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.

See also:

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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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This is a follow-up to:

Adele Framer, a citizen scientist and patient advocate, has studied psychotropic withdrawal syndromes for 20 years. She founded the peer support site SurvivingAntidepressants.org in 2011 and, in 2023, the nonprofit Psychotropic Deprescribing Council for research and medical education. She is an occasional advisor to the medical tapering service Outro Health.

Dr. Aftab mentioned me in his June 13 article, Some Predictions About the Future of “Withdrawal Studies” and graciously invited me to comment. I respect his call for clarity. I’ll try to briefly offer my perspective.

About my bona fides: I am a citizen scientist and the inventor of “withdrawalology,” a term I coined to describe the specialized study of psychotropic drug withdrawal syndromes and their amelioration by tapering. I have no academic credentials in the medical or scientific fields. My interest was focused by my personal experience of developing protracted antidepressant withdrawal syndrome from going off paroxetine in 2004, which has been recounted elsewhere.

As a withdrawalologist, I stand on the shoulders of grassroots activity dating back to the ‘90s. In 2005, I joined one of a dozen forum-type websites full of thousands of people reporting withdrawal syndrome from the new antidepressants and benzodiazepines, long before social media became populated.

Since then, I have researched drug withdrawal syndromes, corresponded with many researchers, and became recognized as an expert in the field. This is not so special, because throughout medicine, iatrogenic effects are poorly studied in general and drug withdrawal syndromes are even more bereft.

In 2006, psychiatrist Richard Shelton, a co-author of Schatzberg et al., 2006. Antidepressant discontinuation syndrome: consensus panel recommendations for clinical management and additional research (a journal supplement sponsored by Wyeth), wrote me this:

“I actually think the discontinuation syndrome is pretty bad in some situations and truly horrible in others …. almost all resolve; that is, except for a very small group, where the symptoms become persistent.”

Another co-author of Schatzberg et al., 2006, psychiatrist Peter M. Haddad, who had published extensively about antidepressant withdrawal syndrome, mentioned the importance of case reports in another correspondence. Subsequently, under the pseudonym Altostrata, in 2011 I started SurvivingAntidepressants.org, an online forum site designed to collect longitudinal pseudonymous first-person accounts while providing peer support for tapering and psychiatric drug withdrawal syndromes, including protracted conditions. The site accumulated 23,740 registered members before it became read-only in January 2026.

Predating the activity on Facebook, Twitter, Reddit, Inner Compass, etc, discussions within SurvivingAntidepressants.org shaped the current discourse about psychiatric drug withdrawal in the scientific literature as well as throughout the burgeoning social media “withdrawal community.”

I invited many researchers to look at the approximately 6,000 first-person longitudinal case narratives collected on the site. Among my correspondents were Giovanni Fava and his colleagues Carlotta Belaise, Fiammetta Cosci, and Guy Chouinard; Michael Hengartner, Paul Andrews, Jim Phelps, and Brian Harvey. Mark Horowitz was a member of SurvivingAntidepressants.org, where he conceptualized his theory of hyperbolic tapering. All went on to contribute to the more recent stratum of literature about psychiatric drug withdrawal syndromes, including Chouinard, G., & Chouinard, V.A. (2015). New Classification of Selective Serotonin Reuptake Inhibitor Withdrawal.

In late 2023, I founded the nonprofit Psychotropic Deprescribing Council, an interdisciplinary organization to collaboratively research and create unbiased medical education about rational psychotropic deprescribing, tapering, and support for what we view as a significant life event. Our membership includes hundreds of pharmacists, mental health professionals, and physicians, some of them psychiatrists, all interested in sharing their experiences and learning more.

A bird’s-eye view

In the US, the population being treated with psychiatric drugs amounts to a general population, not a population selected for severe mental illness. Recent US Census data shows that at any one time, close to 25% of all US adults are taking drugs for a mental health condition alone; while serious mental illness is estimated to affect 6% of the adult population. Approximately two-thirds of those taking psychiatric drugs are taking antidepressants (17% of all US adults). This is a rolling total; at least half of new antidepressant users will shortly quit their drugs, while others will start.

