Stephanie Nelson, PhD, ABPP, ABPdN, is a board-certified pediatric neuropsychologist and founder of The Peer Consult, where she provides consultation and mentorship to assessment psychologists. Her interests include clinical reasoning, psychological assessment, and understanding human behavior through developmental, contextual, and systems-oriented perspectives.

This guest post is the second of a pair of articles by Stephanie Nelson in response to recent posts on Psychiatry at the Margins. It is a comment on:

In his essay, “Adiposity by Self-Report,” Dr. Aftab asks us to imagine a world in which body fat is invisible and impossible to measure directly. How would we diagnose obesity from subjective experiences, self-reports, and associated behaviors? How would we disentangle medically necessary treatment from much-wanted enhancement, or helpful intervention from potential harm? Wouldn’t we face the same epistemic problems we encounter when diagnosing ADHD, which cannot be determined by brain scans or neuropsychological scores?

It’s a thought-provoking analogy. But I think it understates something important about clinical diagnosis without a biomarker. In the absence of a definitive test for ADHD, we triangulate toward a latent construct using multiple imperfect indicators.

We certainly start with subjective experiences. As Dr. Aftab’s essays poignantly explore, our patients share heartbreaking stories of stress and distress. They may have spent years trying to understand their struggles. They long for compassion, clarity, and concrete support, and we long to provide all three. We begin with careful, and care-full, attention to their lived experiences.

But the bright beam of empathic attention can narrow our focus, so clinicians guard against attending only to subjective experience. We must determine whether patients’ descriptions are symptoms at all, and if so, where they belong within the diagnostic space. Descriptions that are unique, universal, incongruent, inconsistent, or improbable can all signal very real distress without being symptoms of the disorder in question. An experience can be clinically important while having little diagnostic value. Symptoms are also shapeshifters. What points in one direction may signal something else, so each symptom must expand curiosity rather than collapse into certainty. Clinicians also attend to symptomatic negative space, cautiously questioning whether expected core symptoms are missing.

Subjective symptoms are also, well, subjective. In our wish to help, and our patients’ wish to be helped, we can miss, mistake, misattribute, or reshape symptoms. Self-inferences can block or blur the diagnostic picture. The temptation to subtly mold symptoms to fit our preconceptions is enshrined in many of our clinical pearls: everything looks like a nail when all we have is a hammer, and we can miss a whole forest by focusing on the trees.

Since symptoms are slippery, we seek other imperfect indicators. While Dr. Aftab mentions self-report and behavioral inferences, and talks about self-perception and other-perception, I don’t think he fully explores the implications of triangulating from multiple lines of indirect evidence. We look for signs, or the behaviors observable to clinicians and people close to the patient. We consider continuity, examining the conditions under which signs and symptoms appear, persist, or diminish. We trace the course to determine developmental timing and trajectories. We evaluate evidence for functional impairment. We weigh relevant family and medical history and the presence of known correlates. We also carefully consider alternative explanations.

If we do neuropsychological assessment, we also bring the concerns into the consulting room. Scores on tests of attention or processing speed do not diagnose, yet the person’s approach can clarify. During testing, did we see signs of fatigue, frustration, fear of failure, forgetfulness, flagging focus, or freezing? Can we get curious about the patient’s experiences together? Research can contribute knowledge about group-level differences, such as distinct patterns of brain activity or discrepant outcomes over time. No one indicator is decisive, and conflicting evidence can reveal as much as agreement. Together, signs and symptoms suggest a clinical pattern, but the other indicators help us judge whether this pattern, in this person, warrants this diagnosis.

So let us reconsider how we would diagnose adiposity if it were literally invisible. We wouldn’t merely ask whether patients felt overweight or engaged in behaviors they associate with obesity. Instead, we would build a syndrome from converging evidence. We would start with subjective symptoms around hunger, eating, physical comfort, or exertion. But we would explore beyond self-report to ensure we were addressing the right problem and proceeding with appropriate caution. We would look for signs, such as specific patterns around eating and exertion, and consider the conditions under which those patterns occur. If we were assessors, we might devise tasks to observe some of those patterns ourselves. We would consider whether difficulty climbing stairs or finding clothes that fit constitutes functional impairment. We would trace the course to look for predisposing and precipitating factors. We would consider family and medical history and the presence of known correlates like physiological markers of inflammation. We would carefully exclude other causes; for example, hunger caused by severe caloric restriction, medication effects, or depression.

This process would be messy. Many indicators would be neither necessary nor sufficient; some would be consequences rather than causes; others would prove misleading. Our constructed syndrome would only imperfectly approximate the underlying inferred phenomenon. Still, triangulating to adiposity from multiple vantage points would give us something to investigate, validate, and revise, in a way that relying on subjective experience alone would not.

This discussion may sound abstract, or like I’m congratulating clinicians on the comprehensiveness of our (idealized) assessments. It may even sound unnecessary or unachievable in real practice: we have limited time, so we do often center our decisions around self-reported symptoms and behaviors. But reminding ourselves, our patients, and the public about how we infer diagnoses from multiple indicators is important and has real consequences.

Consider adult ADHD. Many more adults are reporting experiences and behavior that may align with a missed diagnosis, and we are having a public conversation about what that means. When the discussion focuses primarily on self-report, it can sound like we’re debating whether someone’s subjective experiences are true or worthy of care. This is a profoundly unhelpful frame, ungenerous to patients and clinicians alike. It’s no wonder people feel dismissed, defensive, and distrustful, and the debate quickly devolves. Looking beyond self-report gives us a way out of this impasse. Bringing the other indicators into the frame makes room for more expansive, and potentially more productive, conversations.

Because what worries me is not that more adults are reporting potential symptoms of ADHD. It’s that when we consider their experiences alongside the other indicators, we may be looking at a different pattern altogether. Perhaps the more productive question is whether we’re missing something about the pattern itself.

In clinical and consultation work, and conversations with colleagues, I’ve noticed some striking shifts. Some adults are reporting breathtakingly high levels of executive dysfunction, even compared with those I’ve historically encountered in patients with ADHD and extensive documented impairment. Nonspecific and transdiagnostic experiences such as rejection sensitivity, and seemingly paradoxical experiences such as hyperfocus, are increasingly folded into the ADHD phenotype, despite limited value as discriminating indicators. These experiences are not necessarily new, but their place within the narrative has changed; they sometimes receive more emphasis than the canonical symptoms of inattention, hyperactivity, and impulsivity. Self-report profiles can also be extraordinarily broad, with elevations that cross multiple diagnostic categories, and frequent endorsement of low-incidence symptoms and concerns not traditionally associated with ADHD.

Sometimes these symptoms occur alongside relatively few observable signs, even when we consider observations from people who have known the patient well for decades. Because signs are imperfect (people compensate, observers are biased, memories fail), an increasingly common clinical narrative posits that the absence of signs can never be useful or revealing. We also increasingly see behavioral signs recast as subjective symptoms: not “I routinely fail to complete tasks,” but “it feels much harder for me to complete tasks than it seems to be for other people”; not “I repeatedly lose things,” but “I feel as though I would lose things if I didn’t compensate so intensely.” These descriptions introduce additional layers of inference. What was once relatively visible must now be inferred, sometimes primarily from what the patient imagines might happen if they weren’t compensating so intensely.

These are clinical observations, rather than established population-level findings. But surely they deserve serious investigation, without the questions themselves being treated as evidence of inadequate empathy, disregard for lived experience, or attempts to gatekeep care. Have you noticed these shifts too? Are the distribution and content of complaints changing? Do they converge with the signs, developmental histories, and functional consequences we expect? Are we seeing new expressions of an established syndrome, new ways of describing old difficulties, overdue recognition of overlooked experiences, or something genuinely different?

Broadening a phenotype can be scientifically legitimate, of course, but we would need evidence that its new manifestations belong to the same construct. If this emerging pattern turns out to be associated with less observable impairment, weaker cross-setting corroboration, or different developmental histories, familial patterns, or outcomes, shouldn’t we ask: Are we still talking about the same syndrome? Is this really a different picture of the same diagnosis, or might we be trying to cram a star-shaped peg into a round hole?

This is not the same as asking whether patients suffer or are impaired. Something is happening that is both real and really distressing. We’re asking whether ADHD best explains the pattern and guides our response, rather than assuming a familiar label settles those questions. This matters especially once treatment enters the picture. Interventions can feel profoundly helpful while reinforcing dysfunctional processes or introducing new harms. For example, someone might experience enormous relief from an appetite-suppressing medication without having excess adiposity and without that medication being an appropriate treatment.

Our obligation to ask these questions comes from our desire to provide good care to those seeking our help. But I also feel a duty of care toward the people who are not in my office at this moment. Those include people with more traditional, sometimes severely impairing ADHD, whose difficulties may be less easily articulated or less readily translated into today’s language for accessing care. Expanding a diagnosis can change who qualifies for services, how limited resources are distributed, and whose struggles are recognized. We should be curious about whether the people who have historically experienced the most severe manifestations of a disorder are being helped or displaced as its boundaries change.

Diagnostic categories also ripple outward, shaping self-understanding, family and school responses, clinical attention, research priorities, and expectations of ordinary human functioning. A diagnosis can alter the expectations we place on a child, what we ask of a spouse, or what we attribute to an employee. And as certain experiences become linked to specific diagnoses, they may become less visible as possible responses to mismatched environments, strained relationships, impossible expectations, or the ordinary demands of being human. Meanwhile, the diagnostic explanations we offer influence which of their own experiences people attend to and consider worth exploring. We risk changing not just the boundaries of a diagnosis, but the very meaning of the experiences inside them.

I want us to be able to ask what we’re uncovering, what we might be overlooking, and what follows from the explanations we choose. I’m grateful to Dr. Aftab for providing a space for serious, thoughtful, pluralistic conversations like this one.

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In certain situations when the symptoms are too few, too mild, too many, too severe, or too spread out across many domains, the diagnostic possibilities begin to all blur together. The presentation takes on an undifferentiated quality, a blob of psychopathology that you could reasonably describe using various names for differentiated things if you had to, but anything you call it is too ill-fitting, too artificially precise.

It’s like a low-resolution, pixelated photo.

A blurry photo can be enhanced into a variety of possible faces, and we can arrive at a very plausible but untrue end result.

In the case of a blurry photo, there is usually a truth of the matter. There is or was a face that has lost its features and we can’t reconstruct it anymore with accuracy because of information degradation.

There are other situations, however, where there is no truth of the matter, like generating a low-resolution blur of a face from scratch disconnected from any particular face. There is no truth of the matter regarding what face it really is.

And there are situations where the relevant concepts simply break down or lose their meaning. For example, in the fraction of a second after the Big Bang, the temperature was so high that electromagnetism and the weak nuclear force did not exist as separate forces. There was a unified electroweak state in which neither electromagnetism nor weak nuclear force was a meaningfully separate category. As the universe cooled, the two forces emerged as distinct. It is not that we cannot tell the two forces apart at those high temperatures; rather, there aren’t two forces to tell apart.

Similarly, I feel that there is a point where autism gets too pixelated and hard to differentiate from its cousins; the uncertainty becomes too high. And then there is also a point where it no longer makes sense to talk about “autism” at all because what we are dealing with is just a blob of psychopathology.

In my physics analogy, the dial is energy or temperature. In the case of autism, we have multiple dials to consider: there is developmental history, severity, comorbidities, and the explanatory level of description.

There is too much uncertainty in situations like:

• Diagnosis of autism in adults where developmental history is unknown or unreliable, and years of compensatory behaviors have made assessment difficult.

• Differentiating autism from severe social anxiety, schizoid personality traits, etc.

• Differentiating from “broader autism phenotype” or subclinical autistic traits, in situations where impairments are hard to assess.

Like the photo “enhancement” example above, a clinician can fill in the missing pixels based on educated guesses and priors, but there is no guarantee that the autism reconstructed is the correct reconstruction.

Developmental time is perhaps the closest parallel to the early universe situation. Take a 6-month-old baby; it isn’t that the baby is already autistic, and we just can’t detect it yet. Arguably, there isn’t yet an autism to detect. What exists, probably, is a kind of undifferentiated neurodevelopmental liability that can manifest in different ways later in development, including autism.

At the level of genetics also, there is no such thing as autism, differentiated from other neurodevelopmental and psychiatric conditions.

And then in cases of dense psychiatric multimorbidity, when a person has elevated ratings on many or nearly all psychopathology dimensions, there may be no distinct autism to separate from the rest of psychopathology.

In physics we can distinguish between measurement breakdown and the actual breakdown of phenomena, but in our current science of psychopathology, we cannot empirically distinguish between “measurement is no longer possible due to a high margin of error” and “the concept no longer applies.”

The usual commentary on autism overdiagnosis these days, e.g. Uta Frith and company, leaves me fairly frustrated and dissatisfied. The impression I get is that the diagnostic concept of autism and the composition of people being diagnosed, and those self-diagnosing, has expanded and changed so substantially since the 1980s that folks like Frith, who were used to seeing autism comorbid with intellectual disability or significant speech impairments, struggle to make sense of it. Their instinct is to be skeptical (rather than curious) and to try to preserve some old idea of autism as more real and more genuine. But both the scientific understanding and the clinical landscape of autism have genuinely changed, and the sure ground they hope for doesn’t exist and never existed. This instinct leads them to focus on trying to exclude this or that subgroup—the mildly impaired, those diagnosed late, those who mask, etc., etc.—from the autistic camp. RETVRN!

My interpretation of the situation is different. There are definitely differences between early-diagnosed and late-diagnosed individuals. There are different patterns of severity and comorbidity that lead some people to come to attention fairly early in life and that lead some people to come to attention later in life, but as long as they share the clinical features we call autism, they are all autistic. Heterogeneity is the price we pay for syndromic diagnoses. There are also differences, for instance, between those with severe intellectual disability and mild intellectual disability, or adolescent depression and geriatric depression. Variation in correlates are reasons for specifiers and subtypes, not exclusion from the syndrome.

What makes autism “autism” rather than a different diagnosis? The field has settled on social communication impairments and restricted, repetitive behaviors as the clinical core, and as far as these clinical features are concerned, it is rather clear that they exist on a continuum, with heterogeneity existing within the continuum. There are certainly autistic folks who also have intellectual disabilities or speech impairments, but neither intellectual disability nor speech impairments are autism. To insist that only those with intellectual disabilities and speech impairments are people with “real” autism is to profoundly misunderstand what makes autism autism.

Frith thinks that autism should be reserved for people with severe communication challenges, that people who are fluent in conversation cannot be autistic. When Holden Thorp (Editor-in-Chief of the Science family of journals and diagnosed autistic) asked her that if people like him are not autistic, then what are they, she didn’t quite know what to say:

“That’s the main place where Frith and I diverge. Even someone like me who has most of life’s possible advantages has experienced difficulty from autistic traits imposed by society and the environment — and their preferences for a neurotypical affect. (I told Frith that I had a meltdown at the hotel before I came over; it had to do with technology, as it so frequently does.) Now imagine how that plays out for someone with fewer resources who is also excluded based on their other identities.

Finally, I asked her if people agreed with her, what would she call the rest of us who are no longer autistic. She had noticed I was staring out the window and agreed that was an autistic trait. When I explain why I do that to someone, I just say it’s because I’m autistic. What should I say instead?

She didn’t know. She suggested “autistic-like.” Then she tried “autistic temperament.”

I didn’t think these would fly, and she reluctantly agreed.”

Autistic-like and autistic temperament… woah, it almost sounds like autism exists on a… spectrum?!

We should obviously recognize and better characterize this heterogeneity, and we shouldn’t accept misdiagnosis, but that doesn’t mean we can chop off the spectrum for arbitrary reasons. Frith raises skeptical questions that are fine to raise but is unable to offer a better account of what autism is.

Where I do agree with Frith is that the reliance on self-report, appeals to an overly broad notion of masking (but not masking per se1), social-media-fueled self-diagnosis, and inadequate consideration of other diagnostic possibilities have made diagnosis of autism in adolescents and adults, especially those with only mild impairments and high comorbidity, more uncertain and fallible, and we collectively have not yet come to terms with that fallibility.

My grievance with contemporary autism is neither that people with mild impairments are getting diagnosed, nor that we now recognize and account for masking as a phenomenon. My worry is that at a certain point the confidence interval around diagnostic judgments becomes so wide that we can no longer say with meaningful confidence what we are dealing with.

We need a new clinical vocabulary to talk about this diagnostic blurriness.

In addition to already recognized constructs such as “broader autism phenotype” (no clinical impairments) and social communication disorder (social communication impairments without restricted, repetitive behaviors), there are moments as a clinician when I find myself reaching for descriptions like:

• Autistic features with indeterminate developmental history

• Autistic features with context-dependent impairment

• Autistic features with self-reported impairment, not clinically observed

• Autistic features with psychiatric multimorbidity and uncertain differentiation

I am less concerned with trying to preserve some old idea of autism or restrict it to people with severe impairments. I think people with mild impairments or people who mask also merit clinical recognition. I am more concerned with the margin of error, with epistemic uncertainty. I am worried that when developmental history is uncertain, when impairment is only self-reported, when psychopathology is spread out over multiple spectra, a diagnosis of “autism” conveys a certainty that just doesn’t exist.

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Sam de Selby (pseudonym) is a writer living in Germany with a background in nonfiction and research assistance. She is currently working on Fractal Procrastination, a project detailing the experiential nature of psychosis.

I think it is a mistake to frame treatment adherence as a one-time decision. Taking oral medication means the concession that you are in need of correction is made anew daily, or multiple times per day.

Even at the point when I voluntarily admitted myself to the hospital in the midst of psychosis, I was vehemently opposed to taking antipsychotic medication. If a lobotomy had been on offer, I would have signed the consent forms without hesitation if it seemed likely to stop the pain, yet I baulked at the idea of long-term medication. It wasn’t just fear of side effects or lack of awareness that it would probably help. I didn’t want to make that decision over again every day. I wanted a solution. It was painful to consider what I hoped was a temporary blip could be something deeper.

After about a week in the hospital, another patient persuaded me to start taking my prescribed medication. (I suspect that, where psychiatric hospitalization is beneficial, much of what is therapeutic happens between patients.) He had been in and out of treatment for almost as long as I’d been alive and painted for me a horrifying picture of how my life would go if I remained unmedicated, based on others he had met. I don’t think I would have made that decision without someone telling me I was an idiot not to do so. No amount of education makes it easy to communicate the possibility of escape to someone who is on a different plane of reality and doesn’t know it. I had no idea how much it was possible for things to change as a result.

When I found an antipsychotic that works for me, it was like drinking from a firehose of lucidity. It was too much, too fast, too soon. After years of unrecognized on-and-off psychosis, normal sanity felt alien. Everything I thought I knew about myself was wrong. Suddenly, I re-evaluated my entire life, seeing every single occurrence in a new light. Memories lost all emotional resonance. The nature of state-dependent memory makes it difficult to connect with the past self when your mindset is so different from then. At the time of writing, 5 months after exiting psychosis, I continue to reel at the change in the most basic aspects of experience, like the sense of time and space. I used to feel much older than my age. Now I feel younger, because I’m new to seeing this world without a coating of paranoia.

Every 24 hours still, there is a moment on which everything to follow pivots. Every 24 hours, I must decide which world I want to live in and which person to be. Every 24 hours, I must admit to myself anew that there is something terribly wrong with me. I can only paper over it for a day at a time. It buys me freedom, for one day at a time. The improvement that medication brings in the eyes of others feels like a condemnation of my undoctored self. The unmedicated me becomes the thing to fear. Insight is something that has to be re-enacted over and over, to this day. I take it, and resent it.

It sounds so simple to other people: just take your meds. But that’s a fridge magnet, not a solution to the complicated equation of choosing between living in a world that can feel meaningless and risking incomprehensibility again.

Yet medication also gives you at least a foothold in normality, a little distance to see yourself in cold, clear light. For that, I will always be grateful. The choice to stay in this world feels like a leap of faith anyway. It doesn’t get easier with time, at least not so far. Every pill is a reminder that who I am is not who I want to be. It’s an intervention in basic identity. If it were just about treating a temporary state, it would be easy. The past can be buried. Who I am follows me around. I have to reject that person over again every day.

As far back as I remember, I felt I had access to an extra plane of meaning. I didn’t think I was smarter than other people, but I was sure I knew something they didn’t. The fear setting was always turned up a bit too high. I never quite outgrew having imaginary friends or being scared of the dark. Around age 15, something shifted. That is the point in time where I can clearly see in hindsight how the ambient paranoia solidified, and the voices became problematic.

In the 13 years that followed, the paranoia, social withdrawal, and hallucinations waxed and waned, becoming a nagging background hum after about 8 years. Whether those early features are best categorized as prodrome, schizotypy, or neurodevelopmental difference will always be unclear to me. Certainly, there were previous times before the big episode when I fully detached from reality for days, weeks, or even a couple of months. The difference was that I always maintained some connection to the world, some obligations to keep me grounded, and managed to pull myself back. Looking back, it’s unimaginable that I coped with such intense fear for so long. But you have to get through the day one way or another. There is a widespread misconception that people in psychosis are too disorganized to manage basic functioning and that it should be obvious to other people. Psychosis is not always dramatic. When it starts slowly, you are forced to adapt.

It was only when things worsened to the point of complete functional collapse and suicidality that I was willing to accept help and received a diagnosis. But none of the symptoms were new or surprising to me—some had been worse at prior times. It just took feeling completely defeated by my own mind to break through my innate stubbornness. I no longer cared enough to be in denial. If there was an explanation someone could offer for what was wrong with me, then I wanted to hear it. On the one hand, I regret that I struggled unnecessarily for so long; on the other hand, I know that I would never have been willing to talk about it before. I just wasn’t ready to engage in what ended up feeling like the process of leaving a cult. Involuntary treatment would have only deepened the denial and made me less likely to ever engage with help.

If insight in psychosis is understood to be the awareness of a morbid change in oneself and understanding of how that differs from other people, what happens when there is no clear change, only an alteration in degree or distress? How can the impact on functioning be understood when there is no comparison? When you grow up with unrecognized psychosis, there is no obvious line between disorder and personality. The traits to be relabeled as symptoms may be unwanted, but they are still part of you. In that case, possessing insight becomes about acceptance of defect rather than acknowledgement of change.

Another aspect of how insight in psychosis is defined is recognition of how one’s experience of reality differs from others. This is a difficult ask for a group of people who tend to be socially isolated. If you don’t have much contact with other people, it’s tricky to reality test. If your psychosis is a bolt out of the blue, you’re more likely to have people around you to tell you you’re thinking abnormally. When onset is insidious, relationships erode or never develop in the first place. You need people most at the point where they’re least likely to be around.

Most people in the world are not particularly versed in psychopathology. Most people think everyone thinks like them. When those who’ve studied the mind assume everyone has that knowledge, they’re committing the same fallacy that psychotic people commit when they think they think normally. Until recently, I can’t recall ever having a conversation about the voices because they didn’t register as strange. Most people don’t just talk about how their consciousness is ticking along. There is a built-in assumption that psychotic people should know they’re abnormal. But every time I read this, I think, how should I know what normal looks like?

To accept treatment without ambivalence is then to let a professional carve out the parts of you considered detrimental, to remodel the internal landscape and ways of relating. The blow this strikes to the ego is considerable. Ambivalence in this case can come from the unfamiliarity of inhabiting consensus reality. The change being responded to is the arrival of health, not the arrival of sickness. After all, the gap between normal and psychotic experience is the same size as the one in the opposite direction. This is not to judge it as a bad change, but a drastic and unnerving one. Antipsychotics, when they work, tend to start taking effect relatively quickly compared to, for example, antidepressants. The change they bring is often described as a sudden epiphany, not a dawning awareness. Perhaps sometimes the problem can be that they work too well. They drag you, kicking and screaming, into a different world.

In late 2025, in the middle of a six-month psychotic episode, I found and printed out Aubrey Lewis’ classic paper The Psychopathology of Insight, while obsessively researching what might be going on and how to understand it. Next to Lewis’ definition of insight as ‘the correct attitude to a morbid change in oneself,’ I annotated: ‘but what if it is instead a failure to change?’

I knew, at least some of the time, that what I was experiencing was probably psychosis and was desperate for an explanation to give structure to the suffering. At the same time, I was terrified of being forced to reappraise myself as disordered. The idea that it had all been in my head, all along, was too much to bear. Whatever was wrong with me at that point had never been quite right. When I tried to trace the first appearance of various symptoms, I inevitably found myself going back to my childhood or early teens. In my diary, I wrote repeatedly that I was ‘scared of losing the people in my head’ because I knew they functioned as a shield against loneliness and boredom. I feared what it would do to me to turn something so intimate into a symptom.

Ambivalence about antipsychotic treatment is typically chalked up to lack of insight or intolerance of side effects. While the significant role of both is obvious, the picture is more complicated in the case of insidious, early onset. Where there is a significant duration of untreated psychosis during periods of identity formation, insight cannot mean awareness of a morbid change in oneself. There is no sense of a sudden rupture, no clear division between symptoms and personality—or adaptation to symptoms. In such cases, possessing insight requires acceptance of the self as defective, which is a different demand from recognising a change in the self.

The widely used Positive and Negative Symptom Scale (PANSS) assesses insight by asking if there is a perceived need for prescribed medication. What strikes me about that question is that it is about need — not whether medication is seen as necessary for certain aims, effective, helpful, or simply understood to be the clinical recommendation. Need is assumed irrespective of how well it actually works for a given patient and of whether negatives outweigh positives. Presumably it is insufficient to agree it was needed in the past or to aspire not to need it in the future. It’s unclear if it refers to an internal need, or a need in the sense of being told by others or even coerced.

To me, the question does connote a profound flaw in need of correction. No allowance is made for the possibility of recovery in the sense of functioning unmedicated. Nor is any allowance made for those who don’t respond to medication, would like to change the current one, or who experience intolerable, even life-threatening side effects. I recognise that rating scales are by definition devoid of nuance and are not intended as a full picture of illness. But I also know that no detail of the questions included is left to chance. My argument is about what the operationalisation actually encodes. Treatment ambivalence is cast as a component of sickness, even where there is continued adherence. Insight is not even equated with actual compliance, only with acceptance of fundamental brokenness. The question demands acceptance of its premises, acquiescence to needing fixing regardless of the experience of that repair.

It is hardly surprising to me that higher insight in schizophrenia, in what is known as the insight paradox, is associated with higher risk of depression and lower quality of life. Insight is approached practically, if not defined, in a way that is synonymous with complete pessimism. Schizophrenia has predominantly been seen as a chronic, degenerative disorder of basic brain functioning. While that view is increasingly challenged both by neuroscience and advocates for the recovery model, it remains the assumption underlying assessment of insight in many cases. Newer multidimensional measures of insight still arguably encode the same assumption.

