturalist definition of the scope of medicine that will hold the line against medicalization. No such definition exists. Nor is the answer to artificially restrict the use of the clinical lens and deny people access to clinical care they want and could benefit from. If we are over-relying on the medical framework, the more productive response is to develop other frameworks that can offer people similar or better utility and facilitate more informed and mindful use of the medical lens. The answer is better processes: more transparency, more democratic participation (including the participation of those who receive care), more accountability, more genuine pluralism in the institutions available to people in distress, and more epistemic humility about the limits of any single framework. The answers I ultimately advocate for are thoughtfulness, conceptual clarity, person-centered care, pluralism, and realistic expectations around clinical treatments.

When a problem is inadequately or unsatisfactorily addressed by clinical disciplines and the problem is such that some sort of specialized response is needed or asked for, by all means, create alternative non-clinical institutions that are helpful and accountable. Build frameworks that address the distress and disability more effectively, more humanely, with fewer unintended effects and less epistemic overreach than healthcare currently manages. The future is open-ended, and there is nothing in principle that prevents the development of such alternatives. Indeed, some already exist in nascent form in peer support networks (e.g. those organized around psychotropic withdrawal and tapering, and the Hearing Voices Network), in certain models of community care and peer crisis support, in traditions of religious and spiritual support, and even, dare I say, shamanistic healing. Alcoholics Anonymous and 12-step programs are probably the most established examples.

But there are good reasons why alternatives are scarce and why they haven’t displaced healthcare disciplines. It is difficult to outperform and dislodge professions that have, at their best, rigorous clinical and scientific training, a commitment to understanding human suffering, effective (if imperfect) interventions, and structures of accountability to the scientific communities as well as the society at large.

See also:

Share

My partial agonist stance towards the psychiatric status quo has often left people confused about my beliefs and loyalties (which are to a philosophically informed, pluralistic psychiatry). Some see me as a representative of the mainstream (Robert Whitaker just characterized me as “psychiatry’s attack dog”), while others place me far closer in conceptual space to the critical psychiatrists. On rare occasions, I’ve even been called “antipsychiatry.” All this generally leaves me more amused than troubled and reinforces my impression of how difficult it is for many people to transcend the polarizing binaries that have dominated psychiatric discourse.

I have always liked Erik Hoel’s description of blogging as an “interconnected rope to be braided” rather than a set of stand-alone writings. Thanks to Hoel’s metaphor, when I blog now, I often see myself as adding to a braid I have been weaving for years but readers (especially new ones) often encounter a standalone post and expect it to deliver all the qualifications they desire in one go. Given that many people seem to struggle to locate where I am coming from, I think it will be useful to repost a summary of my points of divergence from the “orthodox” positions of critical psychiatry and other tendencies I see in critical discourse. The most efficient way to do this is through a table I published as part of the introductory chapter of my book, Conversations in Critical Psychiatry.

Conversations in Critical Psychiatry (Oxford University Press, 2024) brought together a selection of interviews published in Psychiatric Times from 2019 to 2022, updated with new and previously unpublished material, including a foreword by Sir Robin Murray and a detailed introductory chapter. In the chapter, Psychiatry and the Critical Landscape, I endorse a position I characterize as “critical and integrative pluralism,” and I describe points of convergence and divergence from the standard positions of critical psychiatry, taking views from the Critical Psychiatry Network as representative.

There is a lot of conceptual detail condensed in this table, and the relevant issues are unpacked at length elsewhere. Some of the differences may seem subtle, but they have significant downstream consequences, generating precisely the sorts of heated debates I have been covering on this Substack since its inception.

Some additional points that are relevant to various ongoing debates.

Agency and the disordered self. Mental health problems can involve genuine impairments of agency. They are often disruptions in a person’s capacity for self-direction and engagement with the world that are poorly understood as intelligible responses to circumstances, devoid of such disruptions. Agency is embodied and enactive, so it can be constrained by neurophysiological, psychological, and situational factors alike, and restoring or supporting it is a legitimate therapeutic aim, achievable via many routes. By contrast, critical discourse tends to locate the principal threat to agency in coercion and medicalization, which can underplay the way in which mental health difficulties can be experienced as alien to, or at war with, the self.

The epistemic authority of lived experience. First-person testimony of suffering, harm, and what helps is epistemically indispensable, but valuing experiential knowledge is not the same as treating it as incorrigible or sacred. A socially objective science has to integrate service-user testimonies and experiences into a pluralistic process of mutual criticism rather than treating any single standpoint as authoritative.

Evidential standards and selective skepticism. Claims about efficacy, withdrawal, and long-term outcomes are empirical questions whose answers can be genuinely uncertain and contested. Critical discourse shows a tendency toward asymmetric skepticism, demanding very high evidence for treatment benefits while accepting strong claims about iatrogenic harm on far thinner grounds, and toward treating industry influence as a reason to dismiss favorable findings wholesale rather than as one bias among others to be corrected for.

The project of classification. There are active, empirically productive programs in classification of psychopathology (e.g. HiTOP, network models, clinical staging, evolutionary and cybernetic frameworks) that take dimensionality, comorbidity, development, and the limits of categories seriously while still aiming at scientifically valid and useful description. Critical stance toward nosology is often largely destructive; it can be effective at exposing reification but doesn’t offer scientifically or clinically credible alternatives.

Reflexivity and the sociology of critique. The sociological lens critical psychiatry trains on mainstream psychiatry should be applied reflexively to itself. Any critical psychiatry worth its name must be self-critical. Critical psychiatry rarely turns the demand for reflexivity inward, tending to position itself as straightforwardly on the side of the marginalized in a way that obscures how its own positions are situated and interested.

Iatrogenic harm. Iatrogenic harm, including things like overdiagnosis, polypharmacy, dependence and withdrawal, are genuine issues of concern and need to be addressed. These are also issues that can be and ought to be addressed within the frame of competent and virtuous psychiatric practice, while acknowledging the reality of mental illness and the necessity of treatment for many. Critics of psychiatry often deploy iatrogenic harm as a delegitimating argument against diagnosis and pharmacotherapy as such. It is notable, for example, that the 2020 documentary film “Medicating Normal” about five subjects harmed by prescribed medications focused not only on drawing attention to iatrogenic harm but also insisted (including in its title) on making the argument that mental health challenges experienced by these people were instances of “normal” suffering that was needlessly medicated. It is not enough for there to be iatrogenic harm, psychopathology itself must be illusory.

Coercion and the values of care. Critics of psychiatry at times present their own value commitments (anti-coercion, autonomy-maximizing) as if neutral or self-evident, when they are in fact trade off against impairments and duties of care. Impairments in decisional capacity cannot be denied. We need to recognize the disability and disruption that accompanies mental illness; it is not a fiction, and systems of care are a necessity. However, we can and we should minimize involuntary care as much as possible by expanding options for voluntary care and by cultivating a social commitment to care that prioritizes human dignity.

In a note on substack, asked in the context of MAHA, “what do we do when our analysis gets picked up by people whose politics we find dangerous? How do we hold onto the legitimate critique without becoming useful to a project we oppose?”

I am inclined to see this in part through a Latourian conceptual lens. The thesis by Bruno Latour in 2004, that “a certain form of critical spirit has sent us down the wrong path, encouraging us to fight the wrong enemies and, worst of all, to be considered as friends by the wrong sort of allies,” is quite relevant to the debates about critical psychiatry and MAHA at hand, and I’ve played with that Latourian thesis here:

References (for the table):

• Aftab, A., & Stein, D. J. (2022). Psychopharmacology and explanatory pluralism. JAMA Psychiatry, 79(6), 522–523.

• Bracken, P., Thomas, P., Timimi, S., et al. (2012). Psychiatry beyond the current paradigm. British Journal of Psychiatry, 201(6), 430–434.

• Double, D. (2015). Giving up the disease model. Lancet Psychiatry, 2(8), 682.

• Double, D. B. (2019). Twenty years of the Critical Psychiatry Network. British Journal of Psychiatry, 214(2), 61–62.

• Moncrieff, J. (2020). ‘ It was the brain tumor that done it!’: Szasz and Wittgenstein on the importance of distinguishing disease from behavior and implications for the nature of mental disorder. Philosophy, Psychiatry, & Psychology, 27(2), 169–181.

• Read, J., & Moncrieff, J. (2022). Depression: why drugs and electricity are not the answer. Psychological Medicine, 52(8), 1401–1410.

• Yeomans, D., Moncrieff, J., & Huws, R. (2015). Drug-centred psychopharmacology: a non-diagnostic framework for drug treatment. BJPsych Advances, 21(4), 229–236.

Share

Daniel Bergner is an attentive and prudent writer who has covered mental healthcare with more care and seriousness than most. His latest piece in the New York Times Magazine, “The Strange Alliance Trying to Remake American Psychiatry,” generously describes this substack as “cautiously thoughtful,” and it is precisely as someone he treats as a fair interlocutor that I want to take issue with the narrative he constructs in the rest of his article. If even a writer like Bergner has these blind spots, that is itself worth examining. It reveals how readily thoughtful commentators can fall into a binary that obscures what is most distinctive, and most contestable, about the Moncrieff-Whitaker-Delano brand of psychiatric critique.

The article builds on a familiar opposition. On one side, “around 1980, mainstream psychiatry adopted a medical model” and ever since, “troubles of the mind have been viewed mostly as physiological diseases of the brain, with treatments focused largely on pharmaceuticals.” On the other side, a movement of reformers and dissidents calling for something… different. Bergner does not say what that something different is, exactly. He gestures at “foundational change” and how some critics want “a true conceptual revamping.” But the alternative remains a kind of negative space in the piece.

I am not defending the particular version of psychiatry Bergner describes. The disease-based, reductive, chemical imbalances-corrected-by-pharmaceuticals account of mental health problems is one I have spent years criticizing. Bergner isn’t wrong about the limitations of that picture. The problem is that in his piece he treats this picture as if it constituted the medical foundation of psychiatry and treats the critics he profiles as if they were the natural and unique alternatives to it.

