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.

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“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.

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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.

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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.

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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.

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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…

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

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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)

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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.

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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.

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REFERENCES

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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.

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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.

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

“You’re back.”

“I’m back.”

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

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

“Flag what?”

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

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

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

“Walk me through it.”

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

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

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

“...all the way down?”

“Yup, all the way down.”

“What about the infants?”

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

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

“You tell me.”

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

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

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

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

“How?”

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

“…”

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

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

“A peculiar, perverted sort of pleasure.”

“Omigod, what a freak show.”

“I told you.”

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

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

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

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

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

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

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

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

But check out the interview and draw your own conclusions!

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Aftab: Thank you!

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

This is a follow-up to:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Here he explains his ideas in his blog:

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

This idea had legs.

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

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

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

These principles are

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Results showed that PHH can replace an inpatient unit.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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In a previous discussion of psychiatric hospitalization, I wrote:

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

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

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

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

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

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

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

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

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

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

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

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

The Case for Psychiatric Home Hospitalization

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

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

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

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

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

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

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

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

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

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

Psychiatric Home Hospitalization: Scarcity Mindset vs Abundance Mindset

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

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

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

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

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

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

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

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

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

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

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

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

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

Why Aren’t Things More Catastrophic?

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

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

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

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

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

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

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

Diagnostic Metaphysics vs Diagnostic Math

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

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

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

Diagnostic Truth as Convergence

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

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

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

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

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

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

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

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

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

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

There, I’ve said it.”

(p 143-144)

And earlier in the book, he writes:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Earlier in March, Psychiatry at the Margins crossed 20K total subscribers. Welcome to all the new readers, and a warm hello to all the longstanding ones. This publication remains one of the most meaningful projects I’ve ever taken on, and seeing how it’s been received has been a gift. Thank you for being a part of it. If you’ve started following the blog recently, do explore the archive.

As I say often, Psychiatry at the Margins is a labor of love and a one-person-plus-friends operation. My gratitude to all my friends, readers across the world, guest contributors, interviewees, and commenters.

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This post is an open thread. All readers are welcome to comment or ask questions. Share feedback, introduce yourselves, point out theoretical or scientific developments that I should be paying attention to, suggest topics for future posts, etc.

• I have been rather slow in responding to comments on recent posts as I am scrambling to finish the draft of my book, Remaking Psychiatry, to submit it to my editor at the agreed-upon deadline. It’s under contract with the trade books division of Harvard University Press. I have conflicted feelings about writing a book at the dawn of, as the word goes, the post-literate society. The process of writing it has been rather intense, and it has not helped that I’ve had a tremendously busy past year (as soon as I agreed to write the book, the universe started sending all sorts of obligations and responsibilities my way, curious) but it has also been clarifying. I believe in the book, and I am eager to send it out into the world.

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

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

• I will also be at the 2026 annual meeting of the Association for the Advancement of Philosophy and Psychiatry (AAPP), May 26-27, 2026, at the University of Texas at Dallas. Following the in-person conference, there will be a virtual conference on May 29-30, 2026. Keep an eye on the website for further details.

• ’s profile on me has been republished in the March/April 2026 issue of Psychotherapy Networker as a special extra feature (free to read but requires an email sign-up). Check it out if you haven’t read it before.

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

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

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

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

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

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

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

Why HiTOP exists

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

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

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

What does the HiTOP model actually represent?

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

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

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

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

HiTOP is not “atheoretical”

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

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

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

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

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

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

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

What counts as “psychopathology”?

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

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

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

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

Making sense of latent variables

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

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

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

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

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

Dimensions, categories, and thresholds

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

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

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

How does HiTOP handle validity?

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

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

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

Values, diversity, and the limits of “objectivity”

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

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

Conclusion

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

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

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

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

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

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

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

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

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

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

• Structure and Dimensions

• Functioning and Quality of Life

• Biomarkers and Biological Factors

• Socioeconomic, Cultural, and Environmental Determinants of Mental Health

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

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

The 4-Domain Model

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

The model consists of 4 interconnected domains:

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

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

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

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

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

Integrating Biological Measures

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

The report highlights 4 areas showing potential:

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

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

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

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

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

Functioning and Quality of Life

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

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

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

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

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

Integrating Social Context

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

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

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

Summary of Proposed Changes to the Future DSM

I. Structural and conceptual framework changes

• Transition to a living document with updates at briefer intervals

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

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

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

II. Integration of biomarkers and biological factors

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

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

III. Enhancement of functioning and QOL

• Make functioning and QOL essential elements of psychiatric diagnosis

• Use brief, feasible instruments for clinical use

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

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

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

V. Diagnostic specification and dimensionality

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

• Integrate transdiagnostic dimensions to better reflect comorbidity and symptom heterogeneity

VI. Procedural and stakeholder changes

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

Personal Reflections and Suggestions

Diagnostic Formulation Needs to Be Linked to Treatment

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

The Missing Domain: Psychological Factors and Personality Traits

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

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

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

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

DSM’s Notion of Dimensionality Is Underdeveloped

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

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

Major Categories Should Not Become the New “Unspecified”

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

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

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

The Definition of Disorder (and the Proposed Name Change)

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

Two strategies are possible here:

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

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

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

Indicate the Degree of Empirical Validation for Specific Diagnoses

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

Explain Why Diagnostic Thresholds Are What They Are

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

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

Include HiTOP in the DSM Appendix

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

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

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

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

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References

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

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

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

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

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

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

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

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