The vast majority of psychiatric patients were initially prescribed antidepressants by primary care doctors, very often without formal diagnosis. The majority of clinical guidelines recommend that maintenance of antidepressants may continue 6 months after symptomatic remission, though this arbitrary rule of thumb is rooted in clinical trials confounded by unrecognized withdrawal symptoms, such as those reviewed in Geddes et al., 2003. Antidepressants are not routinely recommended for mild to moderate depression. According to Luo, et al., 2020, only about 14% of US adults who are taking antidepressants meet the Kessler-6 Index for a severe condition; more than 86% have mild to moderate scores. A meta-analysis showed that in mild to moderate cases, their gradual discontinuation should not lead to the relapse of severe mental illness – though it could lead to withdrawal symptoms.

Psychotropics are psychotropics; regular use of any of them brings about neurobiological adaptation, physiological dependence, and when drug steady-state drops too precipitously, their withdrawal syndromes have remarkably similar features.

As with other psychotropics, psychiatric drug withdrawal symptoms appear among neonates and animals, who have no capacity for expectancy bias or nocebo effect. They occur when people accidentally forget their drugs. They occur when people deliberately stop their drugs with full but misplaced confidence that they’ll be among those who get away with it.

Other post-drug syndromes – emotional anesthesia, sexual dysfunction, hypersensitivity, and neurological kindling – have been documented for many decades in the literature regarding discontinuation after chronic alcohol, opioid, benzodiazepine, and amphetamine use. They can be sequelae of any chronic psychotropic exposure.

Some may be related to homeostatic disruption in the discontinuation process, and therefore true withdrawal symptoms; in other cases, they may be tragically ineluctable consequences of long chronic drug exposure, which so often involves a history of fruitless dosage escalation, bumpy drug switches, forgotten doses, unsuccessful discontinuation attempts, and other neurobiological missteps.

No one knows, because aside from the recent interest in withdrawalology, in-depth investigations of these iatrogenic conditions are rare.

Psychotropic drug withdrawal syndromes offer ample opportunity for misidentification of equally enigmatic ME/CFS, POTS, post-viral syndromes, fibromyalgia, or FND. Throughout the withdrawal literature, including that by psychiatrists regarding antidepressants, common withdrawal symptoms and protracted withdrawal symptoms are described as autonomic. ME/CFS, POTS, post-viral syndromes, fibromyalgia, and FND also have autonomic features.

Differential diagnosis is essential in distinguishing withdrawal syndromes from FND or dysautonomias, which also fluctuate and can be drug-induced. Among the millions taking psychiatric drugs, certainly there are small numbers with any of these conditions, even some with brain tumors. Crucially, the chronology of dosage reduction indicates withdrawal symptoms. If they appear, you’d want to quickly reinstate a low dose of the suspect drug. In protracted withdrawal syndrome, you’d want to be very careful about drug interventions, which, due to withdrawal-induced hypersensitivity, might cause paradoxical reactions or neurological kindling.

How often does withdrawal syndrome occur after discontinuation of chronic psychotropics? In addiction medicine, it is presumed to occur so often that drug substitution is routinely utilized to avert it, while gradual tapering is recommended for benzodiazepines.

There is no reason to presume that antidepressants and other psychiatric drugs are exempted from the general consequences of psychotropic discontinuation. As with other psychotropics, when dosage is decreased, withdrawal syndrome is the horse, not the zebra.

We have no words

Always concerned with ontology and semantics, Dr. Aftab is correct that the vocabulary used in public discourse about prescribed drug withdrawal is confusing. Medical terminology itself is confusing, particularly in psychiatry and addiction medicine, the two medical specialties inescapably fixated on but eternally flummoxed by human nature.

Linguistically siloed, psychiatry itself is prone to paraphrases, poetic license, misnomers, misappropriations, and misinterpretations of pharmacological terms, such as “dependence”, evidenced by the vast numbers of synonyms listed in systematic searches for review articles.