You know what else was published in 1980, by the way? George Engel’s “The clinical application of the biopsychosocial model” in the American Journal of Psychiatry. The “medical model” that Bergner places as having taken over psychiatry in 1980 was already, in 1980, being articulated in a form quite different from the one he describes.

As I have written before, there is a long-standing public confusion in which the medical model is identified with the idea that all psychiatric conditions are discrete biological disease entities of the brain. This caricature isn’t true even of much of general medicine, which routinely deals with multifactorial syndromes, problems shaped by environment and trauma, conditions defined by symptom clusters without identifiable biomarkers, and it certainly isn’t true of psychiatry. What we call the “medical model,” properly understood IMO, is an aspiration to extend the conceptual and practical tools of general medicine to mental health problems: classification and diagnosis, attention to natural history, multi-level causal explanation, and the use of a wide treatment armamentarium that includes, but is by no means exhausted by, pharmacotherapy. It is also a model that, in theory, comfortably exists in a broader pluralism of clinical and non-clinical approaches.

The binary of disease-based reductive psychiatry on one side and “critical psychiatry” on the other nudges us to assume there is nothing in between. In fact, the space between is large and well populated. Various strands of explanatory and methodological pluralism and theoretical developments like embodied cognition, enactivism, complex dynamic systems, phenomenological psychopathology, psychodynamic psychiatry, social determinants of health, etc… these are not minor footnotes. They are scientifically grounded, neuroscientifically and psychologically informed, philosophically aware, humanistically oriented, and deeply skeptical of reductionism.

The critics of psychiatry depend on this binary being invisible. If the only choices on offer are 1980s neuro-reductionism on one side and a self-righteously critical, anti-medical posture on the other, then anyone disenchanted with the first is shepherded toward the second. Once you see the binary, you see that the rhetorical machinery of critical psychiatry runs on it.

Bergner places Thomas Szasz at “the far edge of the movement.” I don’t believe that’s correct. Maybe that’s true in terms of how Szasz exists in our contemporary imagination as some ridiculous antipsychiatry arch-villain, but it’s definitely not true in terms of Szasz’s actual ideas. The Szaszian core, the view that mental illnesses are not illnesses at all, that the medical characterization of psychic suffering is a category error, that what we call “mental disorder” is really a moralized description of problems in living, is not at the periphery of contemporary critical psychiatry. It is at its heart of it. Joanna Moncrieff has openly defended Szaszian conceptions of mental illness. Laura Delano’s own conceptual framing of her psychological difficulties sits squarely in this tradition. The Szaszian commitments are load-bearing. Robert Chapman has traced the persistence of Szaszian assumptions across the broader critical literature.

I’d expect someone like Bergner to ask Delano on the record: what, exactly, do you disagree with in the Szaszian conception of mental illness? I’ve read her book. I can’t say I can articulate that there is a disagreement on the core ideas.

Bergner writes of Delano that her diagnoses “might have been better understood as a reaction to life’s trials.” I find this telling.

What does it mean to characterize something as a reaction to life’s trials in a manner that threatens the psychiatric conceptualization of mental disorders? Does psychiatry have no vocabulary to talk about reactions? Do “reactions” of all variety lie outside the proper concerns of medicine? Reactions can very well be excessive, prolonged, disabling, dangerous… what then makes the concept of “reaction” stand in contradiction to the concept of “disorder”? Reactions can be sticky and can be responsive to a wide range of interventions, including medications. Reactions can be and are shaped by biology and personality.

The dichotomy of “reaction” versus “disorder” is a false one. Some reactions are disorders, and some disorders are reactions. Once you recognize that minds are embodied, embedded, and enacted, these binaries dissolve quickly. Psychiatric conditions have simultaneous neurophysiological, experiential, existential, and sociocultural dimensions. We know this!

The seductiveness of the binary is precisely the Szaszian tradition at work: it requires illnesses to be discrete biological essences and, absent evidence of such an essence, declares the application of illness concepts a category mistake.

I want to note, with some bemusement, Bergner’s parenthetical aside: “Aftab, who is hardly a radical critic of his field…” I do not object to the description. By the standards of Mad in America, I am hardly radical. I also don’t care about being radical. I care about getting it right. If I thought the radical critics were getting it right, concerns about radicalism would not stop me. But I don’t think they are.

The implicit logic seems to be: even Aftab, who is no radical, sees these problems. This is meant to lend credibility to the critique. Fair enough. But who are the radical critics? Delano? Whitaker? Davis? Are we supposed to cheer for the radicals? And why are the radicals bending over backwards to present moderate versions of themselves to the American public?

We are in this weird moment where some woke critics of psychiatry will say things like “Abolish psychiatry!” and when pressed on what they mean by “abolish,” it’ll turn out that they mean something like, “judicious use of medications and comprehensive biopsychosocial services and sociopolitical action aimed at social determinants of health.” Very radical! (E.g. see Emmett Rensin’s review of Empire of Madness.)

But when it comes to the current iteration of the MAHA movement, we are dealing with the inverse phenomenon. There is a deliberate moderation of positions. Over-pathologization, over-medicalization, iatrogenic harm, etc, all the right buzzwords, and when pressed on the specifics of their psychiatric worldview, it emerges that they mean something quite Szaszian.

To Whitaker’s credit, in his comments to Bergner, he’s not playing the moderation game: “I don’t think serious reform is enough.” Language like “overmedicalization” is, for him, “limited in outlook,” “implied call for reduction rather than a true conceptual revamping,” “entrenching instead of displacing psychiatry’s medical model.”

It also tells us what the public face of the movement is doing. “Overmedicalization” and “overprescribing” are popular and sympathetic causes — who could really be against them? — and they function as the moderate-sounding entry points to an underlying program that, if stated plainly, would lose most of its public support.

If someone doesn’t even believe in the reality of mental illness, I don’t quite think they can be seen as having valid concerns about “overdiagnosis,” when, by the logic of their own framework, every diagnosis is overdiagnosis. If someone doesn’t even think medications have clinically meaningful efficacy, their complaints about “overtreatment” sound rather odd.

As I’ve written previously, the Whitaker-Moncrieff version of critical psychiatry, at its core, is a philosophically and scientifically exhausted movement. Despite a lot of effort, it has not persuaded the clinical and scientific communities of the positive account it offers of the nature of psychopathology and its treatment. Having lost the argument inside medicine, the movement has pivoted to the public square, leaning on the popular and sympathetic vocabulary of overdiagnosis and overmedicalization, and finding political traction with a government whose anti-expertise sensibilities make it unusually receptive to its agenda. Where the political and cultural influence of this pivot will peak, I do not know and I am afraid, but philosophically and scientifically, it is already stagnant and degenerating fast.

The one domain in which critical psychiatry has, in my view, gained genuine clinical ground is around antidepressant discontinuation and the practice of hyperbolic tapering. And there, the cause has advanced with momentum because the patient experience of withdrawal and successful use of hyperbolic tapering filled a medical gap where guidance was genuinely lacking; it is still notable that we neither have high-quality scientific evidence for expansive conceptions of protracted withdrawal nor for the specific efficacy of hyperbolic tapering regimens.

A useful diagnostic question for understanding MAHA’s relationship to medicine is: what is the source of MAHA’s ideas about medical reform? These ideas are a dangerous mix of respectable science, fringe science, and pseudoscience… as we have seen in situations like vaccines, psychedelics, autism etiology, and nutrition. MAHA psychiatry is no different in this regard, but proponents are noticeably more cautious in how they present things to the public.

To the extent the MAHA proposals on psychiatry have merit and broad appeal, they generally articulate existing ideals of good psychiatric practice. More awareness of medication risks. Less reflexive prescribing in primary care. Fewer antipsychotics off-label for non-psychotic indications in children. More non-pharmacologic options. More humility about long-term maintenance. Psychiatric mainstream has been moving (too slowly and too defensively, perhaps, but moving) toward each of these positions for years. The MAHA position there is a louder version of existing medical wisdom the field has under-prioritized. Fine.

But what makes MAHA psychiatry MAHA and gives it its distinctive character are precisely the ideas that go beyond existing ideals of good psychiatric practice, that are on theoretically shaky ground, and where the scientific community hasn’t been persuaded because the evidence isn’t there yet to persuade enough physicians.

Furthermore, whatever MAHA psychiatry says, the Trump administration’s broader agenda has been to weaken the public health and social safety net infrastructure that any humane response to mental illness depends on.

This is why I hesitate to endorse even the sensible-sounding parts of MAHA agenda. Bergner’s piece is structured around the optimistic framing of the alliance. What if this works? You can kinda tell that he is hopeful against odds that it will work. But he gives less attention to the structure of the alliance.

Anything MAHA touches today will be studied by scholars in coming decades as the health rhetoric of twenty-first-century American fascism.

Strange alliances are sometimes necessary in politics, but nothing about the MAHA-critical psychiatry convergence is a strange coincidence. It is the natural unfolding of the logic of disability-skepticism, bodily purity, self-reliance, and medical distrust.

Bergner is right that something is shifting. Vibes. Just like the MAGA cultural vibe shift of early 2025, I believe the prognosis of this vibeshift is guarded. Not because of pharma ads on TVs or because of the psychiatric establishment holding on to its scientific authority, but because curbing medical authority will not, on its own, produce better collective mental health. It is the wrong instrument for the goal, like expecting tariffs to stimulate economic growth.

A quarter of the way into the twenty-first century, we are only beginning to scratch the surface of the deep wells of human mental suffering. Psychiatry, clinical psychology, and social work are reaching, and over-reaching, as they search for solutions. They are also, for all their faults, engaged in the project of understanding and remedying psychological suffering through scientific evidence, clinical humanism, and public accountability. For now, they are the only game in town.