The only way to have hope for the future while living with schizophrenia is to, at least partially, reject or question that one is fundamentally defective. To accept the need for lifelong treatment for something innate in you, with no hope of negotiating a recovered state on your own terms, is to give in to despair.

Ambivalence about treatment in early onset, prolonged, untreated psychosis can come from the sheer abrupt shock of consensus reality. Awareness of symptoms and the suffering they bring does not negate the challenges of this transition. Nor does a good treatment response make adherence easy. Disputing the premise can be a claim about identity, not failure to recognise suffering.

It makes a tremendous difference if someone has grown and adapted to symptoms, like a tree trunk warping around a fence. The basic disturbances underlying schizophrenia can, at least sometimes, be present many years before obvious illness. The personality traits comprising schizotypy are potentially lifelong. People may learn to balance inhabiting consensus reality with their own private framework before florid psychosis emerges, carrying a long-term sense of being different. It is a mistake to assume psychotic complaints are always mere states, unwanted and unwelcome.

Where there is no clear premorbid baseline, recovery must be about constructing a new self, not restoring an old one. The remittance, partial or full, of symptoms is only the beginning of this process. Delusional beliefs can be a self-protective mechanism for coping with traumatic life experiences, so simply removing them through medication without replacement complicates coping. Constructing a vision of the future is difficult work, especially for those, like me, who do not have access to therapy or any treatment other than medication and sporadic brief outpatient checkups.

Insidious trajectories in schizophrenia are associated with worse outcomes and only partial recovery, perhaps attributable to slowness to seek help once florid symptoms emerge. Longer durations of untreated psychosis are associated with a reduced likelihood of remission and higher risk of suicide. I wonder whether that has something to do with the difficulty in accepting treatment after you’ve lived with the slow disintegration of reality for years. It’s hard to have a sensible attitude to psychosis when it has crept up on you.

Perhaps rather than asking if medication is needed to assess insight, it makes sense to ask about the ways in which someone would like their experience of reality to change, and whether they understand that this is possible. To me, that sounds like hope. Wanting to change how you live and how you relate to the world does not require immediate acknowledgement that your entire way of thinking is wrong and different from other people. That’s a big ask for anyone. But it does open the door to understanding the ways in which treatment could be beneficial and desirable. Approaching insight this way may not always be possible — after all, assessing insight is pointless if everyone passes. For insight to do discriminatory work, someone has to lack it. But what I am suggesting can be a gentler starting point for those who are distress or impaired by psychosis and aware of it.

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Stephanie Nelson, PhD, ABPP, ABPdN, is a board-certified pediatric neuropsychologist and founder of The Peer Consult, where she provides consultation and mentorship to assessment psychologists. Her interests include clinical reasoning, psychological assessment, and understanding human behavior through developmental, contextual, and systems-oriented perspectives.

This guest post is the first of a pair of articles by Stephanie Nelson in response to recent posts on Psychiatry at the Margins. It is a comment on:

In a recent essay, I Believe in a Radical Abundance of Relational Care, Dr. Aftab makes a compelling case for expanding access to thoughtful and individualized psychiatric care. He argues that many of the problems associated with contemporary mental health treatment arise from scarcity: limited time, limited attention, and limited alternatives to the relatively narrow range of interventions that are readily available. He’s understandably wary of reform efforts organized around reducing diagnoses, prescriptions, or other care when so many are struggling to get the help they need. Instead, he envisions a radical abundance of good care, in which people have access to a wide range of meaningful options. I share his aspirations, and much of his reasoning, but his essay brought into focus a question I’ve been wrestling with about the kinds of care we’ve already made abundant.

I work with children, and early in my career I felt as though I was surrounded by kids experiencing the psychological equivalent of hunger. Empty bellies, aching bodies, nutrient deficiencies. They needed more understanding, more generous attention, more options, and more support. I wanted us to build a world in which there was so much good psychological care available that people could choose among many nourishing possibilities and figure out what actually worked for them. And many of us worked very hard to make more food.

But lately I find myself wondering whether something changed along the way.

We unquestionably have more “psychological food” than we used to. More people are in therapy, taking psychiatric medication, receiving diagnoses, asking for accommodations, consuming mental-health information, and understanding themselves through psychological language. Yet, I’m increasingly uneasy that much of what has become abundant resembles ultra-processed food: highly accessible, easy to consume and provide, often satisfying in the short term, but perhaps not terribly nourishing. In my corner of the world, its ingredients often include a rapid move toward diagnosis, locating the problem inside the individual, accommodations without enough attention to development or environment, and explanations that gradually strip away context and individuality.

Meanwhile, the people arriving at the clinic have changed too. I still see children who are psychologically starving. But I also increasingly see people in genuine distress who seem less like people suffering from caloric deprivation, and more like people eating plenty while nevertheless feeling unwell: micronutrient deficiencies, perhaps, or problems arising partly from the composition of the diet itself.

I want to be extremely careful here, because their suffering is real. I don’t want to resurrect a distinction between people who “deserve” care and people who don’t. Nor do I want fewer possibilities available to people simply for the sake of having less treatment. Indeed, someone might receive a great deal of psychological attention and still be missing precisely the understanding, support, or changes to their circumstances that would actually help them.

But I do wonder whether this complicates the abundance argument.

Ultra-processed food doesn’t merely coexist with better food. Once it becomes cheap, ubiquitous, convenient, heavily reinforced, and culturally familiar, it changes the entire food environment. It shapes preferences and expectations. It changes what producers make. And simply making fresh vegetables abundant alongside it doesn’t necessarily undo those effects.

Could psychological care operate similarly?

Perhaps some forms of psychological care are not merely inferior substitutes that people choose because richer relational care is unavailable. Perhaps what we’ve made abundant changes in how we conceptualize distress, what people learn to ask for, what clinicians learn to provide, what institutions incentivize, and where our precious, scarce attention ultimately goes. And perhaps that helps explain the strange coexistence we now have, of ever-expanding mental health treatment alongside people with serious mental illness and high support needs who remain profoundly underserved.

These are the questions I’m still trying to think through.

I share Dr. Aftab’s desire for a radical abundance of care. I’m just increasingly unsure that the answer can be “keep everything we have and add much more excellent care beside it.” I wonder whether abundance sometimes requires pruning as well as planting. The pruning may involve questioning some of our defaults: reflexive labeling, familiar interventions offered without sufficient consideration of alternatives, a tendency to interpret all problem-in-living as psychological concerns, and institutional incentives that favor what is easy to provide over what might actually be helpful. It may mean being willing to consider whether each form of care we offer truly relieves suffering, deepens understanding, increases people’s capacities or resources, or helps create circumstances in which they can live more effectively. Thoughtful gardening requires watering and weeding, especially when some extremely successful species may be crowding out the ecosystem we were trying to create.

Maybe, in other words, there is a humane subtractive agenda? Not subtraction as austerity, suspicion, or denial of suffering, but subtraction in service of making room for what nourishes.

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I was invited by Psychoanalytic Inquiry to write an article for an upcoming issue of the journal that will feature contemporary voices engaging with classic psychoanalytic papers. The consulting editors for the issue, Nicole Nelson and Adrian Sanchez, suggested Psychoanalysis and Moral Values (1960) by Heinz Hartmann as a suitable target for my commentary, a classic text on how moral values intersect with psychoanalysis, and I accepted. The article has now been published online ahead of print.

I am sharing an excerpt here for the readers of Psychiatry at the Margins.

What Psychoanalysis Can and Cannot Tell Us About Morality

Consider a hypothetical scenario. A woman meets with a psychoanalyst for an initial consultation. Her main reason for seeking psychotherapy is, “I want to be a more ethical person. I realize that for much of my life I’ve acted in a selfish and self-centered manner. Can you help me become a more moral person?” When asked to clarify her conception of a moral person, she says, “Someone close to God, who follows God’s word, is an obedient daughter and obedient wife, a selfless mother, and one who is not vulnerable to temptation.” How might the analyst respond to her, and what should the therapist say about what, if anything, psychoanalytic psychotherapy can do for her in her pursuit?

The classical psychoanalytic answer to this would be that psychoanalysis is not primarily about morality or ethics; it is instead about a certain sort of mental freedom and self-knowledge. The analyst cannot promise any moral improvement whatsoever. They can, however, potentially help the person better understand what motivates their inquiry, why this inquiry has acquired a sense of urgency at this particular moment in life, and why they are drawn to these particular moral values.

Instead of giving an answer about the relationship between psychotherapy and morality, another analyst might focus on discussing the particular vision of morality she brings up. Her moral worldview appears centered around relationships to authority, whether it is God, father, husband, or children. Her own desires and judgments are not only absent, they seem to be a threat. Perhaps what she needs is less guilt and less obedience. Maybe she needs to embrace a degree of healthy selfishness that she has so far rejected.

And yet another analyst might say: psychoanalysis is indeed an ethical undertaking, and genuine concern for others is a developmental psychological achievement, while mere compliance with rules indicates something has gone awry. Psychoanalysis carries its own ethics. It values candor, preaches tolerance of ambivalence, a greater willingness to see one’s real desires. This ethic is not neutral towards patriarchal and religious ideas of obedience. So while the answer to whether psychoanalysis can help her be a better person is yes, the outcome won’t resemble her description of morality at all. It may, in fact, subvert it.

If you, dear reader, are a psychotherapist, how would you respond? In contemplating this clinical scenario, you are also contemplating an old question about the relationship between psychoanalysis and moral values, and one of the first comprehensive treatments of this question comes from Heinz Hartmann.

***

Heinz Hartmann was an Austrian-born psychiatrist and psychoanalyst, and was the leading theorist of ego psychology in the mid-20th century. Psychoanalysis and Moral Values is a short book by Hartmann, published in 1960, as an expanded version of a Freud Anniversary Lecture he gave in New York in 1959. It was an attempt to clarify what psychoanalysis can and cannot contribute to our understanding of morality. The central thesis of the book is that psychoanalysis gives us a psychological account of moral behavior (how moral values and the superego develop, etc.), but it cannot by itself tell us what is morally right or wrong.

As a theory of personality, psychoanalysis is, in Hartmann’s view, well placed to explain the psychological origins of moral feelings and conflicts. It can do so, however, only by maintaining a separation between psychoanalytic practice and the personal moral worldview of the analyst. The analyst’s role is to be a scientific student of morality. To determine how moral valuations arise and are maintained, and how they interact with other psychological processes. The analyst’s role is not prescriptive, it is not to prescribe what ought to be value ultimately.

Hartmann reconstructs Freud’s view on ethics using various scattered sources such as Freud’s theoretical writings, letters, biographies, etc. Freud was not an ethicist and did not concern himself with building moral systems. However, he also saw morality as indispensable to the cohesion of civilization. Freud believed psychoanalysis to be a descriptive science which could, in theory, explain morality in psychological terms, but one that could not offer a moral vision itself. Per Hartmann, any analyst who treats psychoanalysis as a source of moral values is misreading Freud.

In Hartmann’s analysis, moral behavior develops out of early relationships with adults, characterized by a tangle of emotions such as dependence and resentment, love and fear, and identification and resistance. Efforts to manage early sexual and aggressive impulses as well as the internalization of external imperatives from caregivers develop into superego. While Freudian theories provided a description of how moral behavior develops, the explanations do not say and do not determine what should be valued.

[…]

Can analysis lead to moral improvements in a person? Hartmann concedes that this is possible. There are routes from psychological health to ethical behavior. Through enhanced self-knowledge. Integration of previously suppressed or denied impulses and ideals. Better insight into motives and conflicts, such that moral code and actual conduct are brought into closer alignment. Psychoanalysis can produce a more integrated personality, one that is less vulnerable to problematic oscillations between rebellion and submission to authority figures. But Hartmann remains critical of the assumption that successful psychoanalysis necessarily improves moral behavior. The aims of psychoanalysis are clinical; any moral gains are indirect and these moral gains must not become the explicit goal of treatment.

***

Hartmann’s conclusion is that psychoanalysis is a psychological science of moral behavior that can’t itself yield a moral system. This conclusion remains true and is still persuasive. Today, it is understood more readily as a specific application of a more general thesis in philosophy, known as the “is-ought problem.” This philosophical problem was famously articulated by David Hume, and while it continues to be actively debated by philosophers, the core point is now widely accepted. The core is that purely descriptive premises cannot by themselves entail a normative conclusion, unless some normative assumption has already been smuggled in (Sayre-McCord, 2023). In scientific practice, empirical inquiry is usually infused with values of one sort or another, making it difficult to state facts in isolation without values in the background. “Thick concepts” that combine values and facts (Väyrynen, 2025) also complicate this philosophical picture. Classical philosophical examples of thick concepts include character terms like generous, cruel, and tactful. Health is arguably a thick concept as it combines descriptions of physiological and psychological state of affairs with ideas of what is optimal and desirable.

I am more intrigued by Hartmann’s claim that psychoanalysis can explain the ontogenesis of moral values and moral behavior. This is because subsequent scientific and psychological research on moral development has largely displaced psychoanalysis as the central explanatory framework and this raises the question of how much of Hartmann’s claim still holds up…

[…]

What do we know about the effects of undergoing psychoanalysis on moral judgment and behavior? In terms of clinical studies, we know surprisingly little. While there is an abundant literature on the efficacy of psychoanalytic and psychodynamic psychotherapies, studies have not systematically studied moral behavior as an outcome. What we can say with some confidence is that long-term psychodynamic psychotherapy is associated with improvements in personality functioning (De Maat, et al, 2009; Lindfors, et al. 2015; Leichsenring et al, 2023). Personality pathology involves impairments in self and interpersonal functioning, including unstable or exploitative value systems and difficulties with guilt and responsibility. While we cannot really say anything confidently about whether psychoanalysis improves moral judgment and behavior, undergoing intensive analytic/psychodynamic work can improve the psychological conditions under which moral judgments are made. Psychoanalytic treatment can nudge a rigid or fragmented psyche towards more integration and self-reflection, strengthening the patient’s capacity for mentalization and affect regulation. Those changes can, in principle, reduce impulsive or retaliatory behavior, decrease covert exploitation, and soothe self-sacrificing “moral” enactments that are driven by unconscious guilt. Undergoing psychoanalysis can foster a more coherent and humane conscience and thereby tilt moral judgment and behavior in a prosocial direction, but Hartmann is correct that psychoanalysis cannot be pursued as a moral treatment. The aim of psychoanalysis is psychological health, not morality, and any moral benefits are secondary to that.

Hartmann got the conclusions right in 1960, although anyone producing a similar work today would have to focus more on the relationship between moral psychology and moral values. Moral psychology as a scientific discipline can explain how we develop our moral sense without telling us what’s morally correct. While cognitive psychology, social psychology, evolutionary biology, developmental psychology, and neuroscience have now replaced psychoanalysis as the primary lens for understanding moral development, core insights from psychoanalysis remain important to our contemporary understanding. The internalization of moral values from relationships with caregivers, the influence of unconscious conflicts, the opacity of moral motivations, and moral behaviors as reaction formations are insights that remain alive within moral psychology. Psychoanalysis brings a unique attitude of respect for the idiographic developmental complexity of the moral self that distinguishes it from other disciplines and ensures its continued relevance.

Read the paper here.

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As readers of Psychiatry at the Margins are well aware, I have been interested in understanding the phenomenon of overdiagnosis in psychiatry, and I have been frustrated by the tendency of critics to assert or imply that vast proportions of human suffering and impairment that come to clinical attention are simply undeserving of clinical recognition. It is common for critics to invoke “normality,” protecting “normal,” searching for “normal,” with “normal” as being under threat from out-of-control, ever-expanding DSMs. I was once sympathetic to this line of thinking, but now I am skeptical of invocations of “normality,” and I am of the view that the DSM thresholds are rather conservative. The DSM falls short of a comprehensive description of psychopathological presentations, and the categories are not broad enough to capture all clinically relevant forms of psychological suffering and disabilities for which diagnosis is needed. The criteria for specified diagnoses exclude a significant number of patients who experience considerable distress and impairment in their daily lives.

People fundamentally misunderstand the dynamic behind increasing rates of psychiatric diagnosis when they focus on the DSM as being the driver of this expansion. By and large, clinicians are not imposing labels or disorder judgments on reluctant patients who would rather not have a name for what they are experiencing (although it does happen). There is a tremendous demand and appetite for diagnostic labels. Psychiatry legitimized psychological distress and disability as healthcare problems deserving of recognition and treatment, but the profession was unprepared for the magnitude of clinically significant distress out there, and the diagnostic manuals have struggled to keep up. Much clinical practice involves clinicians responding to real suffering inadequately captured by official criteria. This leads to stretching existing diagnoses, not from diagnostic carelessness but due to genuine gaps in the diagnostic framework.

I have organized these ideas into a hypothesis of psychiatric overdiagnosis as diagnostic stretching in response to clinical need. The article describing this hypothesis is currently available as a preprint on PsyArXiv.

I encourage you to read the preprint for details.

Below is some additional overview of my argument.

Psychiatric overdiagnosis, for the purposes of my hypothesis, refers to the observation that there has been a rapid rise in the rate of mental health diagnoses in recent decades (including internalizing disorders such as depression, anxiety, and trauma-related diagnoses, and neurodevelopmental disorders such as autism and ADHD), combined with the suspicion or skepticism that a substantial proportion of these diagnoses are illegitimate, unwarranted, or unnecessary.

Note that this definition differs from how other authors have defined overdiagnosis. For example, Suzanne O’Sullivan (2025) defines overdiagnosis as a diagnosis that, while technically correct, does not benefit the patient and may do harm.

Since the 1990s, there has been a stretching of specified diagnostic categories (e.g. major depressive disorder, ADHD, bipolar disorder) in clinical practice to cover patients who have the relevant symptoms and have clinically significant distress and/or impairment but do not otherwise meet the official diagnostic thresholds for the specified categories. The presentations are either subthreshold (the fall below the required number of symptoms or temporal thresholds) or they are phenomenologically adjacent to the diagnosis (e.g. mood dysregulation being adjacent to bipolar disorder; focus problems being adjacent to ADHD).

Mental health awareness campaigns legitimized mood difficulties, anxiety, focus problems, and social difficulties as legitimate reasons for consultation, on par with bodily complaints such as dyspepsia, back pain, headache, and dizziness. Increased awareness of mental health problems has lowered the help-seeking threshold such that rates of diagnosis are now converging on the population burden of distress/impairment. Specified diagnoses are being stretched to allow that convergence.

This stretching is a clinical response to legitimate patient needs interacting with official classifications that are too narrow (not too broad, contrary to popular perception) and whose thresholds are semi-arbitrary and do not correspond to real-world distress or impairment. The suggested solution is that our clinical classifications should more accurately characterize clinically significant forms of distress and impairment instead of entrenching current gaps in the diagnostic schema.

The hypothesis can be empirically evaluated by measuring the population burden of psychiatric distress and/or impairment directly, benchmarking against common conditions from general medicine, and quantifying the risk of serious adverse outcomes. Because diagnostic stretching is hypothesized to be a response to institutional dependence on specified diagnoses, it also makes predictions that differ from competing hypotheses. My hypothesis doesn’t take a position, one way or the other, on whether diagnosis and treatments do more good than harm.

The individual ingredients of my hypothesis are not new; they have all been discussed in some form or other over the years (e.g. Haslam’s work on concept creep), but I have not come across an arrangement of these ingredients in the manner and with the valence that I see as most accurately characterizing the state of affairs.

The intention of my hypothesis is to offer an explanation for both why diagnoses have increased (this is in response to genuine clinical need and the population burden of distress/impairment) and why this invites skepticism (stretching beyond official thresholds is problematic for various reasons and is met with understandable suspicion).

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Exciting news to share. I am doing a series of articles for the Science desk at The New York Times. The series is called “Therapeutic Window,” and the first article came out today. It is about whether ADHD is better understood as a disorder of “attention” or of something else: What if A.D.H.D. Isn’t About Attention at All? (gift link)

“As a psychiatrist, I increasingly see people seeking help for a familiar constellation of troubles. They have a hard time staying focused. They often forget things. They suffer from disorganization, restlessness and impulsivity. They struggle with spreadsheets and memos, with laundry and food preparation, with showing up at appointments and meeting deadlines — with tackling, in other words, the necessities of daily life.

Increasingly, these patients view their problems as ones of “attention,” as more people identify with the diagnosis of attention deficit hyperactivity disorder, or A.D.H.D.

The rise in A.D.H.D. diagnoses — along with the use of prescribed stimulants like Ritalin or Adderall — has led to great debate among the public and within my field of psychiatry. Has the medical establishment finally recognized a long-overlooked disorder? Or has the diagnosis become too capacious, over-medicalizing ordinary difficulties?

But this debate runs up against a fundamental scientific uncertainty. The condition’s name notwithstanding, “attention deficit” may be the wrong conceptual framing for A.D.H.D. Scientists have been exploring a more basic quandary: What is the condition in the first place?”

Read the rest at The New York Times.

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As I was reading Ezra Klein and Derek Thompson’s Abundance last year, I couldn’t help but think back to a powerful line from the book Health Communism (2022) by Beatrice Adler-Bolton and Artie Vierkant:

“We call for a radical abundance of care that functionally casts off centuries of ideologies of austerity, subjection, and extraction.”

The logic of scarcity, the separation of the “deserving” from the “undeserving” when it comes to clinical care, is deeply problematic. One doesn’t have to be of any particular political orientation to hear the force of that claim.

The answer to the crisis of care, I believe, is more and better care. I do not want to take away the imperfect tools we have to help people. I want us to give people more of what they need. I am of course in favor of curbing inappropriate psychiatric prescribing, unnecessary psychotherapy, waste of community resources, etc. etc., but in my heart, what I really want for all of us is a radical abundance of care.

The problem with medical and psychiatric care is not necessarily that we do too much but that we do too much of some things because we have constrained the supply of all the other things. This is, in effect, the Abundance argument applied to the clinic: the problem is not excess but artificial scarcity.

The more I practice, the more I believe that attention is the rarest and purest form of clinical generosity. The system is organized around scarcity of attention and time. It is relatively easy to ask for and be prescribed medications, but quite difficult to see a physician who actually cares and listens and thoughtfully attends to diagnostic work-up and treatment risks and patient concerns. The default attitude in medicine today is one of impatience.

In a system of scarcity, of course we get inappropriate prescribing and superficial therapy, because we are over-relying on what is easily available. I find it odd that so many smart colleagues in prior decades have focused on expanding access to psychiatric medications as the primary issue, as if the mental health crises we face can be addressed by something akin to putting SSRIs in the water supply. An abundance of good clinical care also means an abundance of support and guidance for deprescribing. Careful, case-by-case deprescribing is good care, and I want more of it.

I have spent my psychiatric career thinking about what it means to help people in states of distress, impairment, and vulnerability, and thinking, too, about the ways our systems of care go wrong. I am genuinely sympathetic to concerns such as over-medicalization and practices such as deprescribing (make deprescribing boring, as I’ve said). These are important issues, I do not think we should neglect them, but they are far from the organizing principles for me.

There are many critics of psychiatry, psychology, and medicine who act as if they hate the treatments we have to offer more than they care about the suffering humans. Or rather, the suffering they truly seem to care about is iatrogenic suffering. Of course, the actual motivations of critics are much more complicated and defensible than that.

Concerns about over-diagnosis and over-medicalization are also driven by a crisis of trust. Conceptualizations and treatments are forms of power, and there are many today who are wary of the power of the healthcare system. And they resist expansion of diagnoses not necessarily because they are blind to the suffering involved and the need for assistance, but because their overarching concern is to limit and oppose the institutional power of medicine. My relationship with medicine and clinical care doesn’t start from mistrust; it starts with the assumption that medicine is deserving of public trust and capable of honoring it, even when it has fallen short of it in practice. Which is one reason why I feel ill-at-home with the overdiagnosis and deprescribing crowd. I am wary of movements that focus on a subtractive agenda, one whose primary ambition is to take things away from people. Too many critics want to take away clinical care they believe to be unnecessary and harmful, and doing so is a bigger priority for them than actually relieving human suffering in effective ways.

In 2023, James Davies, John Read, Joanna Moncrieff, and other co-signatories (over thirty in total) published a letter in the BMJ calling on the UK government to “reverse the rate of antidepressant prescribing.” The priority—reflected in the title of the letter—was not to call on the British government to ensure that people get the right care and supports, whether in the clinic or in the community. The priority was to have fewer people on antidepressants. I do not think I can support a cause that cares more about fewer antidepressant prescriptions than about facilitating access to help that people need.

Most real-world people I’ve met who’ve been unhappy with psychiatric and psychological treatment don’t want less treatment. They want better treatment and more of it. Most real-world patients I’ve met who are worried about medication adverse effects want a prescriber who cares, who is attentive and thoughtful, and willing to inform them accurately and address their concerns, and troubleshoot the tangle of symptoms-comorbidities-iatrogenesis-stressors with them, and discuss trade-offs between symptom improvement and adverse effects, and facilitate their decision-making.

When a patient has ready access to a full range of options, then medication becomes one tool among many, chosen deliberately, not defaulted to out of desperation. Under conditions of an abundance of relational care, the reliance on prescribing becomes easier to remedy. Under such conditions, whether one in six or one in twelve individuals are on psychiatric medications matters far less; it is not a source of alarm, because the people who are on medications are on them because of their informed choice amidst a variety of treatment options available to them and because they believe the ongoing use of medications is a net positive for them and they have the resources and support available to them to safely come off them when they so choose.

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“I do not want to have these problems that are notoriously difficult to solve, about which there is no professional agreement. I do not want to embark on a years-long project dedicated to my own mind.” Lauren Oyler, My Anxiety

“I had 3 young kids and was a touch anxious. So I did what you do… asked a psychiatrist for some Zoloft.” Lindsay Clancy, from a note on her phone.

“I cannot stress this enough—if you are in distress, seek treatment. It works. But, and I can’t stress this enough either, the treatment of mental illness is at a primitive stage.” Paul Bloom, Psych: The Story of the Human Mind

Psychiatric treatment is often enough a frustrating affair, for the patient, for the clinician, for the caregivers, basically for everyone involved. At every step, we are plagued by uncertainties, unknowns, worries, risks, desperate requests for interventions, ambivalence about treatment, and a liability that sticks to providers like tar.

We have highly imperfect tools at our disposal, and more and more we rely on these tools in situations where their use is less-than-necessary. I am focusing mainly on psychiatric medications here, but psychotherapy is no less imperfect and sought after. Neurostimulation, imperfect as well. Psychedelics, don’t even get me started. Anyway, the point is, there is no refuge. Anyone selling you anything better than ‘highly imperfect’ in the realm of mental healthcare is a fool or a grifter. (And this includes deprescribing and tapering…)

I don’t know, man, I feel like the psychiatric profession messed up big in the tone it took when it came to public outreach and mental health awareness efforts. We communicated to people that we have stuff figured out, that we know what to do. Come to us with your problems and we will fix you! Unfortunately, we know jack shit…

We can look at the issue of seeking-help-from-medicine along a number of axes:

• The extent to which addressing a problem requires specialized knowledge possessed by trained clinicians

• The extent to which clinicians control access to effective interventions. This can be a consequence of specialized skills (e.g. performing surgery or specialized psychotherapies) or manufactured (e.g. access to medications restricted by prescription)

• The magnitude of benefit that can be expected from the interventions and how reliable the benefit is.