Withdrawalology has made do with what it can find in the existing terminology. “Withdrawal” has long been used colloquially and medically as a noun for both the process and the consequence. However, across psychotropics, withdrawal clearly proceeds from a chronology after a psychotropic drug dose has been reduced or discontinued, whether the drug has been prescribed or not.

If the literature says “depression” is a possible withdrawal symptom, how does it differ from “relapse”? What does “rebound” mean? What is “protracted withdrawal syndrome”? Defined as following acute withdrawal, which is supposed to only last for a matter of weeks, it is scarcely detailed anywhere, though Lerner & Klein, 2019 listed 11 synonyms for it collected by SAMHSA.

Steering well clear of the acute phase, Chouinard and Chouinard (2015) somewhat arbitrarily put the start of protracted antidepressant withdrawal at 6 weeks of symptomology, with duration of “several months or more.” (Hengartner et al., 2020, of which I was a co-author, estimated median duration to be about 2 years.)

Surely observant clinicians have seen continuous withdrawal symptoms lasting more than 6 weeks – that would be protracted withdrawal syndrome. But how do patient reports of “delayed withdrawal” on social media make sense? In my experience, asking people more questions about their recent history usually revealed that “delayed withdrawal” was preceded by initial mild withdrawal symptoms, perhaps ignored, that had progressed to marked withdrawal syndrome. Due to withdrawal-induced hypersensitivity, one innocent glass of alcohol or a course of antibiotics or a strenuous workout session could trigger or revive more obvious withdrawal symptoms.

(There is also the possibility of individual neurology holding out against withdrawal-induced dysregulation for a time, but finally falling like a trail of dominoes into a more conventional pattern of protracted withdrawal syndrome.)

When human nature meets psychotropic drugs, we’re utterly in the dark, linguistically. No language has the words to describe the symptoms that patients feel when they experience an alien drug-induced neurobiological effect. They struggle to communicate and clinicians struggle to understand them.

Nebulous terms at best, “depression,” “anxiety,” and “anhedonia” only dimly convey withdrawal sensations. I made up the term “emotional anesthesia” to indicate a post-drug symptom that is distinct from the usual use of “depression,” drug-induced “blunting,” and “anhedonia.”

Dr. Aftab may have over-interpreted language that the withdrawal community uses on social media. The participants are doing the best they can, but they are mostly unaware of the existing literature about withdrawal. Like many researchers, they are describing the leg of the elephant closest to them, sometimes in detail that does not stand up to generalization.

Patients’ words are all that clinicians have to go on, and clinicians are confused. The haze around identification of withdrawal syndrome appears to be the appearance of emotional symptoms in the symptom lists. This carries over into research: even if physical withdrawal symptoms were present, Lewis, et al., 2021 put subjects with any appearance of emotional symptoms on the “relapsed” side of the ledger. This is a conceptual error leading to questionable conclusions.

It is a curious blind spot that psychiatry analyzes emotional symptoms out of context. In the midst of drug discontinuation, people may well react to odd symptoms with fear or distress – aside from actual withdrawal-induced emotional symptoms. If the chronology is pointed in the right direction and the patient reports odd physical symptoms, you’re seeing withdrawal whether emotional symptoms are present or not. If only emotional symptoms are present, differential diagnosis should presume the chronology is the key.

“Discontinuation” for antidepressant withdrawal syndrome is an unnecessary euphemism. Very widely used for centuries throughout medicine and society to describe what happens after people stop psychotropics, “withdrawal” will be in use forever. However, as various clinical interests converge on improving the process, the future of withdrawal studies will inevitably shift to “tapering,” a term that has gotten scant attention in medical education.

Start low and go slow

Even in 1904, Watson knew that he had to gradually wean Sherlock Holmes off cocaine over years. Systematically gradual tapering practices have never been applied to the newer psychiatric drugs. Perhaps it’s time to try something different?