See also:

Sluggish

Unshrunk and MAHA: A Diagnosis-Critical Case Study

My foray into Youtube continues! I made this primer on An Introduction to Critical ADHD Studies, a paper that came out last year which outlines the various approaches to understanding ADHD…

Read more

a year ago · 148 likes · 5 comments · Jesse Meadows

Share

I have a new opinion piece in the New York Times, “We’re Thinking About Mental Health Diagnoses All Wrong” (gift link for access) (published with several other titles, including “Here’s What Psychiatrists Mean When They Say You Have A.D.H.D.”). It distills into a single public-facing essay several core aspects of what I have been thinking and writing about for years, especially when it comes to the gap between what psychiatric diagnoses are and what the public imagines them to be. The public conversation about mental health has become remarkably sophisticated in some ways and yet remains tethered to a picture of psychopathology that is far too simple: diagnoses as discrete things you either have or don’t have, rooted in identifiable biological malfunctions, waiting to be discovered by the right clinician. Once official psychiatric categories escape the clinic (as they have over the past decades), they have a habit of solidifying into folk psychology. The distance between the flattened story offered and what is actually happening leaves people alienated from their own experience and generates its own backlash in the form of skepticism toward the whole enterprise of diagnosing mental health problems.

The messy reality, as I try to lay out in the piece, is that mental health problems are dimensional, dynamic, shaped by personality and context, and often more meaningfully understood as patterns of distress and disability. None of this makes them less “real” or less deserving of care… if anything, it makes the clinical encounter richer and more honest. I hope the essay reaches people who have been puzzled or frustrated by their diagnostic experiences and offers them a more honest framework for making sense of what they are going through. (A special thanks to my editor, Alex Ellerback!)

The essay generated quite a bit of engagement on the NYT website. There were 586 comments before the discussion was closed. I also responded to a fair number of them. (You can see the comments here but a NYT subscription is needed.)

Hello and welcome to all the new readers who find their way to this substack through NYT! There were many more things I would have liked to include in the essay but wasn’t able to due to limited space. So, I’ll link here to a few other posts exploring various aspects of these issues in more detail that readers, especially new ones, will find relevant.

• On how statistical clustering of psychiatric symptoms differs from clustering based on clinical observation

• On issues of mental disorders and personal identity

• On experience therapeutic relief from diagnosis

• On systems thinking in clinical neuroscience

• On evolutionary approach to psychiatry (Q&A with Randy Nesse)

• On clinical staging (Q&A with Pat McGorry)

• On demand-capacity mismatches

• On diagnosis as explanation

• On the social construction of disorder judgments

• On alienation from reductive understandings of diagnosis and treatment (book review of Laura Delano’s Unshrunk)

Share

There are two broad mindsets or flavors when it comes to talk of “deprescribing” in psychiatry.

The first is the mindset of competent, collaborative, patient-centered practice, one that treats taking patients off medications that are no longer necessary, are causing harm, or no longer align with informed patient preference as part of routine psychiatric care.

The second is the mindset according to which psychiatric medications are really only helpful in a small number of extreme cases, are generally unnecessary and overall harmful, and people who take them are either misinformed or are using the medications as a crutch to avoid “doing the work” of addressing their psychological hang-ups, making necessary lifestyle changes, or cultivating a stoic attitude.

The problem is that the first mindset has been largely absent from real-world practice. People are started on medications willy-nilly and kept on them willy-nilly. Only a small fraction of patients has providers who do proper evaluations, make medication decisions in an informed and collaborative manner, periodically reassess the need for medications, and then taper them in a safe and gentle way. Mainstream medicine’s failure to embody the first mindset is precisely what created the vacuum the second mindset has filled. For decades, mainstream psychiatry willfully blinded itself to the burden and severity of withdrawal and discontinuation-related difficulties from antidepressants and other psychiatric medications, ceding this ground to radical critics out of a medical bias in favor of ongoing treatment and a tendency to interpret withdrawal and discontinuation-related rebound symptoms as relapse.

In reality, a substantial proportion of people using psychiatric medications long-term struggle to come off them. After getting no meaningful guidance from their physicians or nurse practitioners, they search online for help, discover communities of people who have been dealing with these issues, and find strategies that actually work… but the people offering that guidance have often been radicalized over the years by iatrogenic harm and by selective exposure to literature skeptical of psychiatry. Some of these people end up believing that staying on psychiatric medications is itself what caused their chronic illness and that is what is causing our mental health crisis and there is an urgent need for deprescribing on a massive scale.

For years now, “deprescribing” discourse has been the gateway to a radical critique of psychiatry… that psychiatric medications aren’t really effective, that they are inherently dangerous, that mental disorders aren’t even medical conditions. The term “deprescribing,” otherwise innocuous and with a respectable lineage in medicine, has become charged and critically tinged. It has been co-opted by people who see psychiatric medications as fundamentally suspect and sinister—useful, perhaps, for short periods in some situations, but a practice we should be wary of by default.

As the number of people struggling with withdrawal from psychiatric medications grows, and as more people search online for guidance, an ecosystem of services, largely disconnected from mainstream medicine, has emerged to offer information and guidance about safely coming off psychiatric medications. American psychiatry’s silence on the matter has been a source of embarrassment for anyone in the know.

It is in this landscape that the American Society of Clinical Psychopharmacology (ASCP) consensus statements have arrived (JAMA Network Open, Feb 2026) (see Ellen Barry’s coverage of ASCP recommendations and of MAHA initiatives in the New York Times). The timing is no coincidence in my mind; while work on developing this consensus may have been going on for a while, the publication now reads as a direct response to the public visibility of iatrogenic harm narratives and the alternative ecosystem that has grown up around them. The ASCP is making an effort to reclaim “deprescribing” and situate it within mainstream medicine as a practice that is a fundamental feature of good clinical care. They are late in the sense that they should have been published twenty years ago, at least, but better late than never. The statements address general deprescribing principles, pharmacokinetic and pharmacodynamic factors, adverse effect management, treatment adherence, special populations, and the psychological context of deprescribing.

Most of the recommendations are distillations of sensible clinical practice. I would characterize the statements as generally reasonable, sober, pragmatic, and grounded. They describe the collaborative mindset that needs to be the default in clinical practice.

A few examples illustrate the tenor:

The utility of continuing any particular psychotropic medication should be periodically reassessed, at the very least, on an annual basis. (100% agreement)

A risk-benefit analysis should be conducted before deprescribing any drug to gauge benefits vs lack of efficacy, or benefits vs adverse effects and their manageability. (100% agreement)

Patients who request to stop a medication that seems to be effective for previously poorly controlled symptoms should be guided through a risk-benefit discussion of continuation, discontinuation, or other modification to their regimen.

When considering whether to deprescribe an existing medication based on lack of efficacy, conclusions about perceived poor efficacy should not be made until the prescriber has made a careful assessment of adherence or adequacy of a trial.

Patients prescribed nonempirically supported polypharmacy for conditions for which pharmacotherapy is not indicated as a first-line treatment (eg, borderline personality disorder, PTSD) should be routinely evaluated for systematic deprescribing of non–evidence-based medications.

I was also happy to see a section devoted to psychological and psychodynamic considerations around medication treatment, including statements like:

Patients’ psychological barriers to deprescribing may include unconsciously fearing the loss of medication as a valued object, experiencing loss of medication as a rejection by the prescriber, and a threat to the medical legitimacy of their suffering.

This is the kind of careful, clinically grounded thinking that should be a default rather than an aspiration.

At the same time, it is notable that these recommendations bypass and skirt the most pressing and controversial issues in the deprescribing domain. The guidelines mostly focus on generalities and on the specifics of when to consider deprescribing, but they say almost nothing about how to deprescribe and the little they say is very problematic. There is no discussion of how to approach dose reduction as a valuable goal without necessarily leading to discontinuation, how to manage and prevent antidepressant withdrawal, different tapering strategies that clinicians can consider, how to approach protracted cases of withdrawal, or how to undertake a slow, gradual taper that requires using doses not available in standard pharmacies.

The statements defer to existing evidence on maintenance treatment without considering whether the trial results have been systematically biased by ignoring discontinuation-related effects. They generally recommend maintenance treatment for recurrent depression, bipolar I disorder, and schizophrenia, ignoring controversies in these areas. They assume, for example, that most people are correctly diagnosed when the reality is that there is widespread diagnostic chaos and medication decisions about maintenance are made under considerable uncertainty.

The guidelines operate firmly within the default thinking about maintenance treatment and tinker with it rather than confronting the assumptions that produced the present situation. They are valuable because they emphasize virtuous clinical practices. But they bypass all the big points of controversy around deprescribing, and for patients struggling with difficulties coming off their psychiatric medications and for clinicians treating them, the recommendations offer little of substance.

Mark Horowitz, in the comments he posted on the ASCP paper, has pointed out several major limitations that I also generally agree with. The reliance on Delphi consensus rather than a review of scientific evidence not only glosses over the gaps in empirical data but also allows the same epistemic community that normalized long-term use to now define the appropriate conditions of its reversal. The statements implicitly prioritize relapse prevention over discontinuation-related difficulties; increased post-reduction monitoring is described in terms of relapse risk rather than the possibility that post-reduction symptoms may also reflect withdrawal. The mechanics of deprescribing are sidestepped entirely; there is no engagement with dose-response relationships or receptor occupancy, and no mention of hyperbolic tapering.

There are points where the ASCP experts reveal their disconnect from the iatrogenic harm world in striking ways. The most gauche example is this statement, which achieved 81% agreement:

Medications with a long terminal elimination half-life (eg, fluoxetine, vortioxetine, cariprazine, aripiprazole) or long-acting injectable antipsychotics generally can be abruptly stopped without the need for a downward dose titration because they will auto-taper.

The idea that medications like fluoxetine and aripiprazole can be stopped without down-titration is, in my view, dangerous. I would not recommend that to my patients. It is astonishing to me that 80% of these experts would think that someone who has been on 60 mg of fluoxetine or 20 mg of aripiprazole for 5 years can just stop the medication because these medications “auto-taper.” Yikes! As Horowitz also notes, this claim reflects a simplistic view of neuroadaptation: receptor-level adaptations can take longer than the elimination of even long half-life drugs, and abrupt cessation can still precipitate delayed but severe discontinuation difficulties.

A statement like this one reveals that the ASCP recommendations, for all their virtues, are disconnected from the experiences of the harmed patient community and guided by the knowledge and preconceptions of an insular community of academic researchers who do not, in any sustained way, manage the patients struggling with the complexities of psychotropic withdrawal.

I want two things when it comes to deprescribing.