• The ways in which the interventions can cause problems or leave you worse off.

• The stakes at play and the cost of delay or inaction.

• Degree of disagreement around values and preferences.

• Ecology of alternatives to clinical care. Where else can you go?

• The degree to which a doctor’s judgment is preemptory vs contributory. At one end, it is strongly preemptive; it overrides or replaces your judgment. Whether a breast lump is benign or malignant, the doctor’s judgment takes precedence. At the other end, the doctor’s judgment is contributory. It is one input that exists alongside other considerations, and it is defeasible based on your assessment of the situation.

• Norms of consultation, i.e., whether you are expected to bring a problem to doctors. At one end, it is prescribed, expected or established. You go to the doctor if you have a breast lump. At the other end, it is optional. If you are struggling with grief or marital conflict, you can go to a therapist, but you don’t have to. If you are binge eating, you can go to a therapist or a psychiatrist, but there isn’t a strong expectation that you have to.

When we start treating weak norms of consultation as strong norms, when we assign preemptive authority in areas where only contributory authority is justified, when we destroy traditional cultural means of support to shunt people into medical treatment, we erode people’s capacity to meet suffering with the resources they already have or could have had outside medicine. When we rely on interventions that are weak or unreliable and at times harmful in situations where their use is optional and based on unrealistic expectations, we set ourselves up for frustrations and complications. There are situations that are high stakes, that require specialized knowledge, where there is a scarcity of viable alternatives outside medicine, and where deference to experts makes sense, but these are (were?) also rather circumscribed and uncommon.

Thanks to public messaging colored by delulu optimism, many people showing up at the clinics have a misplaced confidence in our ability to scientifically characterize their problems or help them in a timely, efficient, low-hassle manner.

The real message to the public should’ve been something like: we are an immature science; our treatments are imperfect and flawed; they help some people some of the time, and we don’t quite know who will benefit or how much; they come with risks, at times serious risks, and no one can know in advance how they’ll affect you; when they work, no one can say how your relationship to them will change over time. If the resources of ordinary life, self-help, and support available to you through family and friends have failed you, then these imperfect tools are available for you, but don’t expect any miracles. There is so much suffering out there and we are just scratching the surface. If you seek help, you may find a collaborative doctor who is attuned to your concerns and sensitive to iatrogenesis, but don’t count on your luck.

In some ways, it is impressive that we have effective psychiatric medications at all. Imagine being transported to the early 20th century and what do you have in terms of psychiatric medications? Chloroform? Ether? Morphine? Bromides? Phenobarbital? Thank God for the modern pharmacopeia. Even the much-doubted and much-maligned SSRIs, when they work, they work beautifully. With the right patient, you can see mania and psychosis melt away with mood stabilizers and antipsychotics. It’s a joy to see patients get better with treatment. I scoff at the skepticism of willfully ignorant critics who think we have made no advances in mental health treatment over the past century.

But. But. It is absolutely true that these treatments leave a lot to be desired. The truth is that even wielding the power of placebo, there is only so much benefit to be gained and only so many people to be helped. Sooner or later, the specter of treatment resistance, inadequate response to treatment, treatment difficulties—whatever term you find acceptable—rears its head. And we haven’t even brought up treatment aversion, poor tolerability, and iatrogenic complications to the mix yet.

Could the medications cause weight gain, insomnia, sedation, agitation, suicidal thoughts, dependence, sexual dysfunction, tremors…? Possibly. A certain percentage of people do experience these problems. That could be you, yes, it is a chance. We can monitor closely, address any problems that may emerge, stop the medications in a timely way, etc. But no one can guarantee risk-free treatment. We can be transparent about the risks and be attentive to your concerns, and we can work collaboratively, but ultimately it is your decision whether these potential risks are acceptable to you. Their use requires transparency about uncertainties, mechanisms, trade-offs, and alternatives.

The imperfections of psychiatric medications, their ability to both help and harm, the attitudes of conviction as well as ambivalence toward their effects put prescribers (and patients) in a no-win situation. Damned if you do, damned if you don’t. If you don’t prescribe, you are not taking the person’s suffering seriously; you are not recognizing and honoring their requests for help. Prescribe and something bad happens, and you are now guilty of harming them with unnecessary treatments for their ordinary life problems which should never have been medicalized. Take their concerns about tolerability seriously, and discontinue and switch medications in a timely manner without expecting them to endure side effects, and you are now guilty of subjecting them to irresponsible experimentation and rapid switches that put them at risk of further destabilization. It’s Schrodinger’s pharmacology: the medication is simultaneously a medically necessary treatment for a disorder and a reckless intervention for a problem of living, and the wave function will collapse into one or the other once you open the box.

I am writing this out of a sense of exhaustion. Exhaustion at confronting the flood of human suffering with the flawed instruments. There is a tendency, in a situation like this, to deny or minimize this suffering. Overdiagnosis is the cry of our age. That is not my impulse. I recognize this suffering as legitimate, as deserving of a proper response. I wish we had the means to fully recarve our minds and bodies and readjust our operational settings, but we don’t. Maybe we’ll get there one day, but we are not there yet. Bearing witness to pain goes a long way, but it is not enough.

Patients come to us with deep wells of misery whose depths have not yet been plumbed, and they want the perfect drug, as benign as a multivitamin, as effective as fentanyl. A drug that will silence the alarms blaring in the ruins of their bruised lives. A drug that will restore the will to live in their lonely, adrift existence. There has to be a drug out there, right? Zoloft, Xanax, Adderall, Ketamine… this can’t be as good as it gets, right?

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Eric Caplan is a historian of American psychiatry and the author of “Mind Games: American Culture and the Birth of Psychotherapy” (1998). His forthcoming book, “When Healing Harms” (University of California Press, October 2026), reconstructs the landmark malpractice case of Osheroff v. Chestnut Lodge from primary sources never before examined, revealing how the lawsuit accelerated the transformation of psychiatric practice in the United States.

Aftab: Tell us about the subject of your book. Who was Ray Osheroff, why did he sue Chestnut Lodge, and why did this case attract so much attention? What are some common ways in which the Osheroff story is misunderstood or misrepresented?

Caplan: Raphael Osheroff — Ray — was a nephrologist, a kidney doctor. In 1979, under pressure from his wife and colleagues, he admitted himself to Chestnut Lodge, among the most prestigious and expensive private psychoanalytic hospitals in America, expecting world-class care for a severe depression. Instead he was confined to a locked ward, denied medication, and subjected to seven months of talk therapy. He emerged forty pounds lighter, unable to use utensils, physically frail and emotionally devastated — not because his treatment failed, but because treatment was withheld. His parents secured his transfer to a hospital willing to prescribe the antidepressants he needed. But the damage was done. His marriage, his practice, and his reputation all lay in tatters. He then sued Chestnut Lodge for denying him the standard of care to treat his illness, which in 1979 comprised pharmacotherapy, or pharmacotherapy in conjunction with electroconvulsive therapy (ECT), and supportive psychotherapy.

At Chestnut Lodge, treatment was exclusively psychoanalytic. Four sessions of talk therapy a week and what they called milieu therapy, in a structured and controlled environment. In Ray’s case, the psychotherapy he received was confrontational, not supportive. He was told he was symbolically dead. That he would spend the rest of his life on a locked ward at Chestnut Lodge. When he asked when he might be discharged, he was told, “when you stop using your shirt for a napkin.” He was denied access to a telephone. He was not allowed visitors. He was allowed to pace between 12 and 18 hours a day. His continuing pleas for medication were denied — because, he was told, he “would need every neuron to fight this disease.”

The lawsuit was eventually settled out of court and Chestnut Lodge agreed to pay Osheroff. It was widely seen as a victory for Osheroff and a functional acknowledgement on the part of Chestnut Lodge that the standard of care had been violated.

The Osheroff case is well known among psychiatrists. As it should be. But what is well known — that the case represented the triumph of biological psychiatry over psychoanalysis in the treatment of serious mental illness — is not so much insufficient as incorrect.

A malpractice case is ultimately about one thing: Did the patient receive the standard of care for his condition? If he did not, and his condition worsened as a result, that is malpractice. Full stop.

That is what the Osheroff case was about. It was not about whether drugs were better than psychotherapy. It was about whether Chestnut Lodge violated the standard of care by treating Dr. Osheroff’s diagnosed condition — initially manic-depressive illness, later revised to psychotic depression, agitated type — with psychoanalysis alone, while confining him to a locked ward with eleven other patients, ten of whom had been diagnosed with schizophrenia.

Failing to prescribe medication and/or ECT for Osheroff’s condition in 1979 was akin to treating tuberculosis in 1979 at a mountain sanatorium — think Thomas Mann’s The Magic Mountain — and refusing to prescribe antibiotics for fear that they would interfere with the mountain air. Compounding matters, as Osheroff’s health deteriorated at Chestnut Lodge, his decline was not understood as evidence that the treatment was failing. It was interpreted as evidence that the treatment was working: he needed to get worse before he could get better. That conviction followed from the particular psychoanalytic doctrines that had shaped Chestnut Lodge since the 1930s and had been associated with figures such as Frieda Fromm-Reichmann and Harry Stack Sullivan, who hypothesized that early life trauma was, if not the sole source of disturbances of mood, thought, and behavior, then the primary one. And that “cures” required years of psychoanalytic treatment — first regressing the patient to the point of trauma, and then “reconstructing” the personality from the ground up.

Aftab: I was talking once to a psychiatrist who was early in her career when the Osheroff lawsuit happened, and she remembered feeling disgust at the intellectual “arrogance” displayed by experts from both biological psychiatry and psychoanalytic psychiatry during the trial. What was your reaction as you went through the historical records?

Caplan: Psychiatry has unearned confidence in both its theories of mind and its theories of brain. This is hardly unique to psychiatry. On the contrary, unearned authority — by which I mean strongly held convictions or theories without sufficient evidence to justify that confidence — is ubiquitous. Indeed, it would not surprise me if those reading this transcript accused me of the same, much as I like to believe mine is earned.

Psychiatry has given us both the Oedipus complex and the chemical imbalance — to say nothing of a host of other two-to-five-word catchphrases. What it has not given us, not yet, are mechanisms that correlate with those theories. That does not mean the theories are wrong. It does not mean the mechanisms do not exist. There is no way to know today. I cannot speak to tomorrow.

But not knowing is not a license to do nothing — to tell patients, well, come back in a decade and maybe we can help. We would not send a mission to Mars until we had reasonable confidence that it might succeed. But we cannot simply refuse to treat people with serious disturbances of mood, thought, and behavior who want treatment. For those who do not want treatment, that is a different issue, and it has little to do with what psychiatry has or does not have in its toolkit.

In Dr. Osheroff’s case, he actively sought treatment. He was not naïve. He knew he was ill. And he sought the best care psychiatry had to offer — psychotherapeutic, psychopharmacological, and neuromodulatory. He also voluntarily, if one can ever quite call it that, admitted himself to a well-regarded and expensive psychiatric hospital on the recommendation of his treating psychiatrist at the time, Dr. James Wellhouse. Wellhouse recommended Chestnut Lodge rather than Sheppard Pratt in nearby Towson, Maryland, because a bed was available, and he assumed, erroneously, that Osheroff would be treated with medication and/or electroshock, as that was the standard of care in psychiatric hospitals in 1979. He was wrong.

Aftab: If we look at Osheroff’s life and psychiatric history after the lawsuit, does it offer any simple vindication to either the psychoanalytic or the biological psychiatry camp in terms of the nature of his psychological difficulties?

Caplan: When it comes to providing care that helps patients, there are no sides. There is only the patient; the illness or disorder disrupting the patient’s life and the lives of loved ones; and, in the case of mental illness and infectious disease, the question of whether that illness adversely affects the broader community.

If an intervention of any stripe mitigates that suffering, that is, in most cases, a good thing. If it does not, it is not.

Osheroff’s history after Chestnut Lodge is complicated. He married again, and divorced again, and after his fourth marriage failed he fell in love once more. He practiced medicine until his death in 2012. He never experienced another life-threatening depression, but he continued in psychoanalytic therapy for three more decades, and when a depressive episode struck in 1999, he opted for ECT at Hillside Hospital in Queens, administered by Max Fink, arguably the most eminent and experienced proponent of ECT in the United States, if not the world. With Henry Kellerman, a distinguished psychoanalyst and the author of more than forty books, he co-wrote an unpublished manuscript about his time at the Lodge.

He was widely admired by patients and colleagues — I came to possess hundreds of letters from across his career that attest to it. The praise is effusive. Those who knew him before Chestnut Lodge spoke of his intelligence, his medical acumen, his sense of humor, and his musical gifts; he was a regular banjo player in a bluegrass band and a talented trumpet player. He was loved by many and detested by some. Rachel Aviv documents his DUI arrests and an indictment for Medicaid fraud that ended in a de minimis fine. Yet he never achieved what he most wanted: the love and respect of his three children, all of whom severed relations with him and remained estranged for the better part of his final two decades.

Whether he had a personality disorder — whatever those may be — remains contested, and I am agnostic. Many who knew him best, Kellerman among them, insisted he did not. What he suffered from, Henry told me, was a repetition compulsion: the conviction that if only he could make others understand the horror of Chestnut Lodge, he would be vindicated and his children would love him again.

In any case, I think the personality-disorder question is something of a red herring. Chestnut Lodge held that personality disorders were incompatible with “biological depression,” which is rather like saying heart disease is incompatible with cancer. A narcissist is not immune to depression. Otto Kernberg, among the leading authorities on narcissism, argued not only that the two diagnoses could coexist but that when they did, the depression had to be treated first. And there is no evidence that a narcissistic personality disorder requires years of hospitalization, or any hospitalization at all, which is what Osheroff’s doctors believed his condition demanded.

Aftab: The Osheroff case has been the subject of extensive discussion in the past. There is some discussion of it in Jonathan Sadowsky’s The Empire of Depression (2020). More recently, Rachel Aviv devoted a chapter to it in her 2022 book Strangers to Ourselves. You must have believed that existing discussions were incomplete in some important way and that a book-length treatment of the subject had more to offer us. What does your book add to our understanding of this historical episode?

Caplan: Jonathan Sadowsky’s treatment of the Osheroff case is based largely on the Klerman–Stone debate. Rachel Aviv asked a different question from mine. Her interest was in how psychiatric encounters and psychiatric nosology shape both a sufferer’s perception of his or her diagnosis and the broader community’s conception of that person.

The question I asked was different: How did Osheroff’s lawsuit — and the work of his extraordinarily brilliant counsel, Phil Hirschkop — affect the practice of psychiatry, and of medicine more broadly? That question demanded a different approach from Rachel’s: less biographical, more historical. Each of us, of course, has elements of both; what differs is emphasis and scope. It also required a much larger documentary record. I interviewed Al Scanlon, the attorney for Chestnut Lodge; David Fudala, one of Osheroff’s attorneys; people who knew Ray intimately; and others connected to the litigation and its aftermath. My interviews are recorded and on the record. I also worked through an extensive archive of legal records, correspondence, medical records, and other primary sources.

I began the project wanting to conclude that Osheroff’s lawsuit had transformed psychiatry. The evidence would not let me make that argument. What it supports, I think, is something subtler: the case was catalytic. It mattered. But the post-Osheroff world would probably not look dramatically different from the one we inhabit today, because equally significant secular changes were already reshaping medicine and psychiatry.

That distinction matters to me. The historian’s job is not to make the story more consequential than the evidence permits. It is to determine, as closely as possible, what actually happened and what difference it made.

As for Rachel’s question, my answer is that once a disease or disorder is tamed, the stories that traveled with it largely disappear, and with them the sense of identity the illness once conferred on the afflicted. I wish I could take credit for this interpretation. I cannot. It belongs to Susan Sontag, to her Illness as Metaphor, which remains no less trenchant today than when it was published almost half a century ago, in 1978.

Aftab: The Osheroff lawsuit was four decades ago. Why should we care about it today?

Caplan: Because while theories change and treatments change, if sometimes only a little, the mysteries of the brain and mind remain remarkably opaque. We continually substitute metaphor for mechanism. That is not necessarily to the detriment of patients; treatments can work even when our explanations for why they work are incomplete. But it can be to the detriment of confidence in a profession that cannot afford to be cavalier about the difference between a useful theory and an established mechanism.

Medicine does this elsewhere, too. Think of the familiar language of “good cholesterol” and “bad cholesterol,” which is a crude explanation of a far more complicated biological process. But cardiology also has statins, PCSK9 inhibitors, bypass surgery, pacemakers, ICDs, and even transplantation. Against advances of that magnitude, psychiatry’s best interventions can sometimes appear remarkably primitive.

The Osheroff case therefore remains relevant not because it settled an old war between psychoanalysis and biological psychiatry. It did not. It remains relevant because it asks an enduring question: What do physicians owe patients when their theories are uncertain but the patient’s suffering is real?

Aftab: Do you feel comfortable saying something about your own history of psychiatric diagnosis and treatment? Are there any connections between your experience and what Osheroff went through?

Caplan: I do not think I could have written this book if I did not know what depression is. And I do not think I could know what depression is if I had not experienced it firsthand. I suspect Andrew Solomon and Rachel Aviv would say something similar.

That said, I do not think — though others may disagree — that my experience clouded my judgment. Of course it shaped it. The relevant question for a reader or reviewer is whether my evidence supports my claims.

One of the things I am proudest of is that I made the archive of primary sources available to readers with the click of a mouse. The online supplement, whhsources.org, recapitulates my chapter “On the Evidence” and my notes, with a link appended to each note, where legally permissible, that takes readers and reviewers directly to the underlying primary source.

I believe in evidence-based scholarship. The point is not that readers should trust me. The point is that, wherever possible, they should be able to examine the evidence themselves.

Aftab: It is notable that your book garnered advance praise from prominent figures belonging to, so to speak, antagonistic ideological camps — for example, Peter Kramer, Paul Appelbaum, Andrew Scull, David Healy, and Robert Whitaker. I suppose it speaks to the power of good historical scholarship that it can bring people together in this way. Perhaps there is also the fact that the Osheroff case has a Rashomon-like complexity to it and people see in it what they want to see. What do you make of it?

Caplan: I had only a fleeting acquaintance with Peter Kramer. I did not know Paul Appelbaum or Robert Whitaker before I sent them the manuscript and asked for feedback. I met David Healy at a conference about thirty years ago, and we spoke again when I was beginning this project, but he was an acquaintance, not a friend. Steve Hyman also read the manuscript and gave me valuable feedback. As did William Potter, who both treated Dr. Osheroff briefly after his discharge from Chestnut Lodge and evaluated him as part of the process to restore his medical license and hospital privileges. Potter also testified as an expert witness in the Osheroff case, arguing that Chestnut Lodge had violated the standard of care for manic-depressive illness — the primary diagnosis Osheroff received on his admission to Chestnut Lodge on January 2, 1979.

What interests me about the range of responses is precisely that these people do not occupy a single intellectual camp. They disagree, sometimes sharply, about psychiatry, its history, its treatments, and its institutions.

I do think the Osheroff case has a Rashomon-like quality. It is remarkably easy to find in it whatever argument one arrived wanting to make: psychoanalysis versus drugs, mind versus brain, autonomy versus medical authority, psychotherapy versus biological psychiatry. But that is also the trap.

My aim was to resist it. I wanted to reconstruct what happened from the documentary record and then let the evidence constrain the argument. If readers who disagree profoundly with one another about psychiatry nevertheless find the history persuasive, I take that as a good sign. They do not have to agree about psychiatry. They only have to agree that the evidence has been treated fairly.

Aftab: Thank you!

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

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Daniel Cohrs, MD, is a psychiatrist and researcher in San Diego, California, whose work focuses on antidepressant tapering and withdrawal.

TL; DR: The central thesis of this piece is that common doubts about the mechanistic implausibility of protracted and delayed antidepressant withdrawal are overstated. In response to a recent post by Awais, I defend the mechanistic plausibility by offering a detailed, at times technical, discussion of how treatment with serotonin-reuptake inhibitor (SRI) distorts the native signaling architecture of the serotonin system, yielding a compressed signaling repertoire that is less able to convey information in both space and time. The serotonin system’s adaptations to this relatively flat, unvarying signal elevation may make it less tolerant of perturbations, increasing subsequent risk for withdrawal. Dynamical systems theory can be usefully applied to the serotonin system itself, and used to model the effects of chronic SRI treatment. On this view, a system is modeled as sitting in an attractor basin, or a valley, where the depth of the valley denotes the relative stability of the system’s state. The serotonin system’s adaptations to chronic SRI treatment can thus be modeled as decreasing the depth of the valley the serotonin system sits in, rendering it more prone to being pushed into an alternative state like withdrawal. Protracted withdrawal can be conceptualized as a remodeling of the stability landscape, where persistent or severe withdrawal symptoms yield aberrant remodeling and push the system into an alternative stable attractor basin like protracted withdrawal, which can be self-sustaining. Delayed-onset withdrawal can similarly be viewed as the consequence of aberrant remodeling: this process can unfold over long timescales, and the system may not enter a withdrawal state until sufficient remodeling occurs.

Awais’s post, “Some Predictions About the Future of “Withdrawal Studies,” did a great job bringing some conceptual clarity to the very messy topic of antidepressant withdrawal. It also got me thinking, and helped me crystallize a few different strands of thought I’ve had around what a richer mechanistic picture of withdrawal might look like—one that could help explain protracted and delayed-onset cases while also capturing some of the heterogeneity that exists under this broad umbrella.

I’m a physician, and my research focus is antidepressant tapering and withdrawal, so this is an area I spend a lot of time thinking about. I also have lived experience with protracted withdrawal, which I’ll say more about at the end.

My goal here is to sketch a mechanistic picture of what chronic serotonin-reuptake inhibitor (SRI) treatment actually does to the serotonergic system, because I think that picture is much stranger than has generally been considered. To clarify, SRIs encompass SSRIs, SNRIs, and the serotonergic TCAs—anything with substantial serotonin-reuptake inhibition. My central argument is that chronic SRI treatment may compress the serotonergic system’s signaling repertoire, reducing the range of distinct temporal and spatial patterns through which it can convey information. Put simply, the signal becomes flatter and more unvarying. Over time, the system adapts to operating in this altered mode, which may leave it less tolerant of perturbations when the drug is withdrawn.

Awais and I have been corresponding ever since he published his original piece, and our exchanges shifted both of our thinking in ways I’ll try to make clear throughout, starting with where we agree.

We both agree that antidepressants induce neuroadaptation, that the term withdrawal encompasses a heterogeneous class of phenomena, and that the relationship between SERT occupancy and downstream effects is nonlinear and far more complicated than changes in transporter occupancy alone. We also agree that expectancy effects like placebo and nocebo will modulate outcomes, in terms of how effective a given tapering strategy is. However, expectancy effects operate on shared machinery with the serotonergic system, so this shouldn’t be surprising, and also doesn’t mean that withdrawal is any less “organic” or biological. Expectancy effects modulate outcomes significantly across many areas of medicine. Awais persuaded me that our current terminology around withdrawal is too imprecise, and that’s a good place to start before getting into the mechanistic picture.

In one sense, “withdrawal” can function usefully as an umbrella term describing issues related to medication withdrawal after neuroadaptation has occurred. These issues can arise through different mechanisms, unfold over different time scales, and ultimately require different names as our understanding improves. I don’t think heterogeneity is a conceptual problem here. Medicine is full of umbrella diagnoses that later become divided into more mechanistically precise subtypes. Heart failure, for example, encompasses disorders with very different underlying mechanics, but we don’t conclude that heart failure is not a useful concept. We recognize the syndrome first, and define subtypes as the science advances. Awais and I agree that we need more precision in our terminology here, but I think the solution is to worry less about the broad umbrella term, and more about precise descriptors for each subtype as we gain a clearer mechanistic picture.

So we agree that we’re looking at several related phenomena that probably share neuroadaptation as their starting point, but diverge thereafter. Some patients recover quickly. Others recover slowly. And a small subset appear to become trapped in a persistently dysregulated state that we have been calling protracted withdrawal.

Where I think the term withdrawal is most conceptually inadequate is in the subset of protracted withdrawal patients who don’t respond to drug reinstatement. This clearly happens in some patients: many report this anecdotally, and in the very limited formal data we have (analysis of reports from an online forum, Hengartner, Schulthess, Sorensen, & Framer, 2020), of the 19 who tried reinstatement, 10 did not experience resolution of symptoms. Once this is the case, I think that something along the lines of “withdrawal-induced injury” rather than withdrawal in the classic sense is a better descriptor. (Awais suggested “withdrawal-precipitated persistent iatrogenic dysregulation” as a more accurate and specific descriptor, which I like although it is a mouthful!)

However, whether we continue to call that withdrawal or adopt more specific terminology is, to me, a secondary question. The more interesting question is what biology could plausibly produce a protracted withdrawal state—one that sometimes doesn’t respond to drug reinstatement.

That’s the question I’d like to focus on in the rest of this essay. In doing so, I think we can also begin to understand how delayed-onset withdrawal may occur. But before getting into the mechanistic picture, it’s worth establishing that persistent post-discontinuation states are not unprecedented.

On Post-Acute Withdrawal Syndromes (PAWS)

Awais initially characterized PAWS as remaining “poorly characterized with validity issues” and lacking formal recognition in diagnostic manuals, though he’s since acknowledged this was not quite right. PAWS is actually well-recognized for both benzodiazepines and alcohol. For benzodiazepines, the FDA now includes “Protracted Withdrawal Syndrome” in benzodiazepine labeling (e.g., Ativan), defining it as symptoms persisting “beyond 4 to 6 weeks” and lasting “weeks to more than 12 months.” The 2025 ASAM/ACMT Joint Clinical Practice Guideline on Benzodiazepine Tapering includes a dedicated section on protracted withdrawal management. For alcohol, while it does lack formal recognition in diagnostic manuals, neurobiological correlates persisting beyond the acute period (i.e. 1-2 weeks) have been identified, including changes in evoked potentials, orexins, cortisol, serotonin, and most notably, neuroadaptation in the nucleus accumbens and prefrontal cortex, (Bahji, Crockford, & El-Guebaly, 2022) which persists for at least 6 months after cessation (Marty & Spigelman, 2012). Consistent symptom clusters have also been identified, including anxiety, dysphoria, anhedonia, sleep disturbance, cognitive impairment, cravings, and irritability (Bahji et al., 2022).