Insisting on extensive data before psychiatry acts to recommend clinical deprescribing practices is an insurmountable barrier to addressing avoidable treatment risk affecting millions. With little inclination in the medical profession to study iatrogenic conditions, it is unlikely that large randomized controlled trials will define the process of psychiatric drug discontinuation. (The more recent ANTLER RCT, one of the few investigations that might have true withdrawal symptom data, summarized all their other patient-level data in Lewis, et al., 2021, but not the withdrawal data, which has been sequestered.)

Meanwhile, minimizing drug burden is simply good medicine, as the American Society of Clinical Psychopharmacology agrees.

If we truly want to improve outcomes, we shall have to make do with general medical and pharmacological principles, case reports, clinician experience, and common sense – like so much clinical practice does.

Mark Horowitz, co-author of The Maudsley Deprescribing Guidelines, has attempted to give clinicians some pointers. As he has specified repeatedly, his protocol for hyperbolic tapering is only a place to start. The receptor occupancy curves that he has so painstakingly mapped out allow all parties involved to visualize the process.

The Maudsley Deprescribing Guidelines’ more conservative recommendation is an initial reduction of 25% with smaller reductions from there. (An estimated 5-6 half-lives only reaches the threshold of the mean drug plasma steady-state plateau. Six half-lives plus a stabilization period at least as long between dosage reductions allows re-adaptation to a new lower steady-state, a homeostasis based on lower drug input, or, if you will, receptor occupancy. For psychiatric drugs dosed daily, I suggest this will be a minimum interval between reductions of about 2 weeks. However, re-adaptation is individual; making a reduction while the drug plasma level is still in flux or the patient reports withdrawal symptoms disrupts the re-establishment of homeostasis, elevating risk.)

If you’re a hyperbolic taper doubter, you can design your own nonlinear tapering schedule, as long as you maintain a tolerable drug plasma steady-state, stay in close communication with your patient, and correct course as needed to avoid withdrawal symptoms.

Any taper is better than no taper. Don’t do this:

• Tell your patient to simply stop taking their drug.

• Tell patients to “cut in half, then half again, then off” over a few weeks. These very instructions have driven hundreds of thousands to the withdrawal communities and social media.

• Tell patients to skip doses to taper. How could this even be considered when clinicians know it’s important to maintain drug steady-state?

All of the above are demonstrated failures that create outraged consumers. If 50% reductions are a bad idea, what’s left? Try more gradual reductions. Trial and error is a central tenet in psychiatric drug treatment. Embrace uncertainty. Modify as you get feedback from the patient. Don’t make your patients mad at you.

Expectancy bias goes both ways

All that psychiatry knows about SSRI withdrawal syndromes – the catalog of symptoms, the misinterpretation of acute withdrawal, the high expectation of relapse – comes from early trials that utilized abrupt cessation, placebo substitution, or inadequate tapering, yet almost never included protocols to identify withdrawal symptoms. (Not only were subjects in these trials generally antidepressant-naive, they had no expectation that the drugs might cause withdrawal syndrome.)

No conclusions about rate or relapse or withdrawal can be drawn from these compromised and confounded studies. There is no scientific basis for presuming that relapse is the usual outcome of discontinuation of prescribed psychotropics and withdrawal syndrome is uncommon.

The negativity that is visible in the withdrawal community on social media is a mirror image of clinicians’ expectancy bias. All that the withdrawal community knows about withdrawal comes from clinicians utilizing inadequate tapering practices, which from the patient point of view have produced disasters for many years. And that is why they radiate fearfulness and distrust.

The DSM already expects clinicians to differentially characterize subtle permutations of depression. If clinicians update their priors and stop conflating withdrawal symptoms and relapse, I predict tapers that are gradual and in collaboration with the patient will bring about very little real relapse and protracted withdrawal syndrome will become very rare.

Foster self-efficacy

It is an axiom in the mental health field that a strong therapeutic alliance produces better outcomes. The 2026 International Conference on Deprescribing (where psychiatry was hardly represented) featured a poster titled “Personality traits predicting benzodiazepine discontinuation failure in older adults.” The study found that no personality traits were germane but “discontinuation self-efficacy” was the strongest predictor of successful cessation, “consistent with evidence identifying perceived capability as a key determinant of deprescribing behaviour.”