The first is rather superficial, more to do with institutional interests but still important. I want mainstream psychiatry to take ownership of deprescribing and tapering… to make it routine, boring, to back it with solid evidence about which dose reduction and discontinuation techniques produce the best outcomes, to conduct a dozen RCTs on tapering methods and outcomes so that disagreements can be resolved with actual data and this space is no longer ceded to speculations and no longer functions as a gateway to psychiatric skepticism.

Second, and eventually this is what really matters, I want patients who wish to come off medications to be able to do so successfully, without discontinuation difficulties, and I want patients struggling with withdrawal and unsuccessful tapers to find effective care. I have my doubts about hyperbolic tapering as the default strategy for everyone, but for people who are really struggling with withdrawal, based on what we know today, I would recommend some variety of hyperbolic tapering as the strategy most likely to help them.

Our top psychopharm experts act like the stereotype of out-of-touch elites. They need to step outside the ivory tower and spend time talking to people in the prescribed harm community with an open mind. They need to engage with the work of those who have been helping and guiding people through withdrawal for years.

I have my beefs with prominent figures in the deprescribing and iatrogenic harm communities, due to the antipsychiatry bias, dogmatic attitudes, and refusal to seriously consider the many ways in which a self-diagnosis of “withdrawal” can be erroneous, etc, and many of them see me more as an adversary than an ally (*shrug*). But they have my tremendous respect for stepping up and helping people who found little help or guidance from the medical community. I continue to be embarrassed by the failure of psychiatric leadership to address these issues with the seriousness and urgency they warrant, and I am amazed at the absence of a research program aimed at understanding and addressing iatrogenic harm. The ASCP guidelines are a half-step in the right direction, but we have a long way to go before we can make deprescribing boring and routine.

See also:

Share

Dr. Gonzalo Amador Rivera is a psychiatrist and philosophy graduate. He works at the Hospital de Psiquiatría de la Caja Nacional de Salud in La Paz, Bolivia. He writes online at Psiquiatría Subterránea.

The article is published below in both English and Spanish.

In January 2026, the American Psychiatric Association published a series of five articles in the American Journal of Psychiatry outlining priorities and strategies for the future of the DSM. It is a redesign incorporating sociocultural determinants, biomarkers, quality of life, and a four-domain model intended to supersede the categorical structure inherited from DSM-III (1-5). Awais Aftab, in his analysis published in Psychiatric Times and reproduced in Psychiatry at the Margins, offers a generous but critical reading of this proposal, identifying its blind spots with precision: the absence of an explicit psychological domain, underdeveloped dimensionality, and opacity of diagnostic thresholds (6). I share several of his diagnoses, but I wish to shift the axis of debate toward a question that some analyses leave in the background: can DSM-6 gain scientific legitimacy through descriptive expansion, or must it reorganize its architecture to give structural centrality to those distinctions that genuinely modify practice?

Current proposals from the Future DSM Committee seem to assume that the DSM’s central problem is insufficient description, and that enriching what the manual captures about patients will make it a better guide to clinical action. I want to argue that this premise is mistaken. The core problem of the DSM is not that it describes too little but that it discriminates too little. Its categories group heterogeneous phenomena under single labels, without offering clinicians the tools to distinguish between patients who require different treatments, carry different prognoses, and follow different illness trajectories. Adding contextual, dimensional, or biological layers to a classificatory architecture that does not resolve this internal heterogeneity may produce a broader manual, but it will not necessarily produce a more useful one.

This is a general problem, but it acquires particular urgency in fragile health systems. In Bolivia and throughout much of Latin America, where the treatment gap for moderate-to-severe mental disorders reaches 74.7% (7), psychiatric diagnosis often occurs under conditions of specialist scarcity, absent follow-up networks, and limited pharmacological options. In such contexts, a diagnostic distinction that genuinely changes therapeutic decisions can be the difference between a treatment that works and one that doesn’t or even harms. The structural deficits of the DSM are amplified precisely where resources are most constrained.

The Future DSM committee is taking steps that address some of what I would have liked to see. The biomarkers subcommittee, led by Cuthbert et al., for example, explicitly identifies candidate biomarkers, including inflammatory markers such as C-reactive protein in depression, and proposes their provisional integration into diagnostic assessment (3). The Structure and Dimensions Subcommittee, led by Öngür et al., proposes variable specificity from broad categories to specific diagnoses with specifiers, and a hierarchical organization that moves away from the flat categorical structure of earlier editions (2). The sociocultural determinants subcommittee recognizes contextual and environmental factors as integral to psychiatric assessment (5).

The problem lies in where these advances are positioned architecturally. In the proposed four-domain model, Domain I (contextual factors) and Domain IV (transdiagnostic features) are essentially new descriptive layers added to the diagnostic core of Domain III, without modifying its internal structure (at least, it is not yet clear how Domain III would be revised further). The variable specificity proposed by the Structure and Dimensions Subcommittee uses the ICD’s unspecified codes as its base (2, 6), with the risk of reproducing the marginalization already suffered by NOS categories in previous editions. And the candidate biomarkers, however promising, are framed as supplementary information rather than as distinctions that might reorganize how the manual classifies.

The result is that beneath the diagnostic labels of Domain III, heterogeneous phenomena with different etiologies, different therapeutic response profiles, and different prognoses continue to coexist, without the manual offering the clinician tools to distinguish between them.

Recognizing the importance of psychosocial, contextual, and cultural factors is not the same as assuming that their incorporation into the manual corrects the validity problems that have characterized psychiatric nosology since DSM-III adopted its atheoretical descriptive approach as a pragmatic response to the reliability crisis of the 1970s. That emergency solution became institutionalized as permanent architecture. Four decades of research have not managed to replace it, merely surrounding it with complementary instruments systematically relegated to optional sections of the manual.

My primary objection to the current proposals is not that they are wrong in what they add, but that they do not address what most needs changing: the internal organization of the diagnostic core. The question the DSM ought to answer cannot be answered by multiplying descriptive domains. It requires a different architectural principle. The manual needs to give greater diagnostic centrality to those distinctions that do meaningful clinical work in the form of explanatory, prognostic, or therapeutic value, and it needs to give less weight to those that merely organize clinical conversation, ensure reliability, or serve administrative convenience.

Not all diagnostic distinctions are equal. Some generate substantial inferential power such that they predict illness course, stratify patients into groups that respond differently to treatment, or identify mechanisms that open specific therapeutic pathways. Others survive in the manual primarily because they organize professional discourse, facilitate insurance coding and billing, or have accumulated institutional inertia. A mature nosology should be organized to reflect these differences. As Aftab observes with his image of the house of mirrors, schizophrenia and disruptive mood dysregulation disorder coexist in the manual as though they share the same scientific status, because the manual was not designed to discriminate between them in those terms (6).

I am not demanding that psychiatric classification should already possess perfectly stabilized natural kinds. I am proposing something more modest: that the manual’s architecture be organized so that it can progressively incorporate the distinctions that research validates, restructuring the core diagnostic categories in light of that scientific knowledge rather than appending them as (optional?) specifiers. There is a difference between epistemic humility as an honest scientific disposition (which any DSM reform requires) and institutional agnosticism as a permanent policy that pretends that all existing categorical distinctions carry equal scientific weight.

The biomarkers subcommittee identifies the inflammatory subtype of depression as a promising candidate (3). Elevated CRP levels, detectable through a widely available, low-cost blood test, may help identify a subtype with differential therapeutic implications, including differential response profiles to specific antidepressants. This is the sort of diagnostic advance that is biologically grounded and clinically actionable, and accessible even in resource-limited settings. In Latin American health systems without infrastructure for sophisticated monitoring or plasma level testing, a simple inflammatory marker that guides prescribing decisions has tremendous value. But under the current proposals, such a marker would be appended to the existing architecture of major depressive disorder as supplementary information in a different domain. What I would like to see is that if such a distinction proves valid, it should reorganize the diagnostic boundaries itself, not merely annotate what we have already classified.

The case of the dexamethasone suppression test (DST) illustrates, from the history of psychiatry, that the problem is not always the absence of science but the difficulty of a broad nosology in receiving findings that do not fit comfortably within its categories (8,9). As Shorter and Fink have argued, and as Aftab himself recalls in his reading of the test, it may have had more to offer as a marker of a transdiagnostic process linked to HPA axis dysregulation than as a biomarker subordinated to categories as broad as major depressive disorder (8, 9). Certain biological or pathophysiological signals do not necessarily fail because they lack all value, but because they are forced to legitimate diagnostic constructs too broad to capture their yield.

These examples point toward some general architectural principles. The first of these would be a more hierarchical and explicitly revisable structure, in which current categories function less as stable endpoints and more as provisional working hypotheses. In practice, this would mean broad syndromic groupings as provisional entry points, beneath which the manual would explicitly distinguish dimensional, transdiagnostic, and candidate subtype layers, each marked by its degree of evidential maturity and clinical actionability. The committee’s proposals move in this direction, but the variable specificity model needs to go further in making the hierarchy genuinely functional rather than cosmetic.

The second condition would be a greater capacity to accommodate transdiagnostic markers or processes when they have genuine clinical value, instead of forcing them to justify themselves only by validating inherited categories. A more open architecture should be capable of receiving partial findings without demanding from the outset the full validation of a pre-existing category. Models like HiTOP are relevant here, not because they should wholesale replace the DSM, but because they illustrate a way of organizing psychopathology that is more sensitive to hierarchical gradations and less dependent on closed categorical containers (10).

The third condition would be a more selective logic built into the structure of the manual itself. Stathis Psillos, in his defense of scientific realism, argues that agnosticism is always the safer position but not the most honest. Psillos calls it “divide et impera“ (“divide and rule”), retaining the parts of a theory that generate genuine explanatory and predictive success (the working components) and questioning those that do not (the idle components) (11,12). Here I am envisioning something like divide et impera applied nosologically. By this I mean that the manual would need to give greater centrality to those that do genuine explanatory, prognostic, or therapeutic work, and less weight to those that merely organize clinical conversation or administrative convenience. Today we know considerably more about the internal heterogeneity of many categories, the relevance of transdiagnostic processes, and the need for better clinical stratification than we did in 1980; that difference should be reflected in how the manual organizes itself to receive what research will produce.