I think drawing parallels to the history of benzodiazepine withdrawal is instructive. When benzos were released around 1960, significant withdrawal was thought to only occur with supratherapeutic dosing or cases of abuse. Similar to antidepressant withdrawal, many benzo withdrawal symptoms, such as anxiety, dysphoria, and insomnia, looked like relapse of the original condition. It took over 20 years for withdrawal with normal therapeutic dosing to be widely recognized academically, and only in the last 10-20 years have appropriate tapering guidelines that utilize proportional/hyperbolic tapers become institutionalized (Kaiser has reasonable guidance). So, despite how apparent benzo withdrawal seems to many providers today, proper recognition took multiple decades. Fundamentally, it’s hard to find something you’re not looking for, and the history of benzo withdrawal is a stark illustration of that.

Awais finds delayed-onset withdrawal the most pharmacologically puzzling — a mechanism that produces no symptoms while the drug is clearing and occupancy is shifting, then generates intense symptoms weeks later. I understand the skepticism, but what I’m actually most skeptical of is mechanistic implausibility arguments themselves. We simply don’t have the terrain of these systems mapped well enough to rule things out on those grounds. When the picture is this fuzzy, it’s much harder to say what’s not in it than what might be. And I think once we see what chronic SRI treatment might actually do to the serotonergic system, the plausibility of delayed and protracted symptoms becomes considerably easier to imagine.

Evidence of long-term changes after SRI discontinuation

Awais raises receptor supersensitivity syndromes in his piece, analogizing to tardive dyskinesia, where chronic receptor modulation leaves lasting changes that outlast the drug. “Supersensitivity” doesn’t clearly translate to SRIs, as they cause tonic elevations in serotonin and receptor desensitization rather than hypersensitization. But what tardive syndromes do establish is a more general principle: that the system can become stuck and fail to re-adapt to its prior baseline even after the insult is removed.

And there is actually some evidence of long-lasting changes after SRI discontinuation; Mark Horowitz documented much of it well in this paper. The most recent human PET study found no detectable difference in 5-HT1A binding between previously antidepressant-exposed and antidepressant-naïve patients after as little as two weeks off medication, suggesting that PET-detectable changes in receptor binding may reverse relatively quickly (Metts et al., 2019). But receptor binding is not the same thing as receptor function, which may take much longer to normalize. A study in rats found responses to postsynaptic 5-HT1A stimulation remained blunted 60 days after fluoxetine was stopped, even after the drug had cleared and the measured downstream signaling proteins remained at normal levels throughout, suggesting that 5-HT1A signaling itself remained functionally altered (Raap et al., 1999). Studies in rats have also found reduced serotonin, SERT expression, 5-HT1A sensitivity, and related serotonergic changes for up to 2 weeks after discontinuation (Horowitz, Framer, Hengartner, Sørensen, & Taylor, 2023). Although there are limitations to a simple linear conversion based on lifespan, these persisting changes seen in rats may amount to months and years in human time (Quinn, 2005). So while evidence for persistent functional changes comes primarily from animal studies, these findings suggest that receptor signaling and other serotonergic adaptations may substantially outlast drug exposure, even after PET-detectable receptor binding has normalized.

So there is some evidence of long-term changes after SRIs are removed. However, none of these have been connected to the withdrawal state specifically, and these findings remain difficult to interpret without a better mechanistic picture. To paint such a picture, I think we first need to understand how the serotonin system normally operates.

The serotonin system at baseline

There are two concepts that will be important to remember here: volume vs. synaptic transmission, and tonic vs. phasic firing.

Serotonergic neurons have two fundamental modes of transmission: volume and synaptic (or “wiring”) transmission (Gianni & Pasqualetti, 2023). Volume transmission involves serotonin diffusing from “varicosities” — swellings along the axon that act as release sites — into the surrounding extracellular space, without connecting directly to any specific target neuron (Fig. 1). So volume transmission is one-to-many communication: one axon broadcasting serotonin diffusely to many downstream neurons at once. Historically, this has been considered the default mode. At a minority of sites, however, these same varicosities do connect directly with a specific postsynaptic neuron, forming a true synapse. Here, SERT located around the synapse efficiently recaptures released serotonin before it can diffuse away, confining the signal to that one connection. This yields synaptic or “wiring” communication, which is one-to-one communication. At baseline, the serotonin system primarily communicates via very steady, pacemaker-like “tonic” signaling; “phasic” bursts of increased neuronal activity happen relatively infrequently in response to emotionally salient stimuli (Paquelet et al., 2022)

Fig 1: Illustration of volume vs. wiring (synaptic) transmission from (Gianni & Pasqualetti, 2023)

Recent work by Zhang et al. has challenged the assumption that volume transmission is the default (Zhang et al., 2025). They suggest synaptic or wiring communication may actually be the default mode during baseline “tonic” signaling (slow, continuous, steady), and that conversion to volume transmission is activity-dependent. During “phasic” activity (fast, brief, dynamic), released serotonin overwhelms the local reuptake machinery, spills out of the synapse, and converts these sites from one-to-one (synaptic) to one-to-many (volume) transmission—like switching from making a phone call to sending out a radio broadcast. When SERT is blocked with SRIs, the same switch to volume transmission occurs, and Zhang et al. demonstrated this experimentally.

So Zhang et al.’s work can be interpreted in two ways. If we accept their conclusion that synaptic communication is actually the default mode, then chronic SRI treatment converts the default mode of serotonergic signaling from targeted to broadcast — a wholesale qualitative shift, not just a quantitative increase in serotonin levels. More conservatively, their work shows that SRI treatment prevents the normal activity-dependent gating between synaptic and volume transmission at junctional sites, forcing them into constitutive volume transmission. These junctional sites comprise roughly 38% of serotonin release sites in the cortex (Séguéla, Watkins, & Descarries, 1989). On this more conservative interpretation, which I will operate from moving forward, SRI treatment compresses the system’s signaling repertoire: temporally, the contrast between tonic and phasic signaling is blurred; spatially, signaling shifts from targeted synaptic transmission toward more diffuse broadcast transmission. So I think talking about receptor adaptations alone doesn’t quite do it justice. Awais says that “neuroadaptation should be proportional to the degree of functional perturbation from baseline,” and here the system has undergone a fundamental shift in how it communicates—a huge functional perturbation that may be difficult to recover from.

There is an important counterpoint to the picture I’ve sketched. One proposed effect of SRIs is “frequency-dependent facilitation,” which involves amplified serotonin release as neuronal firing rate increases, and is often interpreted as enhanced phasic signaling (Dankoski, Carroll, & Wightman, 2016). The authors themselves suggested, however, that this effect may initially be masked by the large increase in ambient serotonin produced by SERT blockade, becoming more apparent as extracellular serotonin returns toward baseline with chronic treatment.

The problem with this is that extracellular levels don’t return to baseline—since that paper was published we’ve acquired clear evidence of significant serotonin elevations with chronic SRI treatment in most brain regions assessed, and this is generally considered necessary although not sufficient for their therapeutic effects (note this doesn’t necessitate that serotonin is “low” in depression; it instead suggests that raising serotonin in patients with normal levels can have therapeutic effects) (Fritze, Spanagel, & Noori, 2017). So by their own logic, sustained increases in serotonin would mask this effect.

That interpretation seems to fit the functional effects of SRIs better. In healthy volunteers, chronic SRI treatment reduces responsiveness to both rewarding and aversive stimuli and decreases reinforcement sensitivity, and these changes are associated with reduced anxiety (McCabe, Mishor, Cowen, & Harmer, 2010) (Langley et al., 2023), findings more consistent with dampened responsiveness to stimuli than with enhanced phasic reactivity. Phenomenologically, patients don’t describe being hyperattuned to stimuli; instead they often describe being less affected by thoughts or stimuli that previously provoked strong emotional responses. This can obviously be therapeutic, but it can also manifest as emotional blunting. Of note, the leading mechanistic explanation for emotional blunting from SRIs is that serotonin inhibits dopamine activity, indirectly inhibiting the salience network and prefrontal dopaminergic activity (Jawad et al., 2023). Tonic serotonin signaling inhibits dopamine activity while phasic serotonin signaling promotes it (De Deurwaerdère & Di Giovanni, 2017), so reducing phasic and increasing tonic activity may be an upstream mechanism leading to inhibited dopamine activity and emotional blunting.

So the same shift toward a more tonic and less differentiated serotonergic signal that could plausibly contribute both to some of the therapeutic effects of SRIs and to emotional blunting may also represent another substantial functional adaptation that the system must later reverse during withdrawal. If we think of SRI treatment as compressing the temporal dimension of serotonergic signaling—blurring the distinction between tonic background and phasic activity—then many withdrawal symptoms that are often mistaken for relapse or dismissed as nonspecific start to make more sense. As SRIs are withdrawn, the normal relationship between tonic background and phasic signaling may need to be re-established, and that process could itself be unstable. Phasic serotonin signaling broadly encodes salient environmental information, and has specifically been shown to respond to aversive stimuli (Schweimer & Ungless, 2010). Dysregulated phasic signaling could therefore plausibly contribute to the spontaneous panic or surges of severe anxiety patients often describe during withdrawal; I’ve often heard this described as an intense fear of something, without knowing what that something actually is.

What happens when SRIs are withdrawn

When SRIs are discontinued after years of use, I think it’s quite easy to imagine this system having trouble recalibrating back to its prior baseline. Prior work has proposed a “dual-phase” model of antidepressant withdrawal (Fig. 2), with an initial hyperserotonergic phase, and a subsequent hyposerotonergic state (Harvey & Slabbert, 2014). The initial phase involves rebound hyperexcitability. When the SRI is discontinued, extracellular serotonin levels quickly return toward baseline, but 5-HT1A autoreceptors remain desensitized, meaning they still require elevated serotonin to trigger any meaningful feedback inhibition on neuronal firing. Without that feedback, serotonergic firing is disinhibited and dysregulated (Harvey & Slabbert, 2014). This rebound hyperexcitability has been shown experimentally, and can be recapitulated using a 5-HT1A antagonist (Collins et al., 2024). You might think that buspirone, a 5-HT1A agonist, would help, but it has been reported to worsen acute withdrawal; it’s actually a partial agonist and acts both pre and postsynaptically, which complicates the picture. This phase may more cleanly map onto “acute” withdrawal symptoms, although in some patients these symptoms clearly extend into the protracted window.

This mechanism helps explain why short half-life SRIs are associated with more severe acute withdrawal symptoms. Drug levels drop quickly, and so do serotonin levels. So the system spends more time in a state where serotonin levels are insufficient to restrain dysregulated neuronal firing, and the faster rate of decline in serotonin likely increases the severity of this dysregulated firing.

Fig. 2: Hyperserotonergic and hyposerotonergic withdrawal symptoms, from (Harvey & Slabbert, 2014)

Harvey and Slabbert frame the subsequent phase as a transition to a functionally hyposerotonergic state, where autoreceptor function has normalized, but the extracellular serotonin levels that were previously sufficient pre-treatment are now insufficient to stimulate chronically downregulated serotonin receptors. This dual-phase framing offers a simple explanation for some cases of delayed-onset withdrawal: a patient may not experience the classic hyperserotonergic acute withdrawal symptoms initially, but develop hyposerotonergic symptoms weeks to months later as SERT re-expression slowly occurs, serotonin drops further, and receptors are increasingly understimulated.

So, there is a potentially extended window where the “hyperserotonergic” symptoms have resolved, but where “hyposerotonergic” symptoms emerge as downregulated receptors receive inadequate signal. But as we’ve seen, it’s not just the same receptors getting less stimulated; the zone of extracellular serotonin diffusion is shrinking back towards baseline as the SRI is tapered, so a given varicosity is now reaching fewer downstream receptors. The system is trying to navigate back through the qualitative shift in signaling that occurred with chronic treatment, which may be a genuinely difficult problem to solve. In some patients, it may simply not be able to self-correct to its prior baseline over any reasonable time frame, yielding protracted withdrawal.

Comparing the serotonin system with the dopamine systems

Although the serotonin and dopamine systems are different in many important ways, they are both fundamentally monoamine systems, and we can draw useful inferences by looking at drugs targeting the dopamine system. The most obvious comparison would be dopamine-transporter (DAT) inhibitors, but available DAT-blocking drugs either have important additional mechanisms or produce relatively transient transporter occupancy, making them a poor analogue for the sustained SERT blockade produced by chronic SRIs.

A more useful comparison can be made between SRIs and dopamine agonists; the two share many surprising similarities. Used to treat Parkinson’s disease, they cause sustained, unvarying agonism of dopamine receptors, and this sustained agonism also appears to trigger D2 autoreceptor desensitization, although this is less robust than for the 5-HT1A autoreceptor (Voon et al., 2017). Dopamine agonist withdrawal syndrome, or DAWS, shares striking similarities with SRI withdrawal. It has many symptoms which overlap heavily with both stimulant and SRI withdrawal: anxiety, panic attacks, dysphoria, depression, agitation, irritability, fatigue, suicidal ideation, orthostatic hypotension, nausea, vomiting, and diaphoresis (Nirenberg, 2013). However, these patients were obviously put on dopamine agonists for Parkinson’s, not mood or anxiety disorders, so in general these symptoms can’t be easily misattributed to relapse, as they often are in SRI withdrawal. A hallmark of DAWS is that it may be protracted, lasting for months to years in some cases, and onset is variable (Nirenberg, 2013).

The automatic response to this may be that drug withdrawal is simply unmasking a hypodopaminergic state caused by their underlying Parkinson’s; they’ve been on dopamine agonists for years which masked their symptoms until drug removal. However, DAWS doesn’t respond to any other forms of dopaminergic therapy, including levodopa, and risk tracks with total agonist dose rather than disease severity—all of which suggests that it represents a true withdrawal syndrome. DAWS patients aren’t just suffering from a generic hypodopaminergic state; they’re withdrawing from the specific, unnatural pattern of unvarying tonic stimulation induced by dopamine agonists. Reinstating with a dopamine agonist is the only thing that resolves symptoms, but this sometimes induces impulse control disorders at very low doses, suggesting sensitization and persistent dysregulation (Nirenberg, 2013).

In contrast, levodopa is converted to dopamine via presynaptic machinery and relies, at least in part, on endogenous synthesis, storage, and activity-dependent release, thereby preserving more of the dynamic range of native dopaminergic signaling than dopamine agonists, particularly early in the disease course. As Parkinson’s progresses and endogenous dopamine dynamics are degraded, levodopa yields an increasingly pulsatile pattern of stimulation in line with its dosing pattern, which seems to increase dyskinesia risk during treatment relative to dopamine agonists. However, levodopa lacks a classic drug-specific withdrawal syndrome, and the severity of withdrawal-emergent symptoms tracks disease progression, suggesting drug withdrawal unmasks underlying nigrostriatal degeneration rather than causing a dependence-driven rebound as seen in DAWS (Riederer et al., 2025). This is not to say that withdrawing levodopa doesn’t present issues: it can trigger Parkinsonism-Hyperpyrexia Syndrome (PHS), which can be life-threatening. However, PHS can also be triggered by dopamine agonist withdrawal, and this syndrome responds to any dopaminergic agent, in stark contrast to DAWS—both of which suggest PHS is the consequence of an acutely induced, generic hypodopaminergic state rather than a drug-specific withdrawal syndrome. The contrast suggests that protracted withdrawal risk may depend not simply on how much signaling is elevated, but on how strongly treatment distorts the native signaling pattern. In the case of both SRIs and dopamine agonists, that distortion may involve pushing the system towards a more tonic, unvarying signal over time. In contrast, the more pulsatile distortions produced by levodopa cause issues related to treatment itself, but don’t appear to generate the same protracted withdrawal risk.

So dopamine agonists and SRIs induce similar qualitative shifts. SERT blockade shifts signaling toward volume transmission, degrading an important source of temporal information normally conveyed by the transition from synaptic to volume transmission during high-frequency bursts, while also reducing the spatial specificity provided by synaptically confined signaling. Similarly, dopamine agonists reduce the activity of phasic burst neurons, and continuous agonism of dopamine receptors enhances tonic tone (Voon et al., 2017). In both cases, the signaling repertoire becomes compressed: the system becomes louder, but less informative. It’s like someone with a loudspeaker with only one message, and the system adapts to this unvarying input. Just as someone with OCD who avoids targeted exposures becomes less tolerant of them by way of adaptation, a system becomes less tolerant of perturbations when it sees an unvarying, elevated signal—rendering it vulnerable to perturbations like withdrawal.

A reasonable objection to this may be that tonic elevations cause receptor desensitization broadly; doesn’t that make the system less sensitive to perturbations? Not quite: this conflates the system’s gain (how much output a given input produces) and regulatory capacity (how well the system corrects a displacement). Desensitization lowers the system’s gain, meaning a greater input is required for the same output. But this just means the operating set point has been increased, and tonic, unvarying input could render the system more dependent on that input for stability, representing a loss of regulatory capacity.

One framework that may be useful here is adaptive homeostasis, which states that biological systems contract their homeostatic range in response to unvarying signals (Davies, 2016). In general, biological systems require exposure to normal variation in their inputs to maintain the machinery that handles perturbation. When variation is removed, adaptive machinery is downregulated to conserve energy—basically “use it or lose it.” For example, muscle without load no longer maintains its neuromuscular junctions, and cells without intermittent stress scale back their protective networks. The system seems to operate normally while the environment stays constant, but struggles once conditions change and the adaptive mechanisms are called upon.

All of this, I hope, paints a picture of how profound the functional perturbations are with chronic SRI treatment. The system has been chronically operating with a compressed signaling repertoire—a profoundly altered, relatively flat mode of communication—and the path back to baseline may be genuinely difficult to navigate. What I find remarkable, actually, is that in most cases it does find its way back.

A dynamical systems perspective

Dynamical systems theory provides a useful framework for conceptualizing this problem. On this view, a system sits in an attractor basin — a stable state it returns to after being nudged — and the stability of that state to perturbations is denoted by its depth. The system can be pushed into less or more optimal attractor states by perturbations sufficient to push the system out of its current attractor basin. The landscape also isn’t fixed: as underlying conditions shift, barriers to alternative states can decrease or increase, raising or lowering the probability of the system being pushed into one.

The most recognized invocation of dynamical systems theory in psychiatry recently has probably been Carhart-Harris’s application to mental disorders, where certain disorders represent the brain becoming trapped in a deep attractor (Carhart-Harris et al., 2023), and where psychedelics induce “annealing,” figuratively heating the system and making it more plastic, ideally to facilitate transitions to more optimal states (Carhart-Harris & Friston, 2019). Of more direct relevance, Yano et al. have applied dynamical systems theory to the serotonergic system itself, modeling the reciprocal feedback between extracellular serotonin and autoreceptor regulation. Their model showed that changes in the properties of this feedback system can produce a bifurcation from a single, healthy stable state into a bistable regime with a new pathological attractor; each stable state is associated with different levels of autoreceptor expression and extracellular serotonin. Once such bistability emerges, subsequent perturbations can push the system from one stable configuration into another, where it may remain even after the original perturbation has passed (Yano, Watanabe, Aonuma, & Asama, 2013). Although their model was not designed to explain antidepressant withdrawal, it provides a useful proof of principle: if chronic treatment and withdrawal alter the regulatory architecture of the serotonin system enough to induce multistability, dysregulation of autoreceptor function or acute shifts in extracellular serotonin—both of which may occur during withdrawal—could push the system into a self-sustaining dysregulated state.

With all of this in hand, we can paint a picture of what the progression both to and from the SRI-treated state may look like for the serotonin system from a dynamical systems perspective. Doing so helps us conceptualize both delayed-onset withdrawal and withdrawal that doesn’t respond to drug reinstatement.

One disclaimer—the landscapes below are conceptual stability landscapes rather than calculated energy landscapes: valley depth and barrier height represent the relative stability of a state and its resistance to perturbation, not literal physical energy.

In the model I’m proposing, early on in SRI treatment, the energy barrier between the treated and untreated state is low, making the transitions between each state relatively easy. As time progresses, the system becomes adapted to the tonic, steady elevation in serotonin and becomes both less tolerant of perturbations, and more estranged from the healthy baseline state. These are represented as the energy barrier between the SRI-treated and the dysregulated state progressively decreasing, and the barrier between the SRI-treated and healthy baseline state progressively increasing, respectively.

The process of tapering from the chronically treated state can be represented by another remodeling of the landscape. When done carefully, the barrier back to baseline slowly decreases, and the system eventually returns there as the landscape remodels. However, a sufficiently large perturbation, like a too large dose reduction, can push the system across the boundary of its current attractor and into a dysregulated state like acute withdrawal.

In a patient with underlying vulnerabilities, or if a taper is done too quickly, the remodeling process may not necessarily push the system back towards baseline over time; rather than the barrier towards baseline decreasing, the barrier towards a dysregulated state may instead decrease, and eventually the system settles there rather than back towards baseline. Notice that the system is functionally in the SRI-treated state until the remodeling is complete, so the patient may be largely asymptomatic during this process. This may be one way to conceptualize how delayed-onset withdrawal occurs.

One possibility, then, is that delayed-onset withdrawal reflects an aberrant remodeling process, while acute withdrawal may more often be the consequence of a too-large perturbation that pushes the system into dysregulation.

Patient reports also suggest that some people who ultimately develop protracted withdrawal first spend an extended period in acute withdrawal without reinstating. This suggests to me that protracted withdrawal may also be the consequence of aberrant remodeling. So the stress of continued withdrawal lowers the barrier towards a protracted state over time, and the system settles there. Notice that the height of the barrier back to the treated state is larger than it was when in the acute withdrawal state, so even if the perturbation of reinstatement was sufficient to restore the system back to the treated state when in acute withdrawal, that doesn’t necessarily mean it’s sufficient in the case of protracted withdrawal.

Dynamical systems models have shown that the speed at which conditions change can affect not just where a system is pushed to, but how its stability landscape evolves. When different parts of a system respond on different timescales, rapid change can produce a different pattern of shifting attractors and barriers than the same change occurring gradually (Kaszás, Feudel, & Tél, 2019) (Feudel, 2023). So if SERT inhibition falls faster than autoreceptors, transporter expression, receptor signaling, and other processes can recalibrate, that mismatch could send the serotonin system down a different path of readaptation, potentially lowering the barrier toward a dysregulated state rather than progressively restoring the landscape toward its pre-treatment configuration.

Of course, this framing is not a quantitative model of antidepressant withdrawal. Formal dynamical systems models generally use equations that specify how different components of a system interact and change over time, and we are nowhere near having that level of mechanistic precision for antidepressant withdrawal. But this framework can still be quite useful. Scheffer and colleagues have applied this framework to psychiatric disorders broadly, and stated explicitly that even when the relevant causal relationships cannot yet be quantified, dynamical systems theory can still provide a useful qualitative framework for understanding how complex systems change over time (Scheffer et al., 2024). I’m using it in that spirit here—not as proof that withdrawal behaves exactly this way, but as a conceptual model that I think captures the problem more richly than simply thinking in terms of “serotonin + receptors.”

Does any of this support hyperbolic tapering?

Awais initially raised the challenge that even if the mechanistic picture I’ve sketched is correct, it doesn’t automatically follow that hyperbolic tapering is the right clinical response. He suggested that hyperbolic tapering requires desensitization to be at least partially reversible on taper-relevant timescales, and if it is reversible on those timescales, it is not persistent for months to years after discontinuation. So on my account, if these adaptations can persist for months to years after the drug is gone, then what is a hyperbolic taper with small steps every 2-4 weeks supposed to do?

My answer is that yes, some re-adaptations are happening at each taper step, but it’s less about the system fully re-adapting at each step, and more about 1) staying within a window of tolerability and 2) promoting healthy re-adaptations. I think there are many layers of adaptations of varying time scales, and hyperbolic tapering allows time for these differing scales. As illustrated by the dynamical systems framing, I think hyperbolic tapering both reduces risk of the system being pushed into a dysregulated state by a too-large perturbation, and allows the system to navigate this complex process of re-adapting back to baseline more carefully, leading to more appropriate landscape remodeling. Because the system has received a tonically elevated signal that is less differentiated in both time and space for years, it has become tuned for that more unvarying input and less tolerant of perturbations. Hyperbolic tapering keeps those perturbations within a tolerable window as the system (hopefully) slowly recovers.

In the most canonical form of R-tipping, the landscape doesn’t necessarily deform at all: it can retain its shape while moving along a given axis. If the landscape moves slowly enough, the system (the ball in the valley) can track its moving attractor while remaining within its basin. If it moves too quickly, the system may lag behind, cross a basin boundary, and enter an alternative state such as withdrawal. It’s a bit like a pickup truck accelerating so quickly that cargo in the bed gets left behind. This illustrates a second possibility alongside the aberrant remodeling described earlier: a rapid fall in SERT inhibition could lead to aberrant remodeling, or leave its shape intact but move it too quickly for the system to keep up.

So with the richer conceptual framework dynamical systems theory provides, we can imagine several ways in which hyperbolic tapering is helpful without the system necessarily needing to completely re-adapt at each taper step. Smaller dose reductions may prevent a single perturbation from pushing the system across an energy barrier into a dysregulated state. Allowing more time for adaptations operating on different timescales may promote landscape remodeling toward the pretreatment state rather than toward a dysregulated one. And a slower overall rate may reduce the risk of losing track of a moving attractor, as in canonical R-tipping.

Lack of controlled studies on hyperbolic tapering

There aren’t any controlled studies on hyperbolic tapering, which is a significant limitation, but I think the reason deserves emphasis. There’s historically been essentially no funding for this research. So even if hyperbolic tapering were perfectly effective, we still wouldn’t have satisfying evidence for it. Anytime we discuss iatrogenic harms, the institutional context around the research, or the lack of it, needs to be part of the conversation. Nonetheless, there have been some observational studies using hyperbolic tapering (Groot & van Os, 2021), and two RCTs have now been initiated — RELEASE and DISCARD — though DISCARD’s maximum duration of 4-5 months raises the question of whether tapers of that length will be adequate for the most sensitive patients, potentially creating a floor effect that obscures a real signal.

That said, I think the uptake and clinical impact of the Maudsley Deprescribing Guidelines tells us something. And it’s worth noting that patients effectively discovered proportional tapering on their own, well before the research on hyperbolic occupancy curves was widely published. In the absence of appropriate institutional guidance, they empirically arrived at 10% monthly reductions through trial and error. So although some have said that hyperbolic tapering is mediated largely by expectancy effects, patients developed the need for proportional tapering before they had any scientific framework to form expectations around. The fact that our mechanistic understanding now converges with what they found empirically both validates their experience and lends credibility to the underlying biology.

Also, if only a small proportion of patients are sensitive enough to require very slow hyperbolic tapers, a study enrolling all patients who taper will need to be very large to detect a difference. Enriching enrollment for high-risk patients would make picking up a signal considerably easier.

The asymmetry between going up and going down

The dynamical systems framing makes clear that the path back to baseline is different from the path to the SRI-treated state: the landscape has been altered by chronic treatment. One form of this path-dependence is termed hysteresis, where the route back through a system differs from the route in (Angeli, Ferrell, & Sontag, 2004). It has been shown at the level of brain networks—concentration thresholds of anesthetics used to remove consciousness are not the same as those needed to restore it (Kim, Moon, Mashour, & Lee, 2018)—and Fava’s oppositional tolerance concept, which Awais discussed in his piece, describes treatment course in hysteresis-like terms.

This path-dependence helps explain an asymmetry Awais raises: we jump a drug-naive brain from 0% to 70-80% SERT occupancy in a matter of weeks when starting an SRI, and the brain adapts without anyone proposing a hyperbolic uptitration schedule. Yet, the hyperbolic framework implies that comparable dose reductions on the way down are dangerously large perturbations. The answer here is essentially hysteresis: the path down the occupancy curve after years of treatment is fundamentally different from the path up during initial uptitration. On the way up, the serotonergic system is drug-naive: it hasn’t yet undergone the transmission mode shift, the autoreceptor desensitization, or the compression of its signaling repertoire described above. On the way down, it has, and these changes have rendered the system less tolerant of perturbations.

Awais initially argued that if 70-80% SERT occupancy is required for a clinically meaningful antidepressant effect, the system must have substantial buffering capacity — and that neuroadaptation at subtherapeutic occupancy should therefore be minimal. He’s since agreed that this conflates two different sensitivities: the sensitivity of the mood-relevant clinical output and the sensitivity of the homeostatic machinery, which need not share a threshold. In other words, the therapeutic threshold tells us something about the system’s functional sensitivity for therapeutic effects, not for any effects. 70-80% occupancy may be required for antidepressant effects, but lower occupancies may be sufficient to induce significant neuroadaptation. It’s very plausible that a dose may be insufficient to modulate mood/anxiety or really have meaningful subjective effects on the “way up” or with treatment, but induce significant withdrawal symptoms on the way down—this is true anecdotally for many patients. And since anyone who has been on an SRI has generally been on therapeutic doses, they’ve experienced 70-80%+ occupancy and all of the neuroadaptations detailed above. So although neuroadaptation can absolutely occur at lower occupancies, the clinically relevant question is almost always about returning from therapeutic occupancies—and all that has to be true is that some patients genuinely struggle to reverse the deep neuroadaptations induced by long-term therapeutic dosing.

Beyond occupancy

All of this suggests that SERT occupancy alone is an inadequate map of what’s actually happening during tapering. Awais makes this point too: withdrawal symptoms are downstream consequences of receptor adaptations, second-messenger changes, gene expression shifts, and network-level changes, and the relationship between an occupancy change and those downstream effects need not follow the same curve as occupancy itself; in other words, the relationship between occupancy and clinical effects may be nonlinear. I completely agree. In fact, Bryan Shapiro and I recently submitted a paper modeling extracellular serotonin levels that shows the relationship between SERT occupancy and serotonin is itself nonlinear — technically hyperbolic (preprint here). So even before receptor and network adaptations enter the picture, SERT occupancy is already translated nonlinearly into extracellular serotonin.

The motivation was trying to explain why withdrawal occurs within the therapeutic dose range. If occupancy were the whole story, the fact that it’s nearly flat in the therapeutic range (Fig. 4) would suggest withdrawal shouldn’t really happen there, but it clearly does in some patients. In short, the same law of mass action that causes dose-occupancy curves to plateau also causes extracellular serotonin to rise significantly throughout the therapeutic dose range. It’s far from a complete model of biological effects, but it is a necessary step toward modeling further downstream nonlinear dynamics and individual variations in things like autoreceptor function and SERT/MAO activity. It also ties in nicely with Zhang et al.’s work: the degree of serotonin elevation correlates with the degree of shift to volume transmission, so tapering an SRI involves a transition from more volume transmission back toward synaptic transmission at synaptic sites, and the speed of the taper may influence how smoothly the system can negotiate that transition.

Fig. 4: Dose-occupancy curves for SSRI antidepressants, normalized to the U.S. Food and Drug Administration (FDA) minimum effective dose for the treatment of major depressive disorder (Sørensen, Ruhé, & Munkholm, 2022). Curves are truncated at the F.D.A. maximum recommended doses.

I’ve heard withdrawal in this flat occupancy range attributed to psychological factors. This paper is a good example of why that’s exactly the wrong assumption — a plausible biological mechanism was just around the corner, and that kind of thinking only inhibits proper investigation.

It’s also worth noting that while the focus so far has been on the brain, serotonin receptors are expressed in nearly every peripheral organ (the gut, vasculature, immune cells, adrenal glands, etc.), and the effect of SRIs on local serotonin levels is very context-dependent and hard to predict. So some withdrawal symptoms might be related to changes in peripheral, rather than central, serotonin levels.

Comorbid and overlapping conditions

As with any psychiatric population, some patients will inevitably have FND, ME/CFS, or similar conditions. However, patients with more complex medical histories are probably more prone to withdrawal in the first place, so there’s a selection bias at work. Some will have withdrawal overlaid on prior pathologies, while others may have withdrawal that triggered or worsened an underlying vulnerability. Proving that withdrawal didn’t at least contribute to a given presentation will often be difficult, which cuts both ways: we shouldn’t too quickly attribute protracted symptoms to these conditions, any more than we should too quickly attribute them to withdrawal alone.

The conditions that I think will likely have the most overlap with protracted withdrawal and really need to be considered are central sensitization and nociplastic pain, conditions classically associated with chronic pain. My research partner Bryan Shapiro has explored this question in depth in a recent Substack article, making a compelling case for the overlap between protracted withdrawal and central sensitization. I think he’s identified something genuinely important, although I’d frame central sensitization and nociplastic pain as potential comorbidities rather than as alternative explanations for what protracted withdrawal is. It’s worth emphasizing that central sensitization is not a psychological phenomenon; it is a specific biological pathway in which intense or sustained nociceptive input produces hyperexcitability of central nociceptive neurons, making them respond excessively to normal or subthreshold input.

Nociplastic pain is a broader syndrome that includes central sensitization as an important mechanism but also involves top-down amplification and decreased inhibition of pain processing at multiple levels of the nervous system, ultimately manifesting as general CNS hyperexcitability. The difficulty is that serotonin itself regulates pain processing, autonomic function, arousal, immune signaling, and many of the pathways implicated in nociplastic pain. So the dysregulated serotonergic dynamics that may be present in withdrawal mean the overlap between withdrawal and nociplastic pain may be mechanistic, not just symptomatic. This means that treatments used for nociplastic pain could potentially help some patients with protracted withdrawal. However, we need to be cautious not to conclude that patients who benefit from such treatments must actually have nociplastic pain and not protracted withdrawal: the mechanistic overlap means these approaches may genuinely help without telling us anything definitive about the underlying diagnosis. And the fact that SRI withdrawal and many of these other conditions share some nonspecific symptoms doesn’t itself necessarily point to a shared underlying etiology.

My own experience with protracted withdrawal

Like many who study antidepressant withdrawal, I have lived experience with it. In my case it is mirtazapine, which I have experienced protracted withdrawal from for extended periods—certainly well over a year—multiple times throughout the past 10 years, with numerous failed tapers. I have developed an incredible array of non-psychiatric health issues related to tapering, even when done at an extremely slow rate. Dose reductions of well under 1 mg reliably trigger profound gastrointestinal issues. I do have underlying gastrointestinal issues, but the mirtazapine taper magnifies these exponentially. Most recently, repeated attempts at microtapering have reliably triggered biliary hyperkinesia (confirmed via HIDA scan) and associated bile reflux that caused gastritis with bleeding significant enough to leave me iron-deficient.

Initially, I blindly put faith in the idea that my body would eventually adapt, and I largely held at the same dose for over 1 year, with no improvement in symptoms. Other symptoms come along with withdrawal: extreme night sweats, dyshidrotic eczema and other atopic issues, insomnia—none of which were issues I had pre-treatment. Upon reinstatement, these issues usually vanish within a few doses, although I have been through periods of protracted instability as well. Notably, these dose changes produce little change in my underlying anxiety or mood; the withdrawal phenomena are overwhelmingly physical. Mirtazapine is an extremely potent H1 blocker, and replacing that activity with a peripherally (not centrally, so no effects on anxiety) acting potent antihistamine like desloratadine mitigates the GI and allergic symptoms. But, mirtazapine being such a “dirty” drug, i.e. hitting so many diverse receptors, makes simply replacing its activity to facilitate tapering somewhat complicated—ending up on a slew of new drugs in order to get off of this one isn’t a great solution. I should mention that mirtazapine is an atypical antidepressant, not an SRI, so the specific mechanistic arguments I’ve laid out regarding SRIs previously don’t apply directly to mirtazapine. However, the broader principles do: drugs that render the system more rigid and intolerant of perturbations increase withdrawal risk, and I believe mirtazapine does so through analogous mechanisms.

I know that my case is an extreme outlier, even amongst those with mirtazapine withdrawal. However, my experience has shown me that protracted symptoms related to psychotropic withdrawal are absolutely possible, and can be genuinely biological without needing to appeal to psychosomatic or psychological explanations. Unfortunately, the research is too limited to tell us definitively how common cases like mine are. Although most cases of protracted withdrawal do seem to eventually improve over time, both my experience and my research have taught me that the body and brain can fundamentally become dysregulated by chronic psychotropic treatment, and in some cases it simply cannot independently recover to a pre-treatment baseline over time scales we normally associate with withdrawal.

Disclosure: I serve as a consultant to Outro Health, a company focused on antidepressant deprescribing. This essay was conceived and substantially developed prior to the start of my work with Outro, and the views expressed here are my own.

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“A man will be imprisoned in a room with a door that’s unlocked and opens inwards; as long as it does not occur to him to pull rather than push.”

Ludwig Wittgenstein, Culture and Value

When it comes to the DSM, the vibes are Kafkaesque through and through. It is common for the manual to be portrayed as based on expert consensus, oriented towards the pragmatic needs of psychiatric practice and research, and for its diagnostic categories to be “invalid” in the sense that they don’t represent discrete disease entities or map onto a coherent neurobiology. One would imagine that a manual like that would be attuned to the clinical needs of mental health professionals, that it would be flexible and able to incorporate diagnostic categories based on expert agreement and public significance… but, nope. To gaze into the machinery of the DSM is to gaze into a convoluted bureaucratic contraption that is fueled by an odd mix of tradition and conviction, and that is beholden to a peculiar set of processes and priorities, and that has a pompous self-image that is entirely at odds with its reputation.

The mental health professions are so fractured and divisive that only a manual as deeply flawed and as deeply disliked as the DSM could acquire some sort of symbolic authority. The DSM is an official classification of mental disorders, but it neither reflects new scientific developments nor established clinical wisdom. It is not a compendium of all clinically relevant psychopathological presentations; there are gaps in the current schema. The categories are neither arbitrary nor valid, but something in between… they have the status of being supported by validators to some degree, but without any assurance that this is the optimal configuration for the validators. The manual is continuously revised, but the burden of evidence demanded since the 1990s to make changes to its historically contingent architecture is so onerous and proposed changes are so vulnerable to being vetoed by APA insiders that it is like trying to get blood out of a stone. And when the manual does manage to get new categories incorporated officially, the result can seem mangled. E.g. the only new category to be added to the DSM since 2013 is “prolonged grief disorder,” and it took a huge amount of effort on the part of everyone, backed by a substantial amount of empirical evidence, to get it into the DSM, but arguably, “prolonged grief” is the wrong clinical characterization (the problem is not primarily that grief is prolonged) and the duration threshold of 1 year makes little clinical or scientific sense and was seemingly chosen as an overly conservative cut-off out of fear of public backlash against over-medicalization.

Unsurprisingly, the manual is slowly bleeding relevance and authority. Psychiatric research has increasingly become transdiagnostic. Elements essential to a good psychological case formulation are not covered by the DSM so clinicians look elsewhere. FDA doesn’t require that DSM categories be used as indications for drug development. Clinical communities have created their own specialized alternatives better suited to their needs (e.g. the Hierarchical Taxonomy of Psychopathology and the Psychodynamic Diagnostic Manual). And while many rely on it as a billing manual, you don’t even technically need it for billing, as you can bypass DSM and directly use the International Classification of Diseases (ICD) by WHO.

I say all this as background because it is crucial to understand why the DSM is struggling to incorporate “postpartum psychosis” as a diagnostic category. There are too many stakeholders, too many competing interests, and not enough clarity on what is really important to the DSM. There is an excellent article in the New York Times by Ellen Barry and Pam Belluck (Jan. 20, 2026; gift link) on the debate around including postpartum psychosis in the DSM, presenting the perspective of both the researchers behind the proposal and of DSM insiders.

The proposal for inclusion of postpartum psychosis in the DSM is described in detail in this paper (Veerle Bergink, et al.) in Biological Psychiatry by a team of prominent reproductive psychiatry experts. Postpartum psychosis is a clinically recognizable and clinically well-described psychiatric phenotype with its own distinct characteristics. While pregnancy is not associated with an increase in risk of mania or psychosis, the early postpartum period is well-recognized, both clinically and epidemiologically, as a time period of elevated risk (according to the article, there is a 10-fold increased risk of developing first-onset psychosis or mania). There are distinct biological factors involved in the postpartum, with endocrine, immune, and other physiological changes, all of which seem relevant to the increased risk. There are treatment algorithms specific to postpartum psychosis. Postpartum psychosis is a period of high risk in the form of both suicide and infanticide risk. Short-term and long-term course trajectories are distinctive.

At present, DSM doesn’t have separate categories for postpartum psychosis or postpartum depression. DSM instead has “peripartum” specifiers, referring to the time period during pregnancy and 4 weeks postpartum, for depression, bipolar disorder, and brief psychosis. The fragmented nature of postpartum psychosis in the DSM and the inclusion within the peripartum period mean that postpartum psychosis doesn’t exist as a distinct formal diagnosis in the manual.

The proposal recommends placing postpartum psychosis as a distinct category within the bipolar disorders chapter of the DSM. Within the current organization of the DSM, especially if the choice is between placing it in the schizophrenia spectrum chapter and the bipolar disorder chapter, the experts behind the proposal favor the bipolar disorder because...

1) most women with PP have prominent affective symptoms; 2) treatment response to lithium and electroconvulsive therapy is excellent; 3) in half of the cases, first-onset PP is also the first onset of bipolar disorder; 4) pregnant women with bipolar disorder are at very high risk of PP; and 5) the genetic risk architecture for PP is distinct but overlapping with bipolar disorder.1

Here are the proposed criteria:

the onset of at least one of the following states (at least 1 of 6) within 12 weeks of childbirth, lasting at least 1 week and present most of the day, nearly every day, or for any duration if hospitalization is necessary: 1) mania/mixed state; 2) delusions; 3) hallucinations; 4) disorganized speech or formal thought disorder; 5) disorganized, confusional, or catatonic behavior; or 6) depression with psychotic features.

Experts believe that doing so will facilitate diagnostic recognition, better training, more research attention, better preventive efforts, improved forensic expert opinion, and improved awareness that postpartum psychosis has a strong link to bipolar disorder than to schizophrenia spectrum disorders.

From the DSM perspective, the biggest obstacle is the placement. While postpartum psychosis does indeed have a strong relationship to bipolar disorder, the syndrome remains diagnostically heterogeneous. Around 30% of women with postpartum psychosis don’t meet criteria for bipolar disorder and those presentations are more consistent with psychotic depression or primary psychosis.

Let’s take a look at some of the discussion presented in the NYT article. Emphasis added via bold text is mine.

“Criteria added to the D.S.M. in 2013 allow doctors to diagnose bipolar disorder, psychosis or major depression “with peripartum onset.” This solution captures the disorder’s heterogeneity but doesn’t draw the same kind of clinical attention that a stand-alone diagnostic listing would, some mental health experts said.

“Dr. Bergink stressed the human cost of delaying the move — women who are misdiagnosed, or sent home with reassurances about the “baby blues.” She recalled some of the most tragic outcomes…

“[Members of the Serious Mental Disorders Committee were] split on whether creating a separate diagnostic category was the best way to ensure it. A slim majority favored that option, but a substantial minority voted to remain with the current formulation, in which major disorders can be diagnosed “with peripartum onset.”

“There was not a clear consensus,” [Dr. Carrie Bearden] said, and the narrow margin felt insufficient for a change of this consequence. One reason for this, she said, is a sense that the D.S.M.’s decisions cast such a long shadow over psychiatric practice.

“It’s science, but it’s also a group consensus,” Dr. Bearden said. “It also has a major influence on treatment and on policy. So we can’t just go with, well, this is the best evidence that we have at the moment, so let’s take a very decisive action.”

Experts in maternal mental health said the D.S.M. would have to balance the benefit of raising awareness against the risk of codifying a disorder that is not fully understood.

“Dr. Margaret Spinelli, a specialist in postpartum psychosis at Columbia University, said she worried that placing the condition in the bipolar category would cause emergency room doctors to miss it if “it’s not right there under psychosis.”

But Dr. Spinelli… said the benefit of greater prominence in the D.S.M. outweighed those concerns.”

“Ms. Lodha said she doesn’t care where it appears in the D.S.M., as long as it appears.

“To me, it’s less about the categories, and more about how do we actually legitimize, prioritize, normalize this illness by having it in the D.S.M.,” said Ms. Lodha, who is now on the board of directors of the nonprofit Postpartum Support International.”

Reading this, do you get the sense that there is clarity on what the DSM is really about, what the overarching priorities are, what is considered sufficient evidence for inclusion, and what sort of considerations are legitimate reasons to override available evidence? I know I don’t. For example, there is this general sense that people rely on the DSM for training and treatment decisions and policy decisions, so proponents of postpartum psychosis think that including this condition as a distinct diagnosis is really important, while opponents of the proposal appeal to the same considerations (people rely on the DSM for training and treatment decisions and policy decisions…) so we shouldn’t take any decisive action because we are worried about possible repercussions.

The way I see it, there are 3 separate questions:

1. Should postpartum psychosis be recognized as a distinct condition, and do we have sufficient evidence, including validator evidence, to support that recognition?

2. If the answer to 1 is yes, where should postpartum psychosis be placed within the structure of the manual?

3. What are some downstream consequences (clinical, research, training, advocacy, etc.) of a) recognizing postpartum psychosis as a distinct entity and b) putting it in the bipolar disorder chapter, and should these downstream consequences override inclusion if the evidence is otherwise adequate, or should these downstream consequences be considered sufficient for inclusion if the evidence is not otherwise compelling?

If the answer to 1) is yes, then uncertainty about 2) is a mere detail. An important detail, no doubt, but something to figure out rather than reject the proposal. And if the evidence for 1) isn’t sufficient, then 2) is moot anyway.

If placement in the bipolar disorder chapter isn’t perfect, there is nothing really that stops the DSM from having a separate chapter for postpartum disorders. The only thing stopping the DSM is a bunch of self-imposed rules and conventions.

The DSM chapters are generally organized by symptom patterns, but we already have exceptions. Trauma and stressor-related disorders. Substance-induced disorders. The neurodevelopmental disorders chapter is focused on a developmental period. So a postpartum chapter isn’t disallowed by the internal logic of the manual. In fact, ICD-11 already has a “Mental or behavioural disorders associated with pregnancy, childbirth or the puerperium” section.

What prevents the DSM, I suppose, is a post-DSM-5 loose commitment to a meta-structure based on validator evidence. This commitment is not strictly applied anyway, but a separate postpartum chapter likely draws further attention to meta-structure as a practical construct. Second, the DSM revision committee is supposed to evaluate specific proposals, and the specific proposal here is for placing postpartum psychosis in the bipolar disorder chapter. The bar for restructuring the DSM is understandably high and I suppose it’s unclear what sort of evidence would be sufficient. The DSM editors probably realize at some level that chapter organization can be read naively as claims about psychiatric kinds, and they don’t want to make a kind-claim about postpartum disorders. But again, this leaves everyone unclear about how the manual handles ontological versus practical considerations.

I don’t believe I have seen any clear articulation from the DSM leadership on where it stands on question 3. A diagnostic manual should have clarity on what is its central purpose. Is the purpose of the DSM to present a comprehensive classification of psychopathology? Is the purpose of the DSM to classify those psychopathological states that are supported by a particular threshold of validator evidence? Is the purpose of the DSM to classify clinical problems that deserve recognition and awareness? Is the purpose of the DSM to decide on inclusion based on balancing “the benefit of raising awareness against the risk of codifying a disorder that is not fully understood”? Does the DSM prioritize facilitating clinical recognition or a perfect fit into its existing schema? There are no principled, universally applied answers to any of these. This is what frustrates people about the DSM, why they call the process “political” in a pejorative sense. There is no consistency, no respect for evidence, no clear bar for when downstream implications matter and when they don’t.

And resultantly, I do not believe that DSM deserves the respect and authority we bestow on it. Whether postpartum psychosis receives adequate clinical recognition and whether it is prioritized in terms of advocacy and research does not and should not depend on the DSM. If the DSM can’t be a part of the efforts—whether by principle or by the whims of its editors—to recognize the existence of postpartum psychosis as a serious condition deserving a serious response, then it is the DSM’s loss, another step in the steady deterioration of its relevance. Either the DSM is concerned only with the degree of scientific evidence and not with the “human cost,” in which case we are asking it to do something it is not designed to do, or the DSM is a document that is responsive to clinical and practical needs, in which case it is failing to fulfill its mission.

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“… my account collapses the mad- versus- bad debate in a different way. If we set aside Abrahamic metaphysical assumptions and admit vice behavior as just another kind of human problems worthy of scientific understanding, treatment, and prevention, then ‘bad’ points to domains of experience and behavior that can be pathological like any other domain.” (p 496)

“If we accept that criminal/ immoral conduct is subject to being disordered and criminal justice shifts toward nonpunitive rehabilitation and public protection, then the insanity defense debate disappears, as does the need for a differential social welfare response. If all antisocial conduct is subject to rehabilitation, then the silos of adult and juvenile criminal justice/ mental illness/ intellectual disability disappear and the focus on res­toration of prosocial and healthy conduct becomes the overall goal for social welfare institutions.” (p 509)

John Sadler, Vice and Psychiatric Diagnosis

As I write this post, the jury is deliberating in the case of Lindsay Clancy and has not yet come to a verdict. The choice is between finding her criminally responsible for the deaths of her three children versus finding her not guilty by reason of insanity. Social media and the blogosphere are awash with hot takes of all sorts. Whether Clancy goes to prison or stays at the state psychiatric hospital rests on whether the jury believes she possessed the capacity to appreciate the wrongfulness of her actions or conform her conduct to the requirements of the law, the legal standard in the state for the insanity defense.

In the middle of this obsessive focus on whether this legal standard for the insanity defense is met or not, it is easy to forget the constructed, fallible, human nature of this standard. It was not given to us by God. It is not a principled differentiation of conduct based on a scientific understanding of human behavior. The insanity defense is the product of a human society trying and fumbling to reconcile our desire for punishment—for retribution, for the offender to suffer, for harm to be inflicted in a manner proportionate to their wrongdoing, an eye for an eye—with the awareness of human behavior as a complex, multicausal process, one vulnerable to mental illness.

Whatever capacity Clancy possessed at the time of the crime, whether she was psychotic or not, it is clear that she was psychologically struggling and was severely suicidal. A devoted, loving mother, in the grips of a state of suffering few of us can even fathom, took the lives of her 3 children before attempting to take her own, an attempt that left her paralyzed, and she survived only because of advanced medical care available in the modern world. What does a woman like that “deserve”? What does it mean to determine and declare that she deserves punishment instead of treatment, or vice versa? Who the fuck do we think we are?

Psychiatrist John Sadler has argued in his 2024 book Vice and Psychiatric Diagnosis that the insanity defense is rendered unnecessary in an ideal world. “A nonpunitive, rehabilitative criminal justice system and criminal court obviates the need for an insanity defense,” is how he puts it. The NGRI verdict—Not Guilty by Reason of Insanity—exists in our world only because retribution exists. Retributive punishment works by rectifying a moral harm by inflicting more harm, and in a world without retribution, there is nothing left for an offender, mentally ill or otherwise, to be excused from.

Criminal responsibility rests on “Abrahamic” folk-metaphysical assumptions about free will, individual responsibility, and just deserts. The scientific worldview presents a picture of behavior as a complex, multicausal outcome with many determinants. “people act wrongfully under complex interactions with environment, personal history, and personal biological endowment.” (Sadler, p 495)

The “mad” vs “bad” dichotomy exposes the faultlines of this juxtaposition. We desperately want to hold on to the fiction that some states of madness can excuse badness but other states of madness cannot. We recoil in horror when cases like Lindsay reveal the façade of this distinction. A mentally ill woman kills her children and we confront the absurdity of mad vs bad. Our judgments here are driven more by vengeance, political posturing, and fear-mongering than by an appreciation of how things really are.

In Sadler’s vision, the psychiatric state of mind of a person is relevant to what needs to happen to rehabilitate the offender, but it is not relevant to the verdict of guilty itself. If a mother has killed her child amidst suicidal depression or psychosis and if “retribution” no longer exists as an option, what is left is rehabilitative intervention. Whether she should be in a psychiatric hospital or in a place like prison becomes a pragmatic and predictive question: which setting will most successfully ensure rehabilitation while also protecting the public? It follows from the particulars of clinical and criminological judgment. Folk metaphysics is fine for everyday life, but when the stakes are high, Sadler contends, our decision-making has to be based on complex, multicausal accounts of human behavior.

That this proposed state of affairs is aspirational is an understatement. Most of us can barely imagine a world without retribution. I sometimes doubt if humanity is even capable of it. A world in which criminal conduct, including criminal conduct under the influence of mental illness, is approached in the same manner as we approach medical errors and failures of aviation safety, is indeed possible. Whether that ever becomes a reality is a different question. But as the jury deliberates and as Clancy exists in a superposition of being guilty and not guilty by reason of insanity, I’d like to dream of a world with a nonpunitive, rehabilitative criminal justice system that has rendered the insanity defense unnecessary.

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In his majestic and memorable essay “Over the Borderline” (The Lamp, July 31, 2026) — a long and insightful profile of Laura Delano — (excellent writer, please devote some attention to his growing oeuvre, if you aren’t already following him) says at one point that borderline personality is a disorder that he doesn’t believe “properly exists.” He doesn’t quite elaborate on what that means, and the one example he discusses in some detail—his skepticism about splitting—isn’t particularly compelling.

But before I go into that discussion of splitting, I’ll outline a range of possible things someone who disputes the existence of BPD could mean.

1. The cluster of clinical features we call BPD doesn’t actually exist as a coherent, clinically recognizable cluster.

2. The cluster of clinical features we call BPD is clinically recognizable but it is psychometrically and/or etiologically heterogeneous. It is not a proper taxon, a category, a discrete entity, a natural kind, etc, etc.