I agree with Aftab and other experts that the future DSM cannot continue to be a taxonomy closed upon itself. I believe that the core problem is not resolved by adding descriptive domains to a classificatory architecture that continues to carry internal heterogeneity, opaque thresholds, and a limited capacity to guide intervention. A broader DSM may be intellectually more attractive and morally more sensitive, without being nosologically stronger for it.

In fragile health systems, a classification is not legitimized by becoming more complex but by becoming more discriminating and actionable. The Latin American demand for a more useful DSM requires an architecture capable of hierarchizing levels of evidence, opening space for transdiagnostic processes, and giving greater centrality to those distinctions that genuinely modify practice. If the future DSM wants to be more than a more voluminous manual, it will have to accept that, in psychiatry, describing better does not always equal knowing better, and that knowing better only matters when it enables treating better.

Notas de un psiquiatra sudamericano sobre el futuro DSM

Descripción y diferenciación en sistemas de salud frágiles

Dr. Gonzalo Amador Rivera es médico psiquiatra y licenciado en filosofía. Trabaja en el Hospital de Psiquiatría de la Caja Nacional de Salud en La Paz, Bolivia. Escribe en línea en Psiquiatría Subterránea.

En enero de 2026, la American Psychiatric Association publicó en el American Journal of Psychiatry una serie de cinco artículos que delinean prioridades y estrategias para el futuro del DSM: un rediseño que incorpora determinantes socioculturales, biomarcadores, calidad de vida y un modelo de cuatro dominios destinado a superar la estructura categorial heredada del DSM-III (1-5). Awais Aftab, en su análisis publicado en Psychiatric Times y reproducido en Psychiatry at the Margins, ofrece una lectura generosa pero crítica de esta propuesta, identificando sus puntos ciegos con precisión: la ausencia de un dominio psicológico explícito, la dimensionalidad subdesarrollada y la opacidad de los umbrales diagnósticos (6). Comparto varios de sus diagnósticos, pero quiero desplazar el eje del debate hacia una pregunta que algunos análisis dejan en segundo plano: ¿puede el DSM-6 ganar legitimidad científica mediante la expansión descriptiva, o debe reorganizar su arquitectura para dar centralidad estructural a aquellas distinciones que genuinamente modifican la práctica?

Las propuestas actuales del Future DSM Committee parecen asumir que el problema central del DSM es la descripción insuficiente, y que enriquecer lo que el manual captura sobre los pacientes lo convertirá en una mejor guía para la acción clínica. Quiero argumentar que esta premisa es equivocada. El problema central del DSM no es que describa demasiado poco, sino que discrimina demasiado poco. Sus categorías agrupan fenómenos heterogéneos bajo etiquetas únicas, sin ofrecer a los clínicos las herramientas para distinguir entre pacientes que requieren tratamientos distintos, tienen pronósticos distintos y siguen trayectorias de enfermedad distintas. Añadir capas contextuales, dimensionales o biológicas a una arquitectura clasificatoria que no resuelve esta heterogeneidad interna puede producir un manual más amplio, pero no producirá necesariamente uno más útil.

Este es un problema general, pero adquiere una urgencia particular en sistemas de salud frágiles. En Bolivia y en gran parte de América Latina, donde la brecha de tratamiento para los trastornos mentales moderados a graves alcanza el 74,7% (7), el diagnóstico psiquiátrico ocurre con frecuencia en condiciones de escasez de especialistas, ausencia de redes de seguimiento y opciones farmacológicas limitadas. En esos contextos, una distinción diagnóstica que cambia genuinamente las decisiones terapéuticas puede ser la diferencia entre un tratamiento que funciona y uno que no funciona o incluso que daña. Los déficits estructurales del DSM se amplifican precisamente donde los recursos son más limitados.

El Future DSM Committee está dando pasos que abordan parte de lo que habría querido ver. El subcomité de biomarcadores, liderado por Cuthbert et al., identifica explícitamente biomarcadores candidatos, incluidos marcadores inflamatorios como la proteína C reactiva en la depresión, y propone su integración provisional en la evaluación diagnóstica (3). El subcomité de Estructura y Dimensiones, liderado por Öngür et al., propone una especificidad variable desde categorías amplias hasta diagnósticos específicos con especificadores, y una organización jerárquica que se aleja de la estructura categorial plana de ediciones anteriores (2). El subcomité de determinantes socioculturales reconoce los factores contextuales y ambientales como parte integral de la evaluación psiquiátrica (5).

El problema radica en dónde se posicionan arquitectónicamente estos avances. En el modelo de cuatro dominios propuesto, el Dominio I (factores contextuales) y el Dominio IV (características transdiagnósticas) son esencialmente nuevas capas descriptivas añadidas al núcleo diagnóstico del Dominio III, sin modificar su estructura interna (al menos, no está claro aún cómo se revisaría más el Dominio III). La especificidad variable propuesta por el subcomité de Estructura y Dimensiones utiliza como base los códigos unspecified del ICD (2, 6), con el riesgo de reproducir la marginalización que ya sufrieron las categorías NOS en ediciones anteriores. Y los biomarcadores candidatos, por prometedores que sean, están enmarcados como información suplementaria en lugar de como distinciones que podrían reorganizar la forma en que el manual clasifica.

El resultado es que bajo las etiquetas diagnósticas del Dominio III, los fenómenos heterogéneos con distintas etiologías, distintos perfiles de respuesta terapéutica y distintos pronósticos siguen coexistiendo, sin que el manual ofrezca al clínico herramientas para distinguirlos.

Reconocer la importancia de los factores psicosociales, contextuales y culturales no es lo mismo que suponer que su incorporación al manual corrige los problemas de validez que han caracterizado a la nosología psiquiátrica desde que el DSM-III adoptó su enfoque descriptivo ateórico como respuesta pragmática a la crisis de fiabilidad de los años setenta. Esa solución de emergencia se institucionalizó como arquitectura permanente. Cuatro décadas de investigación no han conseguido sustituirla, limitándose a rodearla con instrumentos complementarios relegados sistemáticamente a secciones optativas del manual.

Mi objeción principal a las propuestas actuales no es que estén equivocadas en lo que añaden, sino que no abordan lo que más necesita cambiar: la organización interna del núcleo diagnóstico. La pregunta que el DSM debería responder no puede responderse multiplicando dominios descriptivos. Requiere un principio arquitectónico diferente. El manual necesita dar mayor centralidad diagnóstica a aquellas distinciones que realizan un trabajo clínico significativo en forma de valor explicativo, pronóstico o terapéutico, y menor peso a aquellas que simplemente organizan la conversación clínica, garantizan la fiabilidad o sirven a la conveniencia administrativa.

No todas las distinciones diagnósticas son iguales. Algunas generan un poder inferencial sustancial que predice el curso de la enfermedad, estratifica a los pacientes en grupos que responden de manera diferente al tratamiento, o identifica mecanismos que abren vías terapéuticas específicas. Otras sobreviven en el manual principalmente porque organizan el discurso profesional, facilitan la codificación de seguros y la facturación, o han acumulado inercia institucional. Una nosología madura debería estar organizada para reflejar estas diferencias. Como señala Aftab con su imagen del house of mirrors, la esquizofrenia y el trastorno de desregulación disruptiva del estado de ánimo coexisten en el manual como si tuviesen el mismo estatus científico, porque el manual no fue diseñado para distinguir entre ellos en esos términos (6).

No estoy exigiendo que la clasificación psiquiátrica posea ya natural kinds perfectamente estabilizados. Propongo algo más modesto: que la arquitectura del manual esté organizada de modo que pueda incorporar progresivamente las distinciones que la investigación valide, reestructurando las categorías diagnósticas centrales a la luz de ese conocimiento científico en lugar de añadirlas como especificadores (¿opcionales?). Hay una diferencia entre la humildad epistémica como disposición científica honesta — que cualquier reforma del DSM requiere — y el agnosticismo institucional como política permanente que pretende que todas las distinciones categoriales existentes tienen el mismo peso científico.

El subcomité de biomarcadores identifica el subtipo inflamatorio de la depresión como un candidato prometedor (3). Los niveles elevados de proteína C reactiva, detectables mediante un análisis de sangre ampliamente disponible y de bajo costo, pueden ayudar a identificar un subtipo con implicaciones terapéuticas diferenciales, incluidos perfiles de respuesta diferencial a antidepresivos específicos. Este es el tipo de avance diagnóstico biológicamente fundamentado y clínicamente accionable, y accesible incluso en entornos de recursos limitados. En los sistemas de salud latinoamericanos sin infraestructura para monitoreo sofisticado o pruebas de nivel plasmático, un marcador inflamatorio sencillo que orienta las decisiones de prescripción tiene un valor enorme. Pero bajo las propuestas actuales, ese marcador se añadiría a la arquitectura existente del trastorno depresivo mayor como información suplementaria en un dominio diferente. Lo que me gustaría ver es que, si tal distinción resulta válida, debería reorganizar los propios límites diagnósticos, no simplemente anotar lo que ya hemos clasificado.

El caso de la prueba de supresión de dexametasona (DST) ilustra, desde la historia de la psiquiatría, que el problema no siempre es la ausencia de ciencia sino la dificultad de una nosología amplia para recibir hallazgos que no encajan cómodamente en sus categorías (8,9). Como han argumentado Shorter y Fink, y como el propio Aftab recuerda en su lectura de la prueba, acaso tenía más que ofrecer como marcador de un proceso transdiagnóstico vinculado a la desregulación del eje HPA que como biomarcador subordinado a categorías tan amplias como el trastorno depresivo mayor (8, 9). Ciertas señales biológicas o fisiopatológicas no fracasan necesariamente porque carezcan de todo valor, sino porque se las obliga a legitimar constructos diagnósticos demasiado amplios para capturar su rendimiento.

Estos ejemplos apuntan hacia algunos principios arquitectónicos generales. El primero sería una estructura más jerárquica y explícitamente revisable, en la que las categorías actuales funcionen menos como puntos de llegada estables y más como hipótesis de trabajo provisionales. En la práctica, esto implicaría agrupaciones sindrómicas amplias como puntos de entrada provisionales, por debajo de las cuales el manual distinguiría de forma explícita capas dimensionales, transdiagnósticas y de subtipos candidatos, cada una marcada según su grado de madurez evidencial y accionabilidad clínica. Las propuestas del comité avanzan en esta dirección, pero el modelo de especificidad variable necesita ir más lejos para hacer que la jerarquía sea genuinamente funcional en lugar de cosmética.

La segunda condición sería una mayor capacidad para alojar marcadores o procesos transdiagnósticos cuando tengan valor clínico real, en lugar de obligarlos a justificarse únicamente validando categorías heredadas. Una arquitectura más abierta debería ser capaz de recibir hallazgos parciales sin exigirles desde el inicio la validación total de una categoría preexistente. Modelos como HiTOP son relevantes aquí, no porque deban reemplazar sin más al DSM, sino porque ilustran una forma de organizar la psicopatología más sensible a gradaciones jerárquicas y menos dependiente de contenedores categoriales cerrados (10).

La tercera condición sería una lógica más selectiva incorporada a la propia estructura del manual. Stathis Psillos, en su defensa del realismo científico, sostiene que el agnosticismo es siempre la posición más segura pero no la más honesta. Psillos lo llama divide et impera, retener las partes de una teoría que generan éxito explicativo y predictivo genuino —los componentes que funcionan— y cuestionar las que no lo hacen —los componentes ociosos— (11,12). Aquí estoy imaginando algo como el divide et impera aplicado nosológicamente: el manual necesitaría dar mayor centralidad a aquellas distinciones que realizan trabajo explicativo, pronóstico o terapéutico real, y menor peso a las que simplemente organizan la conversación clínica o la conveniencia administrativa. Hoy sabemos bastante más sobre la heterogeneidad interna de muchas categorías, la relevancia de los procesos transdiagnósticos y la necesidad de una mejor estratificación clínica que en 1980; esa diferencia debería reflejarse en cómo el manual se organiza para recibir lo que la investigación vaya produciendo.

Coincido con Aftab y otros expertos en que el futuro DSM no puede seguir siendo una taxonomía cerrada sobre sí misma. Creo que el núcleo del problema no se resuelve añadiendo dominios descriptivos a una arquitectura clasificatoria que sigue arrastrando heterogeneidad interna, umbrales opacos y una capacidad limitada para orientar la intervención. Un DSM más amplio puede ser intelectualmente más atractivo y moralmente más sensible, sin ser por ello nosológicamente más sólido.

En los sistemas de salud frágiles, una clasificación no se legitima por volverse más compleja, sino por volverse más diferenciadora y accionable. La demanda latinoamericana de un DSM más útil exige una arquitectura capaz de jerarquizar niveles de evidencia, abrir espacio a procesos transdiagnósticos y dar mayor centralidad a aquellas distinciones que genuinamente modifican la práctica. Si el futuro DSM quiere ser más que un manual más voluminoso, tendrá que asumir que, en psiquiatría, describir mejor no siempre equivale a conocer mejor, y que conocer mejor solo importa cuando permite tratar mejor.

Subscribe now

Share

See also:

REFERENCES

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

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.

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.

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.

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.

6. Aftab A. The future DSM: bold redesign, lingering blind spots. Psychiatr Times. 2026;43(3). Republished in: Psychiatry at the Margins [Internet]. 2026 Mar 6 [cited 2026 Apr 19]. Available from: https://www.psychiatrymargins.com/p/examining-apas-proposed-redesign

7. Kohn R, Ali AA, Puac-Polanco V, Figueroa C, López-Soto V, Morgan K, et al. Mental health in the Americas: an overview of the treatment gap. Rev Panam Salud Publica. 2018;42:e165. doi: 10.26633/RPSP.2018.165.

8. Aftab A. Dexamethasone suppression test – the OG psychiatric biomarker. Psychiatry at the Margins [Internet]. 2023 Oct 12 [cited 2026 Apr 19]. Available from: https://www.psychiatrymargins.com/p/dexamethasone-suppression-test-the

9. Shorter E, Fink M. Endocrine Psychiatry: Solving the Riddle of Melancholia. Oxford: Oxford University Press; 2010.

10. Kotov R, Krueger RF, Watson D, et al. The Hierarchical Taxonomy of Psychopathology (HiTOP): a quantitative nosology based on consensus of evidence. Annu Rev Clin Psychol. 2021;17:83-108.

11. Marshall R. Philosophy of science [interview with Stathis Psillos]. 3:16 [Internet]. [cited 2026 Apr 19]. Available from: https://www.3-16am.co.uk/articles/philosophy-of-science

12. Psillos S. Scientific Realism: How Science Tracks Truth. London: Routledge; 1999.

Follow-up to:

In March 2026, I shared a summary of a new paper I had co-authored with folks from the HiTOP Revisions Workgroup. ‘Examining the Foundational Assumptions of the Hierarchical Taxonomy of Psychopathology’ was published in Philosophy, Psychiatry, & Psychology and provided a structured overview of the framework’s conceptual and philosophical underpinnings.

The paper was published as a “Philosophical Case Conference,” which means it is accompanied by 5 commentaries from authors across psychiatry, psychology, and philosophy. Our response to the commentaries was published online last week, so this is a good opportunity to bring the set to your attention. These commentaries were just the kind of conceptual and philosophical engagement we had been hoping to provoke, and we were excited to see that.

The commentaries and the response are open-access for a period of 2 weeks.

• Sam Fellowes. HiTOP, Objectivity, and Logical Positivism.

• Dost Öngür. HiTOP Enters Prime Time.

• Nick Zautra. HiTOP 2.0 and Validity.

• Miriam Solomon. A Time for Pluralism in Psychiatric Taxonomies.

• S. Brian Hood. Realism Affords HiTOP Explanatory Power.

• Awais Aftab, et al. (HiTOP Revisions Workgroup). Clarifying the Philosophical Foundations of HiTOP

Let me walk through the key themes of our response.

What HiTOP is and isn’t. Solomon suggests at one point in her commentary that HiTOP should be called a hierarchical taxonomy of psychology rather than psychopathology, because it models a broad range of psychological variation and lacks its own account of what makes something pathological. We push back on this suggestion. HiTOP restricts its scope to the traditional domain of what has been described by clinicians and researchers as “psychopathology.” It doesn’t include, say, the full range of personality traits in non-clinical populations or the non-clinical psychological aspects of perception, motivation, and so on. What is true is that HiTOP dimensions span from population-typical to pathological ranges, and we have not committed to a specific philosophical account of where the boundary of psychopathology lies or whether such a boundary even exists. The question of what makes something pathological is substantive and contested, involving dysfunction, distress, disability, social values, etc. However, we believe that the value of classifying clinically relevant features of psychopathology doesn’t depend on having resolved that philosophical question first.

Hierarchy and what the levels mean. Hood raises questions about the justification for HiTOP’s hierarchical arrangement, particularly the placement of symptoms, traits, and disorders at different levels. We address what we see as a fundamental misunderstanding: symptoms and traits are not placed at separate hierarchical levels (there isn’t a separate level for symptoms and a separate level for traits). At the bottom of the HiTOP hierarchy are “homogenous symptom components/maladaptive traits,” however, broadly speaking, symptoms and traits occupy every level of HiTOP. The distinction between symptoms and traits is temporal (symptoms are time-bound, traits are enduringdispositions), but any HiTOP dimension at any hierarchical level can be characterized as either symptom-based or trait-based by modifying the temporal framing of the assessment. The hierarchy itself reflects statistical relationships derived from latent variable models in cross-sectional data. Constructs at higher levels represent patterns of covariation among constructs at lower levels. This is a mathematical relationship based on covariance, not a causal or temporal one.

Latent variables and causation. Öngür notes, correctly, that we describe latent variables in statistical terms rather than as causalmechanisms andd suggested this may create tension with HiTOP’s aspirational goal of informing etiological research. The tension is indeed there. The consortium is contributing to mechanistic efforts, e.g. in the form of research on the genetic basis and neural correlates of HiTOP dimensions, but we remain cautious about baking causal interpretations into the model prematurely.

Dimensionality and pluralism. Fellowes identifies an apparent tension in our original paper: we appeal to assumptions as the basis for objectivity while also claiming that empirical evidence supports dimensionality over categorical approaches. We clarify in the response that our appeal to assumptions was in the spirit of methodological objectivity, emphasizing the theory-ladenness of data and the social dimension of knowledge production. Dimensionality, we argue in the response, is better characterized as a working assumption based on taxometric studies that fail to find discontinuities in the population-level distribution of psychopathological states and traits. The truly foundational assumption would be something more general: that we should choose the form of our variables (whether categorical or continuous) based on empirical observations of their distributional properties. We also agree with Solomon and Fellowes that categorical and dimensional frameworks can serve complementary functions, as long as we are mindful of the different notions of dimensionality at play. What we resist is the reification of DSM/ICD categories as statistically and ontologically coherent kinds when the evidence suggests they are not.

Validity and institutional process. Zautra offers a philosophical analysis of how validity functions in HiTOP and characterizes the thinking offered in our paper as “HiTOP 2.0” with relaxed ontological assumptions. From our perspective, our paper was a clarification rather than a turning point, but we are pleased that our clarifications were welcome. Zautra correctly observes that structural validity is prioritized in HiTOP’s validation process, and he notes that systematic external validation has focused primarily on the spectra level and has not yet been extended to other hierarchical levels. We acknowledge this as an active area of development. Solomon observes that both HiTOP and DSM rely on expert consensus and structured social processes, which is true, but there are also differences in the specifics of how these judgments are constrained and guided by evidence and how transparent the basis for changes is.

The paper closes by acknowledging what remains to be done: linking descriptive constructs to mechanistic understanding, more systematic validation across hierarchical levels, and stronger (though still defensible) ontological commitments about what the models represent. HiTOP does not claim to have all the answers; our collective understanding of psychopathology remains rudimentary. What we hope to offer is a framework built on systematic empirical research, explicit assumptions, and openness to revision.