3. The cluster of clinical features exists but it is a mistake to conceptualize it as a disorder of personality. These features are better conceptualized as some other sort of disorder, e.g. a trauma related disorder or a relational disorder.

4. The cluster of clinical features exists but these features are not disordered or pathological. They are “understandable,” even “adaptive” responses to life challenges.

5. The condition may exist but the diagnosis is too easily abused and misapplied, it is not reliable, it is too imperfect and harmful for clinical use, and cannot be trusted.

I believe: 1 is false; 2 is true, but true for most DSM disorders, nothing unusual; I am sympathetic to 3, although I’d like to think we can still meaningfully speak of BPD being a disorder of personality; 4 is true in a circumscribed sense (these features may once have been adaptive in a certain developmental context), but false generally and based on a misunderstanding of what “disorder” and “psychopathology” mean; and 5 is true in some situations.

Rensin says of “splitting”:

“Splitting is generally understood as a relational failure, its instability the anti-social characteristic that raises it to the level of pathology. But it may also be understood as a desperate, if unstable, search for a coherent story: of who you are, of what the world is, of how to make sense of those phenomena of human life that are inexplicable and painful. It is not so unusual to want that: to feel certain of what is going on, at least for a while, to find a story and stick to it, to feel its stabilizing influence and the control that comes with it. This does not strike me as pathological, or even unusual. It is the premise of sour grapes. It is work undertaken in the aftermath of every breakup, as the ego detaches from what was once irreplicable and precious. It is politics: “polarization” and “epistemic bubbles,”…”

“You have been told for your whole life that there are experts who know what this is and what to do, a story about disease and how to treat it. Imagine that she only gets worse. You are so terribly afraid. What is there to do but find another story, another theory of what is happening, another guide, another guru, and pray that this one proves correct, to think, This better work, because otherwise there is nothing left?”

Ok, but that is not what splitting is. The search for a coherent story is indeed not unusual, and there is indeed nothing pathological as such about switching to a different story or theory once a previous one has been disappointing, but these are not examples of splitting. It is like saying “Delusions can’t be pathological; don’t we all hold on to false or irrational ideas despite evidence against them? Silicon Valley founders seem delusionally optimistic. Isn’t it human to believe in prophets of God, anti-vaccine propaganda, trickle-down economics…?” But anyone saying so reveals their own lack of understanding of the difference between an ordinary, irrational, entrenched belief and a delusional belief, even though the difference between them may be a matter of degree. Splitting is a defense, and in its simplest version, it is employed by almost all of us in some manner, but what makes it pathological is the degree.

The Psychodynamic Diagnostic Manual (PDM-3) describes splitting this way:

““Splitting” refers to compartmentalization (dissociation) of positive and negative perceptions and feelings, with the result that the person views self and others in black and white, either–or, and idealized or devalued categories (e.g., heroes and rescuers, villains and abusers, coldly indifferent enablers of abuse)… Splitting is linked to identity diffusion, or the inability to integrate disparate aspects of identity (self-representations) into a coherent whole, or “stand in the spaces” between different self-states, especially under stress.” (p 658)

DSM doesn’t use the term “splitting” in criteria for BPD, but it describes a very similar phenomenon in a straightforward way:

“A pattern of unstable and intense interpersonal relationships characterized by alternating between extremes of idealization and devaluation”

And like the PDM bringing up identity diffusion, the very next criterion in the DSM is identity disturbance: markedly and persistently unstable self-image or sense of self.

Whatever we may think of break-ups, or political polarization, or people souring on psychiatry, these are not cases of splitting in the clinical sense of the word.

Now someone who already has an unstable sense of self and is prone to alternating between extremes of idealization and devaluation may very well display that in the context of their relationship with the psychiatric worldview, but a phenomenon like souring on psychiatry is over-determined as hell. On its own, it’s neither splitting nor evidence of borderline dynamics, but in someone with bona fide borderline dynamics, it also isn’t out of character.

The issue of borderline personality disorder is a sore point for Delano. Rensin writes in the profile:

“She knows that there are people out there—not in this room, but out there—who have read her book and “decided for me that actually I am borderline, no matter what I say.” They know who they are. “I still have plenty of darkness,” she admits. “I cry all the time. I have intense urges of anger. I’m a very angsty person. I would definitely qualify for various diagnoses”—that is, if she “gave a shit about that. And I don’t.””

It is Delano’s right to not give a shit about it and to understand herself using whatever story makes the most sense to her. But others aren’t obliged to abide by her self-assessment as they make sense of her story. And her story, a story that launched a thousand podcasts, has been thrust on us to make sense of, whether we want it or not.

I don’t know what diagnostic criteria, if any, Delano would meet now, and I don’t think it is appropriate to focus on that. It is not our business. From what we are told, she is not an active psychiatric patient, and in the absence of a clinical examination and given her own explicit preferences, no one should diagnose her in the current state. It would not only be epistemically futile, it would be actively disrespectful. But the Delano of the past, the Delano of the memoir years, the psychiatrized Delano, that version of Delano is now no longer the private story of an individual; it has become the backbone of a national movement seeking to reshape mental healthcare in its own image. And much can be said about this historical Delano.

A common response of psychiatrists to reading Delano’s memoir, including mine, has been that her childhood diagnosis of bipolar disorder doesn’t appear to be accurate. Delano is a likely victim of the pediatric bipolar disorder fad. The condition we call borderline personality disorder — you can use whatever name you prefer (emotionally turbulent self-interpersonal relational style?) — appears to be a far better fit.

Here is, for example, the psychiatrist in her review of Delano’s book Unshrunk:

“For many years, Laura Delano was vulnerable and suffering. She was drawn, as many are, to the exonerating power of a diagnosis. She could then blame her brain, in addition to her parents, her school, and, later, the psychiatric establishment. But perhaps the crowning irony is that psychiatry can explain a lot.

Recall Delano’s first year at Harvard, when she rejected borderline personality disorder? The fact is, seen from afar and based solely on her own account, the designation appears to have fit her. For one thing, borderline personality disorder is a condition for which meds are not especially helpful—but where alcohol, cocaine, and other street drugs tend to be, at least in the short term. Second, it is typical for borderlines to receive many diagnoses over the course of their lives. Third, the personality disorder tends to remit over time, in the sense that patients no longer meet the diagnosis but often retain scattered symptoms, or what psychiatry might call symptoms, such as the ones Delano says she still has.”

We have to distinguish between two senses in which a person could reject the diagnosis of borderline personality disorder:

• They could say that they have been misdiagnosed, i.e., they don’t actually meet the official diagnostic criteria for BPD, and if a proper assessment were conducted adhering to actual criteria, the diagnosis would not be supported.

• They could say that they do indeed meet criteria for the condition but they don’t find it meaningful or accurate or helpful to see their life and their problems through a medical diagnostic lens.

Delano herself leans towards the second interpretation. These are her own words from Unshrunk:

“I was once mentally ill, and now I’m not, and it wasn’t because I was misdiagnosed… In fact, I was properly diagnosed and medicated according to the American Psychiatric Association’s standard of care.” (p xiv)

[While Delano focuses on the diagnosis of bipolar disorder, as she discloses in the book, she was also formally diagnosed with borderline personality disorder and received formal treatment for it.]

That means we can’t ignore and discount the presence of the relevant features, however we frame them.

Let me give an example. Let’s say a person was diagnosed with schizophrenia and was treated as if they had schizophrenia and had a terrible experience with treatment. And then their clinical presentation and history were reassessed and it was determined that schizophrenia was never actually an accurate diagnosis for them and that they more accurately met criteria for autism and substance-induced psychosis. Now imagine that this person says, “Well, I don’t believe in autism. I don’t like to use medical labels to understand my life.” Fair enough, they can think of themselves however they prefer, but for everyone else, there is a huge difference between the features we refer to by schizophrenia and the features we refer to by autism. What is applicable to schizophrenia is not necessarily applicable to autism, and vice versa. Now imagine that this person wrote a memoir, “I was diagnosed with schizophrenia, and I only got worse with treatment, and I found liberation once I rejected the corrupt and unscientific psychiatric enterprise.” And when psychiatrists reading the memoir point out that the schizophrenia diagnosis didn’t really make much sense and autism seemed more applicable, and that also explains why they had this sort of negative experience with treatment, and the person replied, “How dare you decide for me that I am autistic? I don’t give a shit about your diagnostic labels,” it would be apparent to anyone paying attention that the point being made about the existence of relevant features doesn’t depend on whether we adopt a medical conceptualization of the issue. A person may reject the medical gaze but that wouldn’t change the fact that they have impairments in social communications and restricted or rigid patterns of behavior. The problem is not about the right to self-conceptualization. The problem is about the accuracy of diagnostic interpretations and the generalizations being offered on the basis of that.

Here’s the basic problem for Delano. Delano has made her story the face of a movement around deprescribing, iatrogenic harm, and, more recently, MAHA. She has told her story to whoever would listen, whether that is the New York Times or Tucker Carlson or RFK Jr. or psychiatrists in positions of power and leadership. She has testified in front of the US House Committee on Oversight and Government Reform. Her story has been used as the poster for the MAHA agenda to tackle overmedicalization. So whether we like it or not, her story is one of great public interest and relevance and, therefore, invites public scrutiny. And yet, Delano also wants to believe, “I am literally just sharing my own story.” (quote from the Rensin interview)

Rensin describes his own bafflement quite well:

“In the months between the conference and the day that we finally meet, I had prepared myself for several possibilities with Laura. I had been prepared for the firm radical, a child of the movement more willing to adopt the opposition posture of anti-psychiatry with me than she had been on mainstream television. I had been prepared for a cynical Laura… I had not expected this utterly sincere belief—and I can only assure you that it was sincere, firm, plaintive, almost wounded—entirely contained within itself, that Laura believes, more than anything, in “pluralism,” in information, that she is, as she says, a “libertarian” about these things, someone who knows plenty of people on psychiatric medication and accepts that people indulge in “risky” actions all the time to cope with the pain of human life, who has ever only told her own story, and who is baffled—there was no other word that occurred to me over the four hours that we sat together but baffled—by the insistence of so many people, both fans and critics, followers and enemies, that her words, spoken in her book, or from her conference podium, or on television, or podcasts, or radio, over and over, containing phrases like “instruments of behavioral control” and “faith-based ideology” in reference to the D.S.M., or calling for a revolution in West Hartford—that all of this could not be understood to come with the disclaimer this is not intended as advice just because she said so. Who, maddeningly, is perfectly willing to express any number of views and advance any number of claims about science, medicine, and society from which the implied vision for others naturally follows.”

Either Delano’s story is the private story of an individual where she gets to decide what interpretation makes the most sense and its applicability to anyone else is uncertain and undetermined, or Delano’s story is one with generalizable lessons for people in psychiatric care, including people with serious mental illnesses, and it is the story on the backs of which an entire movement around psychiatric skepticism and countering medical overreach has been built, in which case it is not only open to but deserving of public and professional scrutiny, including how to best make sense of Delano’s diagnoses, whether she prefers to think of herself in those terms or not.

See also:

• My review of Unshrunk: A Memoir For the Iatrogenic Age

• ’s review of Unshrunk: Unshrunk and MAHA: A Diagnosis-Critical Case Study

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Nev Jones, Lauren Fowler, and Shannon Pagdon
PathLab University of Pittsburgh, School of Social Work

In response to recent public characterizations that minimize the evaluation’s documentation of harm and due process failures, evaluation co-lead Dr. Nev Jones and evaluation project members Lauren Fowler and Shannon Pagdon offer the following account of what the evaluation and their qualitative work actually found. Note that this post should not be construed as representing the views or opinions of evaluation partner HSRI.

Background. Through ‘Kendra’s Law,’ a 1999 statute designed to enable involuntary outpatient treatment, New York became one of the first states in the US to implement what is commonly referred to as “Assisted Outpatient Treatment” (or AOT). Due to the complex civil rights issues such legislation involved, lawmakers enacted the law with sunset clauses (expiration of the law unless extended by the state legislature). The original statute explicitly required state-funded, independent empirical studies (sometimes referred to as “re-authorization studies”) to present objective findings to lawmakers prior to re-authorization votes. The first such evaluation report was led by a research team at Duke University with a final report published in 2009 followed by a series of academic articles. (The evaluation primarily reports pre-post analyses found improvements in administrative outcomes such as hospitalization and medication adherence and increased use of/access to services). When Kendra’s Law was extended again in 2022, the New York State Legislature explicitly required a new, comprehensive independent study before the law came up for re-authorization again, leading to a competitive bidding process and award of a new (second) evaluation contract to a team co-led by the Human Services Research Institute (HSRI) and University of Pittsburgh’s PathLab.

Study Context. The new evaluation spanned approximately 2.5 years with one year (pre-contract) spent conducting background reviews, site visits and consultation with stakeholders across NY. For example, the evaluation team met with every NYS field office, with the leadership of every Mental Hygiene Legal Services division, with county leadership in large urban areas including the Department of Health – Mental Health (DOHMH) in New York City, and with groups of service users with direct experience of AOT and family members. These extended consultations in turn laid the groundwork for the formal data collection (in depth audio-recorded interviews and focus groups) conducted in Year 2. Ultimately, in Year 2 members of the research team interviewed 46 service users, and over 150 psychiatrists, providers, administrators, family members, legal systems staff and state-level advocates.

Ultimately, the independent evaluation represented an enormous and complex undertaking, tasked with grappling with the tremendous variation in AOT implementation across NY counties, and emerging with numerous serious concerns regarding both implementation and AOT’s impacts. In the relatively short time since its release (access full report here), numerous statements and public reporting have mischaracterized actual findings and, in this post, we seek to set the record straight.

The mischaracterizations: Many public statements and reporting, including statements made by the New York Office of Mental Health or its leadership (e.g. here and here), have, in our reading, mischaracterized, misrepresented or overtly “spun” the evaluation study, its findings and their complexity. For example, all OMH statements to date have led with the putative benefits of AOT, while minimizing (or wholly failing to acknowledge) documented harms, due process failures and the fact that the state’s failure to measure and monitor the implementation- and outcome-related harms that were documented is precisely what prompted the team to adopt a mixed methods approach, and Pitt’s research team specifically to heavily invest in qualitative data collection and analysis, most critically concerning the experiences of individuals (/service users) directly impacted by AOT.

Summary of the (Actual) Major Findings — Quantitative. The evaluation (as publicly reported) compared people under court orders (AOT orders involving ACT services) to a matched group receiving the same intensive services voluntarily (i.e. voluntary ACT). Both groups improved on the administrative outcomes used —the voluntary group did as well as the AOT group on most outcomes and better on arrests. Moreover, a more careful reading of the quantitative findings warrants a much weaker reading of the putative benefits of AOT relative to voluntary ACT. In fact, for example, homelessness fell far more sharply in the voluntary ACT group (29.2% to 17.6%, an 11.6-point drop, cutting homelessness by roughly 40%) than in the AOT group (10.9% to 8.5%, a 2.4-point drop). AOT is coded as “significantly better” on housing only in the evaluation’s adjusted, propensity-weighted rate of change comparison — a statistical (relative slope) artifact that stems from the AOT group starting with far better housing outcomes. In absolute terms the voluntary group achieved by far the larger reduction in homelessness, which is the opposite of what claims that AOT “improves housing stability” imply. The reason the adjusted comparison still favors AOT is that it models a relative rate of improvement after weighting and adjusting for age and treatment duration, not the real-world size of the drop: because the AOT cohort started from a much lower baseline rate of homelessness (11.2%), even a small 2.4 point decline represents a steep proportional slope, whereas the voluntary cohort’s far larger 11.6 point decline is measured against a much higher starting point (29.2%) and leaves a bigger residual — thus the test statistic used rewards the group that had less room for change (AOT), not the group that actually housed more people (voluntary ACT).

Intake characteristics merit the same scrutiny, troubling public claims that AOT is reserved for those who “would not accept services voluntarily”: at intake, medication non-adherence was higher in the voluntary ACT group not lower : only 40.8% of the voluntary cohort were taking medications exactly as prescribed, versus 51.3% of the AOT cohort. The voluntary group also started far more disadvantaged on the very outcomes AOT is credited with fixing — 30.3% homeless or unstably housed at intake versus 11.2% of the AOT group — yet reached comparable or better outcomes without any court order. Those absolute numbers should give every New Yorker pause: the cohort that would meet the obvious criteria for “harder to engage” — less adherent, far less stably housed — did as well or better under voluntary ACT. This finding alone is difficult to reconcile with the claim that coercion is not only necessary but also what makes engagement (and by extension service access) possible.

Major Findings — Qualitative. Turning next to the qualitative side of the evaluation, as briefly noted above, we conducted lengthy audio recorded interviews with 46 people with current or recent past direct AOT experience, as well as over 150 psychiatrists, providers, administrators, family members, legal system staff, and state-level advocates. What those directly impacted by AOT described to our team is not a program, at least in the majority of the state, that “supports individual autonomy and dignity,” as an Office of Mental Health representative recently put it. Instead, the majority of service user participants we interviewed — both those on and recently off AOT — described adhering to treatment out of fear of the consequences of what refusal might lead to rather than agreement with it; being placed under orders during hospital discharge and told they could go home only once they signed away a federal right to a hearing that they didn’t even understand as a right; surveillance experienced as invasive and generative of distrust; and medication effects ranging from serious metabolic and neurological harm to emotional flattening. Others reported psychiatrists who would not allow medication changes and AOT as a legal status that negatively impacted housing applications, employment, immigration, and custody proceedings long after the precipitating crisis, or even the period of AOT itself, had ended.

Many participants broke down crying or even sobbing during interviews when describing how it actually felt to be stripped of rights and not understand what was happening to them and why. Others reported that they had simply stopped raising concerns (or even hoping for them), having learned that it changed nothing. (Several participants told us simply that it would be “futile” to publicly raise or express concerns.). And still others asked some version of ‘why was it necessary to force me under AOT in order to access services I wanted all along?’ (Almost invariably when we asked participants if they would have voluntarily embraced the housing, case management, therapy and other psychosocial services they had access to under AOT, they said yes.)

And yet even among those who described deep gratitude to their case managers or ACT team members, we were alarmed by how few individuals were able to describe any access to high quality / high fidelity psychosocial rehabilitation, a reality sadly reflected in part in staggeringly high unemployment rates. (Viz. competitive, integrated employment rates increased a mere 4 percentage points from 4.1% → 8.2%). The overwhelming majority of participants were unable to describe any attempt on the part of their providers to promote social inclusion or community integration, and supervised residential services all too often functioned as “community” housing in name only.

As one parent, deeply saddened by the lack of attention to quality of life in her child’s case put it:

“I get that they don’t want to be made fools out of with the AOT, and they want to say, “Well, look, we kept her out of the hospital for two years now.” Yeah, but you’re medicating her so much that she can hardly move. She can’t tie her own shoes because she’s so big. It’s like you’re not giving her quality life at all.”

Pivoting to judicial process, particularly due process, half of those interviewed said their (Mental Hygiene Legal Services) attorney was present but did not advocate in any meaningful way, and another 30% had no positive or proactive attorney involvement at all. Legal representation did not lead to modification of any order in our qualitative sample, nor any successful challenge or successful objection to a renewal. High -level statewide advocates concurred that a frequent complaint from both service users and family is inadequate access to sufficiently resourced and responsive legal counsel. Per available statewide administrative data on this point, more than 95% of petitions and 98% of renewals are approved. The odds of fighting an AOT order and succeeding are staggeringly low. Indeed, even psychiatrists who strongly defended AOT in principle noted surprise and dismay at the average legal process, as the following quotes depict:

Psychiatrist 1: “The system, though, the court, although AOTs rarely involve the patient [actually] being in court, when a patient is in court, the entire system is rigged against them.... I’ll tell you how. Every person there, the judge is a state judge; the lawyers are state attorneys; the doctor is a state doctor. We’re, you know, we’re all power. We’re all dressed in a certain way. We all talk a certain way. We all behave a certain way. And we, you know, we’re not all powerful, but in the system of, in the entire system, we know all the procedures, we control all the shots. We can talk to each other. I can talk to the judge privately if I really wish to. And the patient, some of them, are, you know, it’s like a bull in a bull ring. You know, I’ve been to a bull fight, so I know how cruel it is. That they’re just totally, bewildered, like, what’s going on?

Psychiatrist 2: “So for me, like, that was actually disappointing to see that when an AOT is contested, it doesn’t feel like it is contested to me. So you show up there, [but] it goes the same way. No one’s really putting up a real fight, which is okay. I mean, because I believe in what I’m trying to do. However, I did question, like, in my mind, who’s fighting for his rights? You know, who helped him? And so you can look at certain points in the process to understand, well, the lawyer was here, the lawyer advised him, etcetera etcetera. But by the time you get to court, there’s really no way [to win], no chance.”

Replication is central to strong science and the truth is that these findings are not remarkable or different from the extant literature. The only other investigation of due process under Kendra’s Law to date, Candice Player’s 2015 due process study (based on her dissertation) documented findings as troubling as our own — with psychiatrists in the sample describing judges who simply deferred to the psychiatrist, service users who had no real chance of winning an appeal, and significant stigma in the ways that service users were talked about across the legal continuum.

Nor does our qualitative work contradict our quantitative work. When it comes to benefits, participants with direct experience repeatedly credited service access, including access to housing, and those providers who did treat them in caring, compassionate ways, as the source of these benefits, not a coercive mandate. Exactly the ‘elaboration’ and triangulation of the quantitative patterns that increases our confidence in the interpretation that service access is what is most critical, with very limited support for the benefits of coercion (particularly when weighed against harms).

This interpretation with respect to the central role of service access is also by no means discordant with the international literature; indeed many international field leaders have argued that that service access is in fact what drives most (if not all) benefits as evidence bed the repeated finding of seemingly robust pre-post benefits that attenuate substantially in quasi-experimental studies (i.e. that partially control for service access) and then disappear entirely in clinical trials in which service access (and sometimes accountability) is fully controlled for. We’ll quote from the most recent high-quality systematic review and meta-analysis of impacts of AOT (compulsory outpatient treatment) on aggression and criminal outcomes just to drive home the point:

“Results for all outcomes were non-significant, the effect size declining as study design improved from non-randomised data on self-reported criminal behaviour, through third party criminal justice records and finally to RCTs. Similarly, there was no significant finding in the subgroup analysis of serious criminal behaviour.” (Kisely, Bull & Gill, 2025)

In fact, the international evidence on AOT is anything but a testament to effectiveness, as Jorun Rugkasa (2016) notes in a summary review:

“Meta-analyses pooling patient data from RCTs and high quality nonrandomized studies also find no evidence of patient benefit, and systematic reviews come to the same conclusion.”

County Variation. It is also worth underscoring that implementation varies enormously across the state — as multiple providers and administrators put it, “if you’ve seen AOT in one county, you’ve seen AOT in one county” -- and this variation can teach us a lot about what is going right and wrong. For example, we noted particularly pronounced variation in the use of AOT diversion and in the application of least restrictive alternative standards: some administrators reported that “least restrictive” is barely mentioned, much less factored in, before they pursue or approve an order, while other counties — typically those with substantially lower utilization of AOT — did take these standards seriously. Similarly, use of enhanced voluntary agreements (pre-AOT diversion) is wildly uneven: New York City, which accounts for a large share of the state’s orders, never uses them to divert people before AOT, while some smaller counties make substantial use of them, engaging people voluntarily first and pursuing a court order only when everything else has genuinely failed. In such counties, administrators told the evaluation team they believe they could keep many or most AOT eligible individuals out of court entirely through voluntary diversion — again contradicting official characterizations of AOT as a “last resort” (ironically claims that have absolutely no evidentiary basis behind them). Note that the only published research to date that empirically addresses the question of pre-AOT diversion – a Los Angeles County study focused on diversion policy stemming from the County’s interpretation of least restrictive alternatives standards – found that, given a 6 month voluntary diversion support intervention – only a minority of individuals initially eligible ended up receiving an AOT order (Starks et al., 2020).

The Politics of Qualitative Findings. Unfortunately, qualitative findings that speak to serious problems with implementation of a given intervention or harms that result are easily (and all too often) dismissed or downplayed on the basis of “anecdote,” smaller sample size, or “non-generalizability.” Here it is important to reiterate that no data on fairness and due process, or any of the harms the evaluation documents, are monitored or collected by OMH. There is no data that documents how many voluntary service agreements a given county has pursued, whether an AOT recipient was meaningfully involved in developing their plan, whether they met an attorney for an adequate amount of time, whether their questions were answered, or whether they would have accepted the same services voluntarily through an enhanced agreement. And when it comes to harms, there is no statewide monitoring of polypharmacy or dosing, or monitoring of whether requests to modify medications have been approved; no reporting on harms associated with law enforcement involvement, involuntary transport (generally in handcuffs), inpatient hospitalization, or medication over objection; no tracking of serious medication side effects occurring under AOT orders; no measurement of collateral losses to housing, employment, or custody, or of the erosion of agency that renders service users “compliant” on paper while in fact continuing to experience their life as a form of house arrest or de facto institutionalization in the community. Where there is no data — and qualitative findings are minimized or ignored — there can be no accountability.

Participants who spoke to us were told that state officials and legislators wanted to learn from them. At the end of the day, the least they are owed is a public response from state leaders, public accounting and news reports that do not minimize or invalidate findings that raise serious concerns about how AOT has been implemented in New York and that document real harm to those directly impacted. If our goal is to improve the notoriously awful outcomes that most people labelled with serious mental illness experience in the United States (and certainly also New York) our shared path surely involves clear-eyed acceptance of the many ways we continue to fail people and a commitment to undoing harms of our own making. That would be a step towards justice.

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References

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

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

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

• Rugkåsa, J. (2016). Effectiveness of community treatment orders: the international evidence. The Canadian Journal of Psychiatry, 61(1), 15-24.

• Starks, S. L., Kelly, E. L., Castillo, E. G., Meldrum, M. L., Bourgois, P., & Braslow, J. T. (2022). Client outreach in Los Angeles County’s Assisted Outpatient Treatment program: strategies and barriers to engagement. Research on social work practice, 32(7), 839-854.

Recommended Additional Readings

• Barnett, P., Matthews, H., Lloyd-Evans, B., Mackay, E., Pilling, S., & Johnson, S. (2018). Compulsory community treatment to reduce readmission to hospital and increase engagement with community care in people with mental illness: a systematic review and meta-analysis. The Lancet Psychiatry, 5(12), 1013-1022.

• Cossu, G., Kalcev, G., Sancassiani, F., Primavera, D., Gyppaz, D., Zreik, T., & Carta, M. G. (2024). The long‐term adherence following the end of community treatment order: A systematic review. Acta Psychiatrica Scandinavica, 150(2), 78-90.

• Johnston, E. L., & Klein, A. (2024). Assisted Outpatient Treatment: A State-by-State Comparative Review. Clevland Student Law Review, 73, 723.

• Johnston, E. L. (2025). Coercive Compassion: Theorizing Assisted Outpatient Treatment. University of Florida Levin College of Law Research Paper Forthcoming.

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

• Maylea, C., Zirnsak, T. M., Edan, V., Armitage, P., Robert, H., & Brophy, L. (2026). Ensuring compulsory treatment is used as a last resort: a narrative review of the knowledge about Community Treatment Orders. Psychiatry, Psychology and Law, 33(3), 583-602.

Catherine Jensen, MA, LPC, is a psychoanalytic psychotherapist working in private practice in Colorado. She sees adult individuals and couples in treatment.

“The following complex statement has to be made. The infant can employ a transitional object when the internal object is alive and real and good enough (not too persecutory). But this internal object depends for its qualities on the existence and aliveness and behavior of the external object. Failure of the latter in some essential function indirectly leads to deadness or to a persecutory quality of the internal object.” DW Winnicott

In Winnicott’s “Playing and Reality,” he describes the importance of the transitional object in the life of an infant or small child (Winnicott, 1971, p. 1). The transitional object (stuffed animal, blankie, etc) mediates between the internal life of the infant and the harsh realities of the external world. As the infant becomes a toddler and starts to individuate from her mother, a transitional object, imbued by the infant with powers of warmth and affection, can help the small child navigate the external world with less anxiety.

It would be cruel to insist to a small child that their beloved transitional object is not “real.” It would be equally cruel for a caregiver to treat the transitional object in every way as a sentient being. To shriek with horror and panic if the transitional object were torn, as if the object were in actual pain. This would be confusing and terrifying to the infant. Thankfully, most caregivers intuit, without having to be told, that the appropriate way to interact with the child’s transitional object is in the realm of “as if.” A playful suspension of reality without complete denial of it.

This realm of transitional space, an “as if” relationship, is vital within the psychotherapeutic relationship, as it allows for helpful exploration of all transference and countertransference dynamics. An essential aspect of effective psychotherapy is the consistent focus on exploration of the patient’s thoughts and feelings, in service of greater self-understanding. Part of this exploration includes the patient’s thoughts, feelings and fantasies about the therapist. The patient should be able to freely express what they imagine the therapist is thinking and feeling about them, at any given moment. For these possibilities to stay alive, the therapist must deploy great caution when disclosing any of their own feelings towards the patient, so as not to shut down this explorative space.

Which Sexuality? Which Self?

In Roy Barsness and Brad Strawn’s chapter from Core Competencies of Relational Psychoanalysis, “Core Competency Seven: Courageous Speech/Disciplined Spontaneity,” Barsness shares an instance in which he disclosed erotic feelings to a young female patient (2018, p. 94). He describes the patient as having grown up in a religious household where sexuality was seen as bad/sinful, thereby creating shame within the patient around her own sexual feelings.

Barsness disclosed out of a hope that his expressed attraction towards the patient would be experienced as affirming of her adult sexuality. While an understandable intent, the article does not discuss how overconfidence around the motivation for such a disclosure could prohibit the therapist from exploring other, more unconscious motivations. It also does not discuss the possible negative consequences of disclosing in the midst of a strong Oedipal transference.

In the article, Barsness and Strawn argue that countertransference disclosures may serve the therapeutic function of affirming a patient’s budding adult sexuality while simultaneously not exploiting it (2018, p. 194). Yet a safe parent knows that sexual feelings between parent and child are the feelings, perhaps more than any other, that must stay in the “as if” realm. Gabbard notes, “a father would not tell his daughter that he had sexual feelings for her, even though the daughter might sense such feelings through interactions with her father. The fact that a father does not disclose such feelings towards his daughter allows her to engage in an important developmental task involving a complex fantasy about him as a love object, knowing there is an aura of safety to do so, created by the boundaries the father establishes (2004, p. 142).”

Psychoanalyst Jonathan Slavin highlights this aspect of the parent-child relationship rarely discussed outside of analytic literature, due to the incest taboo: namely, that there is a sensual, affectionate, playful relationship most parents naturally develop with their young children that can contain erotic elements (2002). He emphasizes that while this relationship can feel meaningful for both parent and child, a parent must (obviously) never exploit it by making the relationship overtly sexual, as we all know the worst tragedies and traumas unfold from that violation.

Likewise, there can be a mutual, unarticulated knowing of erotic connection between a therapist and patient. But an argument can be made that the therapist is like the parent in this specific regard (Gabbard, 2004, p. 142), tasked with upholding firm boundaries in service of the more vulnerable, less powerful other. The patient gets to share all they want about their desires, feelings and fantasies; and the therapist upholds the relationship by exercising restraint, in order that the patient’s exploration of their feelings can continue without having to worry about whether the therapist will violate or contaminate the space with their own longings.

Barsness and Strawn bring an interesting question to the fore: in noticing co-occurring erotic and parental feelings towards the patient who has an eroticized transference, is it therapeutic to disclose one’s erotic feelings directly? If the intent is to facilitate the emergence of the patient’s adult sexuality, a worthwhile goal, what are the pitfalls? Psychoanalyst Jody Davies warns against disclosing erotic countertransference in the midst of a drawn out, Oedipal enactments. She explains, “from within a model of therapeutic action that equates analyst with Oedipal parent, the sharing of any kind of erotic countertransference by the analyst can be viewed only as a parent sharing sexual desire with an Oedipal-age child—a seductive acting-out that undermines the patient’s already ambivalent strivings to relinquish ultimately unsatisfying infantile ties” (1998, p. 754). Barsness was hoping his disclosure would help his patient’s emerging adult sexuality. However, disclosing during a period in the treatment when the female patient was experiencing intense, erotic Oedipal longings towards her therapist, according to multiple analytic writers (Davies, 2018; Celenza, 2017; Gabbard, 1994), would be a seductive acting out on the part of the therapist.

A more restrained and protective response to a patient’s erotic transference, compared to Barsness and Strawn’s arguments, can be seen in Jonathan Slavin’s article, “The Innocence of Sexuality.” In it, Slavin writes of a male therapist’s work with a female patient who expresses erotic transference, mainly, that she would like to know, “Do I turn you on?” (Slavin, 2002, p.70).

He takes great care not to shut down flirtation or erotic longing as expressed by his patient. Importantly, he also does not shut down these erotic feelings nor impulses within himself. However, rather than verbalize them, the therapist instead allows his own feelings to exist within the transitional space of the therapy room without directly disclosing them (Slavin, 2002, p. 69).

An important reason for this kind of restraint is that when it comes to countertransference disclosure, we can never be certain which “self” within the patient will be impacted, or in what manner. As Gabbard explains, “I cannot be certain if the patient’s sexuality I am disclosing to is pre-Oedipal or Oedipal (1994, p.10 ).” As psychoanalyst Philip Bromberg articulated, we are not one unified self. Rather, the younger, more regressed and traumatized self-states remain a part of us, even if dissociated (1993). Long-term psychoanalytic therapy often puts patients in touch with aspects of the self that have long been dissociated or repressed. Many of these self-states may feel traumatic when unearthed (Davies 1994, p. 92). Therefore, every therapist must tread carefully with their disclosures, knowing that a patient’s response may be very “adult” and mature-seeming, while more regressed or traumatized reactions remain hidden from the therapist’s view.

Sex and Gender

Heterosexual male therapists with female patients are in a uniquely fraught position vis a vis this subject, given the sociocultural context both patient and therapist are imbedded in. While many contemporary analytic writers have offered provocative and necessary criticisms of the gender binary (Saketopoulou, 2023; Hansbury, 2017), along with its repressive sex and gender norms, we still must hold the “reality principle” in mind regarding the world our patients live, work and love in. A reality that includes the recent #metoo movement, which brought to light how widely prevalent sexual harassment and assault of women still is, and how widespread is the act of men violating the ethics of their professions.

Even more recent to the news cycle, the sordid details of Jeffrey Epstein’s sexual crimes against women and girls, and the many powerful men who were complicit. For the analytic community to assume that because the average analyst or analytic candidate is progressive and queer affirming means that talk of “women and men” and power dynamics within this binary is outdated or gender essentialist seems reckless to this author. And yet, that is some of the critique I have received from colleagues when broaching this topic. Is there a defense at play here, perhaps covering a fear? One cannot know for certain, but it has left me curious.

Contained in each of us is the polymorphous and perverse, the male and female, the heterosexual, bisexual and homosexual. Characteristics considered traditionally masculine and feminine, to varying degrees integrated, exist in each psyche; shaped by genetics, the early caregiving environment, and society. A female therapist is also capable of mishandling erotic countertransference and scaring or overstimulating a patient of any sex/gender identity. Any sex or gender dyad could fall prey to the concretization of erotic feelings in the therapy room. My hope, by focusing on one specific gender dyad, is to provide an opportunity for close examination of particular dynamics. Who really has the phallus, after all? Can a woman, queer or transgender analyst, wield their power in the therapy relationship in a harmful way? Could they indulge in their own narcissism or sexual desires, or intervene to soothe their own anxieties, to the detriment of a treatment? Of course.

Mutual Yet Asymmetrical

Several Relational analytic writers, on the topic of erotic countertransference disclosures, have emphasized the need for mutuality in the treatment (Bonovitz 2010; Barsness & Strawn 2016, Davies, 1994). To disclose is to offer the patient an opportunity to know the analyst, to experience a healing and authentic relational intimacy, and to integrate their experience of the therapist with the therapist’s own self-reports. The “blank screen” has been helpfully deconstructed by Relational writers, forcing psychoanalysts to contend with their own subjectivity, and the inevitability that patients will notice things about them, whether stated explicitly or not. Yet we must wonder when a stance towards mutuality may veer into unhelpful, even traumatic.

For the “as if” nature of the therapeutic relationship to remain in tact, the therapy must remain asymmetrical. Lewis Aron talked of the mutual, yet asymmetrical, relationship between therapist and patient (1999, p.245). Mutuality exists, and is important. The therapist shows up in an authentic way, is committed to listening, remaining as neutral as possible in regard to the patient’s own conflicts, and brings with him an attitude of care, genuine affective engagement and often, over time, love. The therapy relationship, however, is also asymmetrical. The focus of any given session is on the feelings, thoughts, desires and fantasies of the patient. The patient has come to receive help for something; the therapist is tasked to help. Insofar as any countertransference disclosure is concerned, it must always be in service of the patient.

Christopher Bonovitz is one psychoanalyst and writer who has provided us a vignette, an example of how the therapist’s desire to provide a mutual experience for the patient can result in a jettisoning of the asymmetry which holds the therapeutic frame together (2010, p. 636). His case example in the article “The Interpersonalization of Fantasy: The Linking and De-linking of Fantasy and Reality” brings to the fore questions of how to balance mutuality with asymmetry, and whether traumatic reenactments can ultimately be helpful to the patient. In it, he describes a disclosure of erotic countertransference which was experienced by his patient, Martha, as a traumatic impingement (2010, p. 638). The clinical vignette is moving, with Bonovitz paying attention to his patient’s reactions, devotedly working through the fallout from the disclosure with her. What I would like to challenge are some of the ideas around mutuality found in this piece. Bonovitz states, regarding countertransference disclosures that are received poorly by the patient:

“The analyst feels hoodwinked, filled with shame, and the patient feels imposed upon by the analyst’s unhinged desire. The fantasies, what had felt to be mutual, devolve into a concrete reality devoid of imaginings and symbolic potential; the bridging of subjective experience in patient and analyst becomes reduced to blame and misattributions (p. 636).”

The claim I want to make here is that within a Relational framework where mutuality reigns, and the intersubjective matrix is seen as perhaps the main vehicle for change, the reasons why asymmetry is so important can become obscured. An overemphasis on mutuality may create a therapeutic environment in which the therapist’s own feelings in response to the patient are assumed to be more valuable than they are to the process. Countertransference, in this paradigm, may start to take on an almost magical quality, presumed to always tell us something of the patient. Ironically, this can take the therapist out of the “as if” relationship. If the therapist cannot tolerate the uncertainty involved in not fully knowing the patient’s mind, let alone their own, the transitional space can collapse under the weight of the therapist’s assumptions.

In long-term therapy, part of what we may be called to help the patient bear is the opacity of the Other’s mind. An important aspect of good reflective functioning is the ability to tolerate that we cannot read another’s mind (Fonagy, Bateman, 2008). Being able to accept that we never have the full picture, when it comes to another’s thoughts and feelings about us, is a key indicator of healthy psychological functioning. In order to assist our patients in growing this capacity, we must also be able to bear this opacity. When we insist to ourselves that what we are feeling, the patient must also be feeling, we may be at the mercy of our own poor reflective functioning. We may, as therapists, assume a mutuality as a way to soothe our own anxieties. This risks pulling a patient into an enactment where they feel pressured to reciprocate in a way that feels either inauthentic or intrusive.

The opacity of the mind is particularly relevant to human sexuality. Repressed awareness of sexuality has been theorized to be the root of the unconscious (Laplanche, 2007, p. 202). For the therapist to disclose feelings directly could be seen as a demand to be known and seen in a particular way, which may be experienced as a traumatic reenactment, evoking an infantile terror in the patient. It may also pressure a patient into agreeing with the therapist’s experience of the relationship. It may leave a patient feeling overexposed. As Avgi Saketopoulou states, “something in us always resists being grasped and understood, and in that sense, opacity may be seen as a sturdiness in us... that connects to self-sovereignty (2017, p. 8).”

A mutual yet asymmetrical relationship in the therapy serves to protect the patient from feeling pressured into communicating love to the therapist. All speech, Jacques Lacan claimed, is a bid for love; a desire to be understood (2001, p. 418). Psychoanalyst Bruce Fink elaborates on why self-disclosure on the part of therapist can be seen as an unhelpful flip of roles: “Analysts must not speak much in their own names or talk about themselves so as not to demand to be loved in return by their analysands (2015, p. 97).” The analyst, Fink states, needs to be able to love the analysand without expecting love in return (2015, p. 91). We must be careful with how we, as therapists, handle what Lacan referred to as our lack: the inner emptiness in all of us and its concomitant longings. No time in treatment will rid an analyst or therapist of this lack; the best we can do is accept ours enough to not burden the patient with it.

Psychoanalyst Andrea Celenza states, “the asymmetry in the analytic relationship is not an asymmetry of desire, but an asymmetry of the communication of desire” (2017, p.75). A therapist may communicate their desire for the patient, with the conscious intention of facilitating an understanding within the patient of a mutual desire existing in the room. What can be neglected are the dangers of unintentionally or unconsciously pressuring the patient into sharing only of their desire and not of their sexual disgust, fear, rage or hatred. In what ways may the patient protect the therapist in these situations, or ingratiate, in order to preserve the Good Object? In what ways may a therapist unconsciously find themselves honing in on erotic feelings in the dyad, as a defense against more hateful feelings that exist in the treatment room?

On Narcissism

The occupation of psychotherapist is isolating. Glen Gabbard and Andrea Celenza have both discussed the profile of the therapist most at risk of committing sexual boundary violations: the narcissistically needy or lovesick analyst: often male, middle-aged and either single or unhappy in his marriage (Celenza, 2007, p.210; Gabbard, 2007, p.90). It is perhaps a comforting fantasy to imagine such therapists who commit violations as outliers or sociopaths. Yet this is not what the research shows. Up to ten percent of male therapists commit sexual boundary violations at some point in their career (Celenza, 2007, p. 209). Most express remorse and profound guilt in the aftermath. This is not the portrait of an antisocial predator. It is a description of a narcissistically vulnerable, sexually lonely therapist. If such a significant percent of male therapists commit sexual boundary violations, it isn’t a great leap to imagine that a not insignificant portion of male therapists may disclose sexual or a romantic feelings towards a patient in a moment of overwhelm, desperation or arousal: in a way that is narcissistically gratifying and harmful.

In regards to the therapist’s unconscious motivations, Gabbard writes, “The problem is that we cannot know in any thoroughgoing way what we are up to when we decide to engage in self-disclosure. Our capacity for rationalization and self-deception in analytic work is remarkable (p. 10, 1996).” Every analyst must inspect his motivations carefully, with particular respect paid to the power of unconscious wishes and feelings, along with the therapist’s own defenses against acknowledging embarrassing or shameful parts of the self.

One scenario where narcissistic vulnerabilities can lead the therapist astray involves the everpresent desire for appreciation and satisfaction in our work. An unacknowledged need within the therapist to be admired or appreciated can be acted out in myriad ways. It could make a therapist too eager for the patient to accept an interpretation or disclosure, or even unconsciously seek to justify acting out: if it feels good, it must also be good for the patient. But effective therapy often does not feel good in the moment, and this is true for the therapist as much as the patient.

For the therapist to be helpful, he must be capable of receiving and containing negative, unmetabolized affects from the patient. He must be willing to tolerate repeated criticisms and projections.If a patient has been repeatedly critical and devaluing of the therapist, would erotic transference not feel like a very welcome departure from this demoralizing norm? Is it not possible that a therapist may find himself indulging in the erotic transference and countertransference dynamics, justifying mutuality and the “real” relationship along the way?

Therapists are human, flawed like everyone else. We may have intense feelings or urges erupt in session which leave us feeling ashamed; a pull to sexualize a negative transference when we are discomfited by the patient’s hatred (Celenza 2007, p. 12); a wish to merge with a patient in our loneliness (Gabbard, 2007, p. 76); incompetence in the face of a therapeutic impasse; a want to feel desired (Fink, 2015, p.102). While none of these countertransference reactions are inherently shameful or “bad,” it is imperative that we acknowledge them to ourselves; or at least, acknowledge their possibility.

One clue that narcissistic vulnerabilities are at play when it comes to erotic countertransference disclosure, in particular, is that no one seems to advocate disclosing sexual disgust towards the patient. Perhaps that is because it is universally intuited that such a disclosure would be deeply humiliating and potentially traumatic to the patient. How can we be so confident that a disclosure of our attraction and arousal, the other side of the same coin, couldn’t also be experienced as humiliating and traumatic? Desire and disgust aren’t mutually exclusive, after all (Saketopoulo, 2023) and we can never be sure that one feeling won’t follow the other.

The Relational Turn

An openness within some analytic communities towards the use of disclosure of erotic countertransference is a partial outgrowth of the Relational turn in psychoanalysis. A number of psychoanalysts who identify with the relational tradition have written about the positive uses of countertransference disclosure within the therapeutic dyad (Maroda, 1994; Davies, 1994; Aron, 1991). When used judiciously, these analysts describe how disclosure of certain affective states can help: facilitate mentalizing, break through an impasse, clarify an enactment, and promote deeper self understanding within the patient.

Jody Messler-Davies has written perhaps the most well known Relational psychoanalytic paper detailing a disclosure of erotic countertransference, in her 1994 paper titled “Love in the Afternoon.” It is a particularly compelling case example of the possible therapeutic benefit of sexual countertransference disclosure. It is also diverges from the examples involving male therapists referenced earlier in this paper, in important ways.

Foremost, Davies disclosed in a state of irritation and exasperation, not arousal (1994, p.165). She seemingly was not seeking to name some sort of mutual attraction in order to minimize overwhelm over her own desire. Rather, she was at a loss in regards to her male patient’s insistence that she could never return his feelings. He was unconsciously determined to not recognize Davies’ sexuality as a traumatic reenactment of the Oedipal dynamics in his childhood. This refusal was not only creating an impasse in the therapy, it was ruining his romantic life. So, Davies made a chess move. In stating directly yet decidedly not flirtatiously, that she has had sexual thoughts and feelings about him, she essentially forced her patient to face reality (1994, p. 165).

The gender/sex dynamics of this disclosure are paramount. As Jessica Benjamin has argued, for a boy to recognize that his mother has her own subjectivity is the next developmental achievement following rapprochement. If this achievement is never realized, misogyny flourishes (1988, p. 64). Women are forever seen as objects more than subjects. This is likely still of particular importance for men, as we continue to live in a society and culture where women are seen as the desired and men as those who desire. For a woman to share that she has her own sexual feelings and thoughts apart from the fantasies and imaginings of a man is an assertion that she is a whole object and subject. In a world where a man is largely assumed to desire, a disclosure from a male therapist to a female patient holds very different connotations.

Relational psychoanalysts often discuss the turn from a “one person” to a “two person” therapy relationship, or a transition from a sole focus on the subjectivity of the analysand to a treatment focus that also takes the analyst’s subjectivity into account. Barsness and Strawn, in their article advocating for the use of erotic countertransference disclosure, interpret the “two person” approach as non-heirarchical. Barsness argues that the patient deserves access to the analyst’s mind (2018, 190). This stance confuses mutuality with symmetry (Aron, 1991) and is an abnegation of the power dynamics inherent within the therapeutic relationship. Andrea Celenza cautions that an egalitarian attitude towards psychotherapy “is an assertion made solely from the therapist’s conscious point of view, essentially sidestepping the perception and experience of the therapist’s power from the patient’s point of view” (p. 61). This power differential is heightened within the male therapist/female patient dyad, given the patriarchal power structures imbedded within our cultural and systemic contexts.

In a “two person” psychoanalytic therapy, the therapist, of course, still has obligations and responsibilities to the patient. With the freedom to disclose countertransference comes great responsibility. In a more classical analytic treatment, the analyst could hypothetically retreat behind the safety of the “blank screen,” attempting to remove a portion of their subjectivity with a more rigid analytic stance, which included an almost total lack of deliberate self-disclosure. By comparison, a therapist operating out of an intersubjective or relational stance must think about, deliberate, and practice discernment around countertransference, arguably even more, with even greater care; with a sizable dose of self-doubt, and a profound respect for unconscious forces and motivations always present within themselves. If an intervention is on the table, it must be deliberated carefully, especially when it comes to the erotic.

Barsness and Strawn state, “as there is no such thing as a blank screen, everything we do is some form of disclosure, so it seems wise to talk about it, rather than try and convince ourselves that we can hide it” (2018, p.139). This articulation assumes that the primary reason a therapist would decide against countertransference disclosure is in an attempt to “hide” themselves from the patient. This excludes another option, one in which the therapist creates an environment where the patient can explore endlessly, without fear of being shut down. Ideally, a space in which the patient can feel, think and say anything, and the therapist can feel and think anything.

As Gabbard points out, “There is, however, a vast middle ground of exploratory activity between inaction or projective disavowal, on one hand, and open disclosure of erotic feelings on the other” (1996, p.10).

Another argument Barsness and Strawn make for disclosure is that to share one’s feelings is to be authentic. They state, “when an authentic response is offered, the patient is able to gain a greater sense of what his/her actions mean” (2018, p.139). Unfortunately, this perspective is at risk of conflating authentic with intrusive; even lascivious. Curiosity can be authentic. What of playful, transitional space? What of an allowance of the patient’s flirtations towards us, without either overtly rejecting or reciprocating them? Are these reactions to erotic transference really inauthentic, or a show of good clinical discernment and self-restraint in service of the treatment.

The Trauma of Sexuality

The caution I am advocating for here is informed by Laplanche’s theory that we are traumatized as infants by our caregiver’s sexuality (2007, p. 201). While the very existence of unconscious sexuality in the parent becomes traumatic to the infant, a more severe and harmful trauma occurs when there is sexual abuse or violation. Then, the sexuality of the person who has more power in the relationship is experienced as a traumatic intrusion, which has the power to fragment the child’s psyche. I believe there is a powerful parallel between the caregiver/infant dyad and the therapist/patient dyad in the case of sexuality and countertransference disclosure.

While a patient will notice our sexuality in the room, our task is to help them translate what they experience into their own meaning, not to intrude with our own explicitly stated or acted out desires. While the arguments for disclosures I have referenced thus far would argue that the patient knows on some level about the therapist’s feelings, anyways, I would argue that it is often more helpful for the therapist to help the patient tolerate opacity in these scenarios. To explore with the patient their imaginings, arousal, excitement or terror regarding their own sexuality, in relation to the therapist’s. To help the patient find their own translations and meanings, while also learning how to tolerate the uncertainty always involved in relationships and sexuality. One can do all of this, while staying alive and fully human in the treatment room, without directly disclosing feelings in return.

How is sexual countertransference disclosure uniquely threatening to the “as if” relationship, thereby necessitating extra caution? For starters, the nature of sexual arousal is singularly excessive, shame-ridden, unsymbolized and potentially traumatic (Stein, 1998, p. 596). Davies has posited that sexual arousal is perhaps the only affect that parents do not symbolize for their children via language (2013, p.172), making the experience of arousal in the therapy room particularly prone to accompanying feelings of shame, overstimulation and/or threat. Many patients in psychoanalytic treatment come into adulthood with sexualities containing ancient unresolved elements of “power, control, feelings of being used and using, hurting and being hurt,” (Slavin, p. 51). Sexual countertransference disclosure may cause any number of these elements within the patient erupt to the surface in a traumatic and terrifying way.

Can Erotic Countertransference Disclosure within the Male Analyst/Female Patient Dyad Ever Be Helpful?

While I have spent this article criticizing several written defenses of the positive use of erotic countertransference disclosures, I would like to also include one example of disclosure from the psychoanalytic tradition which may be counted as the exception which proves the rule.

In Slavin and Rhamani’s article, “Moments of Truth in Psychoanalytic Treatment,” a vignette is shared in which the male therapist, Dr. S, is working with a young female patient with a history of childhood sexual abuse. There occurs a moment when Dr. S looks at his patient, noting to himself that he finds her sexually appealing (Slavin, p. 57). The patient notices the look, and frantically asks, “What are you looking at?” (p. 57). The disclosure already happened, and it caused an immediate rupture. Dr. S had an unfortunate choice to make in the direct aftermath of that moment. He could refuse to acknowledge the look, thereby leaving the patient in not only an extremely frightened state, but also in a place of doubt as to whether what she had seen was real. Or, he could affirm her perception, and ground her back to reality, albeit a frightening one. Dr. S chose the latter (Slavin and Rhamani, p. 58).

If we take the vignette of Dr. S in the Slavin and Rhamani article as the notable exception to the enjoinder for male therapists not to disclose erotic feelings to the female patient, the exception could be articulated as such: erotic countertransference disclosure may be necessary when the therapist’s erotic feelings have already compromised the “as if” relationship, due to non-intentional, indirect, yet obvious (to the patient) disclosure. In this case, it may be helpful to affirm what the patient has already noticed — if the patient is frightened and acutely distressed by the knowledge of her analyst’s feelings. Disclosure of erotic feelings in this specific instance may actually be necessary for repair, depending on the patient’s response to such an unintentional disclosure. This follows Celenza’s first guideline regarding erotic countertransference disclosures, that the patient already knows about the therapist’s feelings (2017, p.81). Interestingly, the Slavin and Rhamani example does not follow Celenza’s other guidelines, mainly that a disclosure may be beneficial only near the end of a treatment relationship in which the patient is at a high-functioning, post-Oedipal place in their sexual development. Yet, when a patient not only knows about a therapist’s erotic feelings and is frightened by them, the transitional space has already collapsed, and a “last resort” disclosure may be necessary.