See also:

Subscribe now

Share

Robert Haim Belmaker and Pesach Lichtenberg, Psychopharmacology Reconsidered: A Concise Guide Exploring the Limits of Diagnosis and Treatment (Springer, 2023).

There is a particular kind of book that can only be written late in one’s career or at a critical juncture in one’s profession. It is the book in which a scientist of established reputation takes stock of the promises made in the field and their own aspirations at the beginning of their work and asks, with as much honesty as can be managed, which of those promises were kept. Psychopharmacology Reconsidered is such a book. Robert Haim Belmaker, former president of the International College of Neuropsychopharmacology, has a fifty-year career spanning laboratory neuroscience and clinical psychiatry. With co-author Pesach Lichtenberg, also an accomplished psychiatrist, he has produced a textbook (part clinical manual, part confessional) of psychopharmacology organized around the collapse of what can be characterized as diagnosis-centered psychopharmacology (not a term they use).

The book covers the major medication classes along with discussions of the biochemical basis of psychopharmacology, DSM diagnosis, clinical trial methodology, and future directions. A chapter by psychiatry resident Alexander Moshe Clayman provides a trainee’s perspective (respectful but not obsequious). The tone throughout is conversational and opinionated, and the volume functions as a guided tour by two clinician-scientists who share their hard-won conclusions of how to think about psychiatric medications.

The introduction is structured as two sequential personal narratives, first by Belmaker and then by Lichtenberg, each tracing a trajectory of progressive disillusionment with what they see as psychopharmacology’s foundational promises.

Belmaker organizes his account across multiple domains of disappointment. On genetics: the confidence of the 1970s that molecular genetics would yield discrete disease genes and rational drug targets has given way to the reality of hundreds of common variants of small effect, mimicking the architecture of traits like height and weight. On lithium: despite decades of mechanistic research in which Belmaker himself was deeply invested, all purported mechanisms of lithium action proved speculative, and no rational lithium-like alternative has ever emerged. Lithium works in many but not all cases of bipolar disorder, and so do carbamazepine, valproate, and second-generation antipsychotics… pharmacologically disparate compounds that network meta-analyses show to be equally effective (see a detailed discussion of lithium by Belmaker in a guest post for Psychiatry at the Margins). On antipsychotics: Snyder’s dopamine hypothesis seemed to validate the disease model of schizophrenia, but dopamine blockers act primarily on positive symptoms of psychosis, work across many diagnoses, and affect normal thought and motivation. On antidepressants: SSRIs were developed on the premise that serotonergic specificity would yield greater efficacy, but they are not more efficacious than imipramine and other TCAs; the diagnosis of depression has expanded so dramatically that placebo-drug differences have collapsed to near zero; the chemical imbalance narrative remains on scientifically shaky grounds. On biological markers: limited progress in translating transdiagnostic biological associations into clinical relevance. On clinical trials: reliability was prioritized over validity; meta-analyses contradicted each other; the commercial trial apparatus became self-serving.

Lichtenberg’s portion narrates a parallel arc. Having entered psychiatry during the ascendancy of biological psychiatry, he describes a growing conviction that the standard neurochemical tools of psychopharmacology were inadequate and the minds of his psychotic patients were “too fascinating and complex to be reduced to the blockade of dopamine receptors.” He invokes Moncrieff’s distinction between a disease-centered model of drug action (the drug corrects an etiological cause, like an antibiotic) and a drug-centered model (the drug produces psychoactive effects that provide symptomatic relief, like a shot of whiskey). Lichtenberg is dissatisfied with the neuro-reductionism prevalent in the field and believes that psychiatric diagnosis is fundamentally personal and behavioral (rather than brain-based) and that the meaning of a patient’s symptoms can only be found in the psychological realm. He comes to see that there is “a role for medication, and occasionally it is crucial,” but ultimately many patients require care that goes beyond medications and brain-based interventions. Lichtenberg’s trajectory culminates in his founding of the first Soteria home in Israel, a supportive, dialogical environment where medication is one component among many.

“If the result of this textbook will be to nudge clinical psychiatry to accept the limitations of psychopharmacological solutions for the complex problems of extreme emotional distress, and to reinvigorate the search for other means of providing succor for our patients, we will have accomplished our purpose.” (page 10)

It is an engaging and curious opening. The book is inspired, in part, by work in critical psychiatry (Whitaker and Moncrieff are both cited). I was in a similar kind of state at the very beginning of my career, circa 2018-2019, and reading this book, I was strongly reminded of my own sense of disillusionment back then. Resultantly, I was interested to see where Belmaker and Lichtenberg would go from there. In my own case, once I had come to terms with critical psychiatry, I sought to understand the new scientific and philosophical landscape of dimensionality, complex systems, pluralism, systems neuroscience, and Mad studies, and how it applies to psychopharmacology. Belmaker and Lichtenberg’s impulse, in many instances, is to retreat to the clinical past, to an older and simpler pharmacological era when imipramine treated melancholia, benzodiazepines were the norm for anxiety, and stimulants were reserved for children with minimal brain dysfunction.

Reading across the full book, a coherent, if not always explicit, framework emerges, which can be articulated as a set of general principles. (Belmaker and Lichtenberg themselves do not present any such list; I offer it here as a form of summary.)

Non-specificity of psychiatric medications. No existing psychiatric medication is specific to any DSM diagnosis. Antipsychotics work across schizophrenia, mania, psychotic depression, severe anxiety, and agitation. Antidepressants work in depression, panic disorder, OCD, and anxiety. Lithium works in bipolar disorder, schizoaffective disorder, augments antidepressant treatment, and helps in episodic aggression. The penicillin analogy (a drug that specifically targets a defined pathological process) is fundamentally misleading for psychotropic drugs. These are compounds that alter basic neurochemical systems involved in mood, arousal, salience, and reward, and their effects cascade (rather unpredictably) across multiple domains.

Drug-centered rather than disease-centered drug action. Drugs produce psychoactive effects that may provide symptomatic relief, rather than correcting biochemical abnormalities. No psychiatric disorder has a confirmed biochemical etiology that the relevant drug class corrects. While Moncrieff is approvingly cited in the first chapter, the disease-centered vs. drug-centered distinction isn’t really examined in the book, and like many other commentators, I think Belmaker and Lichtenberg work with a rather superficial impression of the assumptions guiding Moncrieff’s distinction and its implications.

Diagnostic non-validity undermines pharmacological algorithms. DSM diagnoses are not biologically valid. Many patients presenting for care don’t meet specific DSM criteria. Treatment should be guided by symptoms and syndromes (psychosis, insomnia, panic, melancholia) rather than diagnoses.

Diagnostic expansion dilutes drug efficacy. As diagnostic categories broadened from DSM-III through DSM-5, prevalence increased, but placebo-drug differences in clinical trials have narrowed. The drugs that worked well in narrowly defined populations appear far less effective when applied to the expanded diagnostic pools.

The clinical trial enterprise has become degraded. Head-to-head trials almost never find differences within drug classes; the volunteer pool is contaminated; academic trialists rarely see patients; the FDA allows publication of only positive trials; meta-analyses contradict each other; guidelines bias toward newer drugs; findings based on group means don’t meaningfully allow personalization of treatment.

All psychotropic drugs carry subjective costs that tend to go uncatalogued. Antipsychotics reduce pleasure and motivation; antidepressants may blunt emotional life. Beyond pharmacology, the medical model encourages passivity, and biological framing deepens some forms of stigma. These costs must be weighed against benefits for each patient.

Psychopharmacology is one component within a broader biopsychosocial approach. Medication should often not be the first-line treatment, especially where distress is psychosocially mediated or where the patient’s problem is unresponsive to pharmacology.

The totality of “evidence” should be considered rather than a narrow emphasis on RCTs. The idealized hierarchy from basic science to RCTs to meta-analyses to clinical practice is misleading; they propose instead a four-pillar model where basic science, epidemiology, clinical trials, and individualized clinical interpretation all independently support clinical decision-making in a non-hierarchical and continuously evolving way.

The book’s clinical chapters apply these core principles (somewhat unevenly) across drug classes. Antidepressants illustrate the non-specificity and diagnostic-expansion theses most fully: early imipramine studies in narrowly defined melancholia showed robust effects, but as “major depression” expanded to encompass most human sadness, placebo-drug differences collapsed. B&L believe antidepressants remain effective for melancholic depression with vegetative features, classic panic disorder, and relapse prevention, but are likely no better than placebo for the broader DSM-5 population. Antipsychotics similarly demonstrate non-specificity: their efficacy across mania, psychotic depression, agitation, and anxiety marks them as symptomatic dopamine receptor blockers rather than disease-targeted therapies, and second-generation agents proved no superior to first-generation ones per CATIE. They pose pointed questions about the standard treatment model: placebo responders shouldn’t be exposed to side effects, non-responders shouldn’t be maintained on ineffective drugs, and a schizophrenia diagnosis shouldn’t automatically mandate lifetime medication. Benzodiazepines, surprisingly, receive the most favorable treatment; B&L argue that hesitation around prescribing has led to undertreated anxiety and recommend benzodiazepines over antidepressants for many anxiety conditions, reserving antidepressants for well-defined panic disorder.

Their discussion of stimulants exemplifies both the strengths and the limits of the book. Belmaker and Lichtenberg open that chapter with the tension that the same stimulant drugs prescribed to millions of children for focus have a well-documented history as addictive substances and psychosis-inducing agents in adults. They note that the two literatures have developed in near-total isolation from each other, with therapeutic papers on childhood ADHD rarely citing addiction research and vice versa. Belmaker and Lichtenberg acknowledge that stimulants produce clinically significant reductions in hyperactivity and can meaningfully help children remain in their school settings, but they view both the ADHD diagnosis and treatment with stimulants with broad suspicion. They raise the concern that college students and adults who seek stimulants are often responding to the drugs’ euphoriant properties rather than treating a genuine deficit, and warn that adolescents continuing stimulant treatment may develop dependency patterns indistinguishable from adult amphetamine addiction. The chapter closes with the “unresolved” paradox that dopamine-enhancing stimulants somehow help rather than worsen hyperactivity.