Of particular importance here is the affective state of the patient. In Slavin and Rhamani’s vignette, Dr. S’s patient is acutely frightened. The “as if” relationship had collapsed, and the therapeutic space was filled with persecutory objects (Winnicott, 1971). Yet another important difference between Dr. S’s disclosure and the other examples discussed earlier in this paper is that there is no indication Dr. S disclosed his feelings in an enactment; or, in other words, to discharge his own intolerable affect. Dr. S’s disclosure did not seem to be the consequence of not being able to tolerate his own sexual feelings towards the patient. Notably, Dr. S also did not blame his patient for his sexual feelings or attempt to interpret those feelings as mutual. He also kept the focus of the disclosure on the patient’s reactions and perceptions, attempting to maintain asymmetry.

Dr. S disclosed his feelings because he knew the treatment was hanging in the balance. He took responsibility for frightening his patient and knew that repair was necessary. The playful, expansive space of the “as if” relationship had already died. He made a decision to disclose what his patient already knew, in an effort to revive the transitional therapeutic space (Slavin and Rhamani, p. 58).

In summary, erotic countertransference disclosure on the part of the male therapist, towards his female patient, is a therapeutic action particularly likely to harm. To disclose sexual feelings to a patient is to potentially turn the “as if” space of the therapy room into something too real and potentially frightening. Disclosure of sexual arousal within the therapy space, with all of its intensity, along with the consequent affects of fear and shame, is not like “any other” affective disclosure. Its unique potential to obliterate the treatment must be respected.

For a proper level of restraint to be possible, the therapist must be sufficiently aware and tolerant of his erotic longings and sexual feelings towards the patient. To be comfortable enough with these feelings, so as for them to become neither disavowed nor enacted. He must be aware of the narcissistic vulnerabilities which can lead him down paths of grandiose fantasy and pull him into the patient’s unmet longings for merger. Lacan pointed out our universal lack (2015). This is a sense of incompleteness that the infantile, narcissistically wounded parts in us would rather avoid addressing. To see a patient in distress, enraged or even suicidal, expressing their need to know they are desired: what a comforting fantasy to believe that granting their wish would fill not only their lack, but ours. When the therapist cannot tolerate feeling inadequate, refuses to accept the limits on their power to help, thereby obstinately denying their lack, they will intrude on the patient to soothe their own anxiety, and collapse the transitional space.

The male therapist must be accepting of sexual transference from the female patient and aware of his impulses to merge with or soothe the distressed female patient. While erotic countertransference disclosure is not necessarily a boundary violation, it is of fundamental importance for therapists to be ever aware of the possibility that disclosure of erotic feelings may unconsciously serve the need of the therapist. Gabbard has made the argument of the “slippery slope” in this regard: every sexual boundary violation has likely been preceded by an erotic countertransference disclosure (1994, p. 7).

Perhaps Jay Greenberg, one of the founding fathers of the Relational movement, summarizes it best: “There are always multiple perspectives on the participation of each party. This means that whatever is revealed is simply one person’s understanding at a given moment - never... the last word on the subject... I am not necessarily in a privileged position to know, much less to reveal, everything that I think or feel” (1991, p. 197).

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References

• Aron, L. (1991). The patient’s experience of the analyst’s subjectivity. Psychoanalytic Dialogues (1)(1), 29-47.

• Barsness, R., Strawn, B. (2018). Core Competency Seven: Courageous Speech/Disciplined Spontaneity. In Barsness, R.(Eds): Core Competencies of Relational Psychoanalysis

• Bateman, A., Fonagy, P (2008). Mentalizing In Clinical Practice.

• Benjamin, Jessica (1988). Bonds of Love.

• Bonovitz, C. (2010). The interpersonalization of fantasy: the linking and de-linking of fantasy and reality. Psychoanalytic Dialogues, (20)(6), 627-641.

• Bromberg, P. (1999). Shadow and Substance. In Mitchell, S., Aron, L. (Eds): Relational Psychoanalysis: The Emergence of a Tradition

• Celenza, A. (2007). Sexual Boundary Violations: Therapeutic, Supervisory and Academic Contexts.

• Celenza, A. (2017). Erotic Revelations.

• Cooper, S.H. (1998). Flirting, post-Oedipus, and mutual protectiveness in the analytic dyad: commentary on paper by Jody Messler Davies. Psychoanalytic Dialogues, 8, 767-779.

• Davies, J.M. (1998) Between the Disclosure and Foreclosure of Erotic Transference-Counter-transference: Can Psychoanalysis Find a Place for Adult Sexuality? Psychoanalytic Dialogues 8: 747-766

• Davies, J.M. (1994) Love in the Afternoon: A Relational Reconsideration of Desire and Dread in the Countertransference. Psychoanalytic Dialogues 4:153-170

• Davies, J.M. (2013) My Enfant Terrible is Twenty: A Discussion of Slavin’s and Gentile’s Retrospective Reconsideration of “Love in the Afternoon”. Psychoanalytic Dialogues 23: 170-179

• Fink, B. (2015). Love and/in Psychoanalysis: A Commentary of Lacan’s Reading of Plato’s Symposium in Seminar VIII: Transference. Psychoanalytic Review: 102(1):59-91

• Gabbard, G. (2004). Long-term Psychodynamic Psychotherapy

• Gabbard, G. (1994). Sexual excitement and countertransference love in the analyst. Journal of the American Psychoanalytic Association (42)(4).

• Greenberg, J. (1986). Theoretical Models and the Analyst’s Neutrality. In Mitchell, S. Aron, L. (Eds): Relational Psychoanalysis: The Emergence of a Tradition

• Hansbury, Griffin. (2018). The Masculine Vaginal: Working with Queer Men’s Embodiment at the Transgender Edge. Journal of the American Psychoanalytic Association (65)6

• Lacan, J. (2015). The seminar of Jacques Lacan: Book VIII. Transference (1960-1961) (B. Fink, trans.). Malden, Mass.: Polity Press

• Laplanche, J. (2007). Gender, sex and the sexual. Studies in gender and sexuality: 8(2): 201-2019.

• Maroda, K. (1991). The Power of Countertransference.

• Nagoski, E. (2015). Come As You Are: The Surprising New Science That Will Transform Your Sex Life.

• Saketpoulou, A. (2023). Sexuality Beyond Consent.

• Slavin, J. (2002). The innocence of sexuality. The Psychoanalytic Quarterly (V. LXXI)(1), p. 51-80.

• Slavin, J., & Rahmani, M. (2018). Moments of truth in psychoanalytic treatment. In S. Lord (Ed.),

• Moments of meeting in psychoanalysis: Interaction and change in the therapeutic encounter (p. 45-64).

• Stein, R (1998) The Enigmatic Dimension of Sexual Experience: The “Otherness” of Sexuality and Primal Seduction. Psychoanalytic Quarterly 67: 594-625

• Winnicott, DW. (1971). Transitional Objects and Transitional Phenomena. Playing and Reality

You’ve probably heard that Sigmund Freud used cocaine and that he prescribed it to people as treatment, but odds are that you likely don’t have a good sense of the extent and duration of his use or how he employed it in his clinical practice or scientific experiments.

You may also be familiar with this famous quote from a letter to Martha Bernays, his future wife:

“Woe to you, my Princess, when I come. I will kiss you quite red and feed you till you are plump. And if you are froward you shall see who is the stronger, a gentle little girl who doesn’t eat enough or a big wild man who has cocaine in his body.” (June 2, 1884)

(“Froward” is often misquoted online as “forward.” Froward is an outdated word meaning contrary, willful, or disobedient, with the intended meaning here of “if you defy me,” used playfully.)

You may also have seen a version of this letter circulating on social media, which I used to think was fake, but it’s real:

“So yesterday I gave my lecture. I spoke quite well despite my lack of preparation and without any hesitation, which I attribute to the cocaine I’d taken beforehand. I talked to them about my discoveries in cerebral anatomy, a lot of very complicated things that the audience certainly didn’t understand, but it was enough for them to have the impression that I did.” [Letter to Martha Bernays, source]

(Freud pulling a Karl Friston here!)

That was the extent of my own familiarity with Freud and cocaine until recently when I started reading more about it and discovered that this historical episode has numerous fascinating details. Freud was experimenting with cocaine before its medical uses were well-characterized, and he could’ve been the person who developed modern local anesthesia; he saw the local anesthetic potential in cocaine before Koller did (the person who got the credit for introducing cocaine as a local anesthetic) but didn’t follow through with it. Freud treated a close friend with morphine addiction with cocaine, with initially promising results but later disaster, and got accused of unleashing a scourge on humanity. He used cocaine on himself both as self-experimentation and to use it to lift him out of bouts of depression and was amazed enough to call it a “magical substance.” Freud’s colleague hypothesized a “nasal reflex neurosis,” treated by cocaine in the nose. There were scandalous psychoanalytic interpretations: a patient having recurrent bleeding from a surgery-gone-wrong-involving-cocaine is said by Freud to be “hysterical” and bleeding “out of longing.” And his own dream involving cocaine becomes fodder for his psychoanalytic interpretation. And of course, the question that has generated much head-scratching among scholars: what, if anything, do Freud’s experiments with cocaine have to do with psychoanalysis?

Let’s start with the basics.

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Wicked problems, as characterized by Rittel and Webber, are problems that resist definitive articulation, it is hard to know when the problem has been solved, and solutions cannot be judged as true or false but only as better or worse and there is no metric standing above the interests and values of the judging parties. Once a solution is tried, it can’t be undone, and attempted solutions can generate their own uncertainties and repercussions. There’s no criterion that proves all plausible solutions have been identified, and every case is in some way unique, often nested within or symptomatic of larger issues. Wicked problems are complex but their wickedness arises from the plurality of legitimate value positions and the absence of any agreed criterion for what would count as a solution. (In case it needs to be said, “wicked” here means vicious or tricky, not ethically deplorable.)

Wicked problems resist definitive resolution in part because there are conflicting perspectives and values, extending to how the problem should be defined and what outcomes are desired or ought to be considered optimal. These conflicts may arise between different stakeholders or even within the same stakeholder group or within a single person over time. Multiple solutions will be valid, depending on whose values are given weight and how trade-offs are handled.

In a new co-authored paper led by Helene Speyer published in BJPsych Bulletin, “Clinical guidelines addressing complex and ‘wicked’ problems,” we suggest that the notion of “wicked problems” is a conceptual tool that can be used to better understand the challenges of deprescribing of psychiatric medications.

The goals and desired outcomes of deprescribing vary considerably. Some want to discontinue because of a perceived low risk of relapse and others because of the burden of adverse effects and others because of a desire for a medication-free life, and many others for many reasons. Heterogeneous illness course, degree of insight, clinical support available, and patient vs caregiver preferences yield multiple, competing framings of a person’s desire to come off medications. Patients, families, and clinicians weigh desired outcomes differently, and this plurality of evaluative standards means there may be no single correct answer, only complex negotiations.

Each attempt at deprescribing or maintenance has consequences that cannot be cleanly undone. A psychotic/manic/depressive/anxious relapse can be severe enough to alter one’s life, lose jobs, housing, relationships, treatment providers. A prolonged continuation of medication can entrench movement disorders or metabolic problems. A taper may appear to work for months before an abrupt decompensation is experienced. Continued maintenance may look like it’s working by reducing relapse but may functionally impair a person from neurolepsis. Feedback can be delayed and confounded by biological noise, so there may be no immediate test that settles the question of whether maintenance or deprescribing was the right choice. There are different ways to taper and different medications to utilize for maintenance. And each case is essentially unique with peculiarities of pharmacodynamics and psychodynamics. Prior response patterns, comorbidities, trauma history, social supports, local service capacity, and personal aims interlock in idiosyncratic ways, making rule-like generalization perilous.

Another dimension is the tension between individual autonomy and the responsibility to safeguard society. Clinicians’ primary obligation is to the patient, but this responsibility also extends beyond the individual to the society at large, creating situations in which the interests of the patient and the broader societal obligations may come into conflict.

In the case of wicked problems, deciding which explanatory framework to adopt determines the nature of the resolution. If a person is struggling after tapering their medications, whether we construe this as disorder relapse, withdrawal, rebound, disorder evolution, or something else entirely, in some ways, not entirely settled by the data; how we characterize it tells us what the appropriate resolution will be.

For each individual, not knowing whether they can remain well without medication and thereby reduce the burden of adverse effects, or whether they should accept the risk of relapse, is a deeply personal question tied to the dignity inherent in risk-taking. No one can substitute for a person’s own evaluation of what risks are worth taking. This is one of the fundamentally wicked dimensions of deprescribing that can never be reduced to recommendations in clinical guidelines.

Check out our thoughts in the paper on how clinical guidelines may approach this.

“Clinical guidelines aid decision-making, but their simplifying strength becomes a limitation in complex, value-laden situations. Once meant to summarise evidence, they now function as prescriptive standards used in quality and legal assessments. Overly rigid directives can undermine autonomy, hide uncertainty and restrict clinical judgement. Using complexity science and ‘wicked problem’ theory, we introduce ‘wicked complexity’ to better match guidelines design to real clinical challenges. Applying this to deprescribing psychoactive drugs, we show how traditional, adherence-focused guidance can prompt defensive practice. Guidelines for wicked complexity should instead clarify risks, support moral deliberation and support shared, iterative decision-making across healthcare.”

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I often think about how the “invisibility” of mind — the inability of others to access our inner, subjective experiences through anything other than self-report and behavioral inferences — complicates the recognition and management of mental health problems. What if obesity were invisible in the same way as ADHD is? Such a comparison is hard to imagine and requires some suspension of disbelief but bear with me.

What if we couldn’t see adiposity, couldn’t measure it in terms of BMI, waist circumference, or body fat percentage, and had to rely on something indirect like self-perception and other-perception of being obese? This clinical construct of self/other-perceived obesity would not be identical to our current conception of obesity, a chronic state of excess adiposity that impairs health. It would be heavily mediated by subjective perception and shaky behavioral inference. The clinical criteria would invoke items like feeling heavy or weighed down; feeling full or bloated out of proportion; short of breath or fatigued on exertion that others manage; a persistent sense of occupying too much space; eating without hunger or grazing; difficulty stopping once started; eating in response to affect; preoccupation with the next meal; avoiding activities because of perceived size, etc, etc. People would obsess over whether your parents thought you were fat as a child or you’ve only become fat as an adult, and if that “counts.” Who gets believed in the perceived obesity world? The conspicuous eater, the person who visibly labors up stairs. Who gets believed in ADHD? People resembling the hyperactive-boy template. It would not even be clear to many that perceived obesity can be or should be reconceptualized in terms of adiposity because so many clinical features, such as feeling heavy or preoccupation with food or feeling fatigued on exertion are not specific to excess body fat.

Obesity is a clinical problem and weight loss for obesity is the treatment. But we also understand very well that even people in the (non-obese) overweight and “normal” weight range desire weight loss. They desire it for sociocultural reasons, for psychological reasons, for physical fitness reasons. Weight loss in the absence of clinically excessive adiposity is considered enhancement rather than treatment per se, but the boundaries are fuzzy. And we also know that some people desire weight loss for “pathological” ends, to fuel their eating disorders, for example. We can adjudicate these cases because we can measure body fat percentage, or more commonly, we have anthropometric surrogate measures like BMI. But what if you couldn’t? How would you reliably, unproblematically distinguish weight loss for pathological, enhancement, and treatment goals if you had no way to measure body fat percentage or use surrogate measures like BMI? In such a world, it’s easy to imagine that individuals with eating disorders would self-diagnose as obese and would want access to GLP-1 as a treatment for obesity. We would have entire communities dedicated to explaining how anorexia is a poorly recognized form of obesity and if only we didn’t gate-keep access to GLP-1 and believed patients when they told us they are fat.

Such a state of affairs would also lead many to be skeptical of the existence of obesity itself. It’s all a sham! It’s all enhancement and self-destruction! People need to live with obesity. Diet and exercise if you want. Focus on social determinants of health, don’t make it a problem inside a person.

Studies conducted in samples inadvertently enriched for excess adiposity would show tremendous benefits of weight loss treatments across a wide range of measures, including quality of life and mortality. The default medical stance would be that obesity is under-treated, rightly so. And yet, anorexics claiming to be obese and starving themselves with GLP-1s would also be a well-recognized phenomenon, leaving many people confused and vexed, generating endless commentary on how the diagnosis of obesity had been stretched too far, had lost all validity, had been gentrified. And much of this confusion would be dispelled by a definitional physical substrate (adiposity) or a physical proxy measure (BMI).

This is the situation we find ourselves in with ADHD and stimulant treatment. ADHD is as real a clinical problem as obesity, but our epistemic access to it is indirect and mediated via self-report and behavioral inference. Unlike obesity, we do not (cannot?) define it in terms of something we can objectively measure. We do not, e.g., define it in terms of attentional impairments on neuropsychological testing. Perhaps ADHD is as muddled and heterogeneous as “perceived obesity” in my thought experiment which can’t be strictly defined in terms of adiposity either. ADHD is a construct that seems to encompass motivational and task initiation difficulties, executive function difficulties, and impulse control difficulties. And stimulants are attractive to people for a lot of reasons. They offer significant benefits to many people who meet diagnostic criteria for ADHD, but they are also desirable for people who don’t technically have ADHD but have some other problem. People who are struggling to manage motivation, boredom, energy, focus, sleep, etc. Individuals with obsessive and perfectionistic tendencies can worry about having attentional impairments without actually having any attentional impairments. Similar to weight loss treatments being used in the service of an eating disorder, stimulants can be used in a harmful way. Addiction and abuse is one example, but also situations where people are desperately trying to maintain an unsustainably active or productive lifestyle as well as people who are in a stimulant-fueled mania or psychosis. Fitting for our analogy: stimulants are also actively sought and misused for appetite suppression by people with eating disorders.

Nearly everything people cite as evidence against ADHD — contested thresholds, shifts in thresholds and prevalence, the demand for treatment, the simultaneous visibility of medication misuse, swinging clinical opinions between suspicion and enthusiasm — follows from the epistemic situation alone, and would appear just as reliably around a condition few otherwise doubt. (This is a defense of ADHD’s reality only in the negative sense of removing some bad arguments against it.)

Physical measures and shared external yardsticks don’t resolve all the problems of clinical diagnosis. Obesity demonstrates that. Thresholds can still be contested. Surrogates can be highly imperfect. We still have to appeal to evaluative judgments like “excessive” and “dysfunctional.” The appropriate response — intervening on the person vs intervening on the environment — can still be debated. A physical substrate doesn’t tell us what the causes are. And effective treatments can end up targeting processes tangential to causes with the potential for uses and misuses. But at least a public anchor allows us to adjudicate, however imperfectly, between interventions being employed for treatment, enhancement, and pathological ends.

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This is a follow-up to:

When Alan Levinovitz and I developed the concept of the “Rumpelstiltskin effect” last year (see “The Rumpelstiltskin effect: therapeutic repercussions of clinical diagnosis” in BJPsych Bulletin), we were unaware that anyone before had named the relevant concept. A search of the literature using the usual means had turned up nothing, and no one we spoke to knew that this phenomenon had been given a name. So we proceeded. As it turns out, a psychiatrist had described the central concept a half-century earlier… and had reached for the same fable and the same name. In The Mind Game: Witchdoctors and Psychiatrists (1972), E. Fuller Torrey – yes, the E. Fuller Torrey – laid out what he called the ‘principle of Rumpelstiltskin.’

This was brought to our attention by Josh Richardson (thank you, friend) and serves as a good example of independent intellectual convergence.

In the paper, we describe the Rumpelstiltskin effect as: “The therapeutic effect of a clinical diagnosis, independent of any other intervention, where clinical diagnosis refers to situating the person’s experiences into a clinical category by a clinician or the patient.”

Torrey lands on the same core idea that naming a problem can itself be therapeutic but he develops this in the context of psychotherapy. Torrey opens Chapter 2 of the book with an excellent example. Penicillin cures an infection without any shared language or worldview between doctor and patient. In fact, the patient doesn’t even need to be aware that they are receiving penicillin for it to work. For psychotherapy as a treatment, however, communication is the substance, and meaningful and effective communication requires a shared language as well as a shared worldview. Where that shared frame exists, the therapist can put a name on what is wrong, and that act of naming acquires power and therapeutic significance.

Torrey gives further examples. A psychiatrist offers an interpretation about buried anger at a father; the patient breaks down sobbing and blurts out a forgotten history of paternal neglect, and improves. A witch doctor reads scattered shells and announces that a family taboo was broken, offending an ancestral bear-protector; the family, relieved to finally know, performs the sacrifices, and the patient improves. These are structurally identical acts for Torrey. The naming reduces anxiety because a trusted authority demonstrates that they understand the problem and they identify an offending agent (whether it is a childhood experience or a violated taboo) and for the afflicted and help-seeking, this can bring about confession, abreaction, and general catharsis.

Torrey and we reach for the same Grimm tale and for the same reason: the queen is saved by getting the name right, and once the name is spoken, the problem dissolves. Both of us treat this as a cross-culturally recurrent structure. Torrey brings up Lévi-Strauss on shamanic healing and we invoke Aarne–Thompson 500, exorcism traditions, and Le Guin.

Torrey cites Lévi-Strauss to the effect that shamans and psychoanalysts alike make unconscious conflicts available through a language in which otherwise inexpressible states can be voiced. The naming process is universal, but its content is culture-bound. A psychiatrist telling an illiterate African his phobia expresses fear of failure, and a witch doctor telling an American tourist his phobia expresses ancestral possession are useless because neither shares the relevant worldview.

Rumpelstiltskin is the first of Torrey’s four universal components of psychotherapy: a) shared worldview enabling naming (the principle of Rumpelstiltskin); b) therapist personal qualities; c) patient expectancy; and d) techniques of therapy. Torrey contends in the book that both psychiatrists and witchdoctors are species of the same genus (psychotherapist). The naming principle is what makes psychiatric diagnosis continuous with divination rather than with penicillin. Its efficacy runs through meaning and shared belief.

“Both therapists are able to name what is wrong with their patients. The very act of naming it has a therapeutic effect… the principle illustrates the magic of the right word.” (p 16)

“Every therapist who has ever had the experience of observing a patient’s relief after solemnly telling him that he was suffering from idiopathic dermatitis or pediculosis knows how important the name is. It says to the patient that someone understands, that he is not alone with his sickness, and implicitly that there is a way to get well.” (p 16)

Torrey’s bio at the start of the book describes him as “a psychiatrist who has slowly come to realize that he is also a witchdoctor.” And the opening lines of the first chapter are memorable:

“Witchdoctors and psychiatrists perform essentially the same function in their respective cultures. They are both therapists; both treat patients using similar techniques; and both get similar results. Recognition of this should not downgrade psychiatrists; rather it should upgrade witchdoctors.”

This is a version of Torrey very different from his contemporary public image, and he is writing from a bygone era of psychoanalytic dominance in psychiatry. The man who wrote that psychiatrists should recognize themselves as witchdoctors later became psychiatry’s most fierce advocate of schizophrenia as a biological disease. There is no self-contradiction here but the shift is significant.

Despite the same core concept, there are some interesting points of divergence in the way Torrey and Levinovitz and I develop the concept. The biggest one is that Torrey is interested primarily in psychotherapy while we are interested in diagnosis and classification. Torrey’s principle is the first of four components of psychotherapy. Our effect is explicitly defined as independent of any other intervention and extends to include considerations around self-diagnosis.

Torrey’s exemplary acts of namings are interpretations, understandably so. Latent anger at the father, violations of ancestral taboo, etc. Our Rumpelstiltskin effect runs in the opposite direction, from the idiographic to the nomothetic, from one person’s particular story to a recognized category with a textbook description and a cohort of fellow sufferers. Torrey is aware that this also works with nomothetic logic, but he walks past it. Torrey gives readers the example of idiopathic dermatitis to show that the phenomenon is present across medicine, and we have a list of similar examples in our paper doing the same.

Our reading of the Grimm tale emphasizes that no ordinary name will do, and a layperson’s description (“funny little man”) doesn’t substitute. That’s what makes “ADHD” different from “I get distracted.” Torrey doesn’t make this explicit because he isn’t primarily interested in the diagnostic label as such, more in the interpretive act.

In terms of mechanisms, Torrey offers anxiety reduction from the realization that “someone understands, that he is not alone with his sickness, and implicitly that there is a way to get well.” We focus on a hermeneutical framing (Fricker), the sick role and ritual/conditioning account (Parsons), affect labeling, and identity/community formation. Our paper devotes a full section to nocebo, looping effects, internalized stigma, foreclosed agency, and the imposition of a deficit narrative on people who understand their experience as gift or transformation. Torrey was writing before the labeling-theory critiques fully matured and long before Hacking.

One thing Torrey emphasizes that I wish we had is the shared worldview as an explicit precondition. We don’t say it that way, but we do nod toward how the effect works within cultural contexts that treat medical diagnoses as authoritative and transformative.

Torrey develops it as a principle of psychotherapy; ours is an effect of diagnosis. Different explananda, arrived at independently, which is what makes the convergence interesting rather than merely awkward. The shift in the framing of this phenomenon, from psychodynamic interpretation to nosological labels, from a universal component of healing to a placebo-like intervention with its own potential harm profile, mirrors broader shifts in the medical and psychiatric culture.

Because we arrive at the concept through different intentions and different goals, I do believe that the way we define and explain the effect retains value. We were right to say in our paper that the Rumpelstiltskin effect as a medical phenomenon is striking and neglected, but we were simply wrong to call it “unchristened.” But with error comes the possibility of correction, and without that error, I might have remained ignorant of this delightful work from 1972 on psychiatrists as witchdoctors.

A note on a common misreading

Since the publication of our 2025 paper, the most common misunderstanding of the Rumpelstiltskin effect I come across is that idea that a diagnosis is overall more beneficial than harmful for the patient. The Rumpelstiltskin effect is not a claim that receiving a diagnosis is a net benefit or a net positive. It is a claim that the mere act of receiving a diagnosis can be beneficial. There is where the analogy with placebo effects is illustrative. The claim in the case of placebo is not that taking a medication is a net positive (that actually depends on a variety of factors). The placebo claim is that even taking an inert medication can be helpful because the act of taking a medication can have beneficial effects. So, one way to think about the Rumpelstiltskin effect is: would a scenario in which a diagnosis is relatively inert (e.g. say descriptive) still produce benefits of the sort seen with etiologically/mechanistically driven diagnoses? We still don’t know empirically what mechanisms best account for the benefit of receiving a diagnosis, or a clinical name, or an interpretation, but we have a variety of hypotheses, and different hypotheses can be investigated using different sorts of controls.

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