The book was published in 2023, and given the timeline of academic book publication, the draft may have been finalized ~2021-2022. I am highlighting this because we cannot blame B&L for not being aware of research that came out in subsequent years and also because anyone reading the book today needs to be aware that important developments from recent years are missing.

Here are some conceptual, clinical, and scientific points of critique.

The book treats “non-specificity” as a singular phenomenon, but it encompasses several conceptually distinct claims that require different analysis. Pharmacological promiscuity (a drug acts on multiple receptor systems) is a fact about molecular pharmacology. Transdiagnostic efficacy (dopamine blockers work in schizophrenia, mania, and psychotic depression) could mean the drug targets a transdiagnostic dimension, or that diagnostic categories carve nature incorrectly, or both. Mechanistic convergence from pharmacological divergence (lithium, valproate, and olanzapine all help in bipolar disorder) could mean the diagnosis is heterogeneous and each drug works on a different subgroup, or that multiple routes lead to the same downstream effect. B&L slide between these senses in ways that sometimes weaken their argument.

The disease-centered vs. drug-centered dichotomy doesn’t say what most readers think it says. Moncrieff’s distinction is the philosophical scaffold the book nods towards in the beginning and it stays in the background. The distinction is widely thought to assert that either a drug corrects a specific pathological process (like an antibiotic) or it merely produces psychoactive effects that mask symptoms (like alcohol for anxiety). On this casual reading, the framework simply says that psychiatric drugs are symptomatic treatments rather than disease-modifying ones, an interpretation that, for many readers, makes the binary seem reasonable. But this is not what Moncrieff actually claims. As I have discussed elsewhere, her framework makes quite specific commitments that most of its sympathetic readers do not realize they are taking on. Moncrieff classifies symptomatic pain medications like acetaminophen and ibuprofen as disease-centered, because they act on the physiological pathways that are involved in pain. Symptomatic medications targeting fever, cough, edema, blood pressure, etc., all are disease-centered in her usage because they act on physiological processes involved in symptoms even when they do not address primary etiological causes. The “drug-centered model” is reserved for a narrower and more specific claim: that psychiatric drugs work like alcohol or opiates, through psychoactive effects (sedation, cognitive slowing, euphoria, emotional blunting) that suppress or distract from symptoms without acting on the physiological mechanisms that produce them.

This conflation of disease-modifying and symptomatic treatments under “disease-centered” injects intentional confusion into discussions of psychopharmacological mechanisms. It severely restricts which mechanisms one is allowed to invoke for psychiatric drugs: hypotheses involving prediction-error attenuation, neuroplasticity, cognitive flexibility, neurogenesis, or inflammatory pathways are all dismissed as “disease-centered” and therefore disallowed. What remains are intoxication-like mechanisms: sedation, blunting, suppression. The framework also enables a motte-and-bailey: the defensible motte (“the medication doesn’t correct a confirmed dysfunction”) is defended while the contentious bailey (“the medication works only by numbing or masking your symptoms”) is the position actually being asserted. There are better ways to think about this terrain but Belmaker and Lichtenberg unfortunately endorse the disease-centered/drug-centered distinction without examining what it actually entails, and the book inherits its problems.

The philosophy of mind is underdeveloped. Lichtenberg articulates a non-reductive physicalism: mind derives from brain, but subjective experience belongs to persons, and meaning can only be found in the realm of the mind. This is defensible, but its implications for psychopharmacology are never developed systematically. The drugs can work in part through biochemical mechanisms, but the gap between synaptic physiology and phenomenological experience cannot be crossed by a single level of explanation. This points toward something like explanatory pluralism: the view that psychiatric phenomena require multiple irreducible levels of explanation (biochemical, psychological, social, phenomenological). B&L come close to this position in spirit but never develop it philosophically. (See my thoughts on explanatory pluralism and psychopharmacology.)

Here the theoretical developments in levels of biological organization/explanation, complex systems, and embodied cognition/enactivism would have given B&L richer conceptual resources. The enactivist tradition in particular offers a principled account of why the organism–environment relationship cannot be reduced to neurotransmitter levels. And why pharmacological intervention, while genuinely affecting neural dynamics, can never fully substitute for the relational, embodied, and situated dimensions of mental life.

The benzodiazepine position overcorrects. I am sympathetic to the judicious use of benzodiazepines, and I am more open to using benzodiazepines than some of my colleagues, but it’s still a stretch to advocate for benzodiazepines as being the first-line treatments for generalized anxiety today. B&L substantially understate the clinical problems that surround the use of benzodiazepines. Their clinical vignettes depict idealized time-limited use that bears little resemblance to complicated real-world presentations where time-limited use is often aspired to but infrequently achieved.

The melancholia thesis is on shaky grounds. The claim that antidepressants work well for narrowly defined melancholia but poorly for the broader population is clinically intuitive (especially for an older generation of psychiatrists, I’ve noticed) but poorly supported by empirical evidence. The clearest finding from the literature is not that antidepressants are specifically efficacious in melancholia but that tricyclic antidepressants outperform serotonin reuptake inhibitors on core melancholic symptoms… an advantage that, on the available meta-analytic evidence, appears to extend to non-melancholic depression as well and so does not establish melancholia as a pharmacologically privileged target. The Undurraga et al. (2020) meta-analysis found near-identical antidepressant response rates in melancholic (39.4%) and non-melancholic (42.2%) depression, with the lower placebo response in melancholic patients doing much of the work in apparent drug-placebo separations. Subjects responded better to TCAs (50.6%) than SRIs (30.0%). Imai and colleagues’ (2021) individual-patient-data meta-analysis showed that melancholic features were prognostic of overall symptom reduction but did not moderate the drug-placebo difference.

I just don’t think it’s true that melancholia is the population in which antidepressants genuinely work while the rest is diagnostic dilution. (See here for my discussion of antidepressant efficacy and mechanisms).

The stimulant skepticism is selectively sourced. Belmaker and Lichtenberg don’t engage seriously with the substantial evidence base for stimulant efficacy in carefully diagnosed populations. Their clinical vignettes are chosen to illustrate the problem cases rather than the straightforward ones. They apply their diagnostic-expansion-dilutes-efficacy argument to antidepressants with more nuance than they apply it to stimulants, where the tone becomes broadly dismissive. Research on brain circuits has also begun to dissolve the central paradox that stumped B&L: stimulants act on arousal, salience, and reward networks rather than on attention networks proper, helping with sustained engagement on unrewarding tasks rather than amplifying selective attention. This reframes stimulant action in a way that dispenses with the supposition of paradoxical pediatric calming and clarifies why both inattention and motoric restlessness in ADHD are best understood as motivational rather than purely attentional problems.

There is, strangely, no discussion of deprescribing. In fact, the term doesn’t even appear in the book. For a book adjacent to critical psychiatry, I was expecting at least some discussion of it.

The framework doesn’t engage with the new sciences of psychopathology. A significant scientific omission is the absence of any meaningful engagement with dimensional, network, clinical staging, and biotype approaches to psychopathology. These frameworks offer a principled response to many of the problems B&L identify. The HiTOP structure, for instance, provides a framework within which the transdiagnostic efficacy of dopamine blockers (effective across the Thought Disorder spectrum) or SSRIs (effective across the Internalizing spectrum) becomes not a failure of specificity but a positive finding about the spectral structure of psychopathology. B&L’s clinical observations are largely compatible with dimensional models, but they don’t seem aware of or interested in this literature. Computational psychiatry and predictive processing approaches are also absent. The network approach in which mental disorders are constituted by causal interactions among symptoms rather than by underlying latent diseases also provides hypothetical explanations for diagnostic non-specificity. If depression is a self-reinforcing network of interacting symptoms, then a drug that intervenes at any node could disrupt the network without being “specific” to the “disease.”

The relational dimension of prescribing is ignored. B&L never examine the prescribing relationship itself as a site of therapeutic pharmacological action or therapeutic failure. Psychodynamic psychopharmacology is entirely absent. If the prescribing psychiatrist contributes more to outcome variability than the pill (a finding they themselves cite in their placebo chapter), then the meanings patients attach to medications, the transference dynamics that shape adherence and response, and the countertherapeutic uses of prescribing that can chronify illness are relevant concerns to psychopharmacology. They catalogue the failures of the pharmacological treatment without really examining how the relational context in which drugs are prescribed and consumed might account for some of those failures. (See my interview with David Mintz on psychodynamic psychopharmacology.)

What I’m trying to say is that Belmaker and Lichtenberg’s diagnosis of the field’s predicament can be accepted, and yet the inferences can be taken in a quite different direction. Their response is, in essence, a chastened and humble clinical humanism-and-pragmatism: prescribe less, prescribe more narrowly, return to the prescribing sensibility of psychopharmacology pioneers, attend to the patient in front of you, resist the totalizing claims of either pharmaceutical marketing or anti-psychiatric critique. Psychopharmacology Reconsidered does not really say what a positive framework of understanding the transdiagnostic effects of psychiatric medications would or should look like. My own view is that the failures of a diagnosis-centric and disease-centric view should drive us toward richer multi-level mechanisms situated within the new clinical and scientific landscape of dimensions, networks, computations, biotypes, enactivism, and phenomenology.

Psychopharmacology Reconsidered is best understood as belonging to a clinical wisdom tradition, an accumulation of hard-won practical insights from decades of prescribing and scholarly work. Every psychopharmacology textbook is aware of the transdiagnostic effects of psychiatric medications, but few address the relevant tensions head on. B&L are refreshing in their willingness to do so. Reading this book is like talking to and learning from two experienced colleagues.

The book occupies a transitional space: it documents the exhaustion of one pharmacological framework and the necessity of continuing on. It is a book written at dusk, unsure of what the night will bring. It is a book written amidst the ruins of diagnosis-centered psychopharmacology, looking back at the early days of syndromic psychopharmacology, but not yet oriented toward the emerging outlines of a post-DSM, post-critical scientific psychopharmacology.

Subscribe now

See also:

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.”

See also

Share

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!

Share

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.

See also:

Share

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.

Share