For a successful discontinuation process, a positive attitude on the part of the clinician should facilitate patient self-efficacy – recognized as a central goal of mental health interventions.

Wherever people go, there they are. They’ll react to discomfort or pain in characteristic ways that are not necessarily pathological. Among the millions taking psychiatric drugs, some may be querulous, some may dramatize because they think they’re being ignored, some may expect bad things to happen, some may be inclined to the nocebo effect. Or, most likely, they may be reliable narrators. This is where a clinician who knows their patient and asks questions can calibrate — who needs reassurance, who needs the taper slowed, who needs both. If a withdrawal-induced symptom is suspected, stop or slow down the taper until vague symptoms resolve. Respecting the patient’s report and acting to reassure them if needed can only strengthen the therapeutic relationship.

Patient confidence in the process of deprescribing depends on the clinician’s skill and attitude. If the clinician radiates uncertainty about the deprescribing process and expects patient fragility and relapse, that will elevate patient apprehensiveness and corrode their confidence, producing worse outcomes.

Give consumers what they’re asking for: They want to go off their unnecessary drugs without having the risk of withdrawal syndrome hanging over them. Try gradual tapering with a positive attitude in cooperation with your patient! If it’s slow enough, what can you lose?

If you go slowly enough, you’ll be able to tell if your patient is in trouble. As you guide your patients off their drugs, if you have good communication with your patient, you should be able to forestall both withdrawal symptoms and relapse. This is your responsibility. If you see a lot of relapse, you’re doing it wrong.

It’s a consumer movement

Twenty years ago, as now, fear of and anger about withdrawal syndrome from inappropriate discontinuation techniques were fueling the patient complaints now being broadcast on social media. Theories about this movement being driven by ideology or outside agitators are an irrational defense.

The vast majority of people in these online communities would not know who Thomas Szasz is if he reared up from his cold, cold grave and bit them on the leg; they don’t read journal articles; and they have no ideology except the very human impulse of looking for someone to blame. People can avow any identity on social media, but there’s no reward in a “withdrawal identity” – there’s too much misery.

Except for those in forced treatment, every one of those consumers was once a hopeful patient. Now they’re customers who think they’ve been lied to. Their ranks are constantly replenished by what now amounts to treatment error. If clinicians stopped creating outraged consumers, there would be much less noise from social media.

If appropriate tapering methods were adopted, the picture of psychiatric drug withdrawal syndrome as a clinical and personal disaster would become history. There will be no resistance to this from the online “withdrawal community.” It’s an amorphous consumer movement, not a crazed monolithic beast.

No patient is going to stand in the way of clinical practice improvement.

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

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

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

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

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

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

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

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

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

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

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

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

How I Listen to My Voices’ Messages

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

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

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

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

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

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

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

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

What One of My Voices Says—A Miniature Case Study

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

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

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

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

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

Example One

Me (opening the conversation): Windy out.

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

Me: But what is this?

Her: Our forever cousin, our dark goodbye.

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

Example Two

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

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

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

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

Her: Rage makes us reticent in our worldview.

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

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

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

Example Three

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

Me: How will you help?

Her: Gentle guidance.

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

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

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

— , in conversation with

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The Epilepsy Comparison

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

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

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

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

Extending the Epilepsy Comparison

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

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

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

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

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

Enduring Disposition Towards Recurrent Psychosis

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

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

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

Psychosis as Multidimensional Space

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

1. Symptom dimensions

• a. Positive

• b. Negative

• c. Disorganization

• d. Affective admixture

• e. Catatonia

2. Course and staging

• a. Acute/chronic

• b. First-episode, recurrent, persistent

• c. Onset character (abrupt vs insidious)

• d. Premorbid functioning and prodromal decline

3. Cognitive functioning

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

4. Functional impairment and disability

5. Etiology

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

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

6. Treatment response

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

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

Where “Schizophrenia” Sits

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

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

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

Agreeing on the Contours

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

What is it doing there?

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

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

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

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

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

And what is it, anyway?

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

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

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

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

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

• (not suicidal)

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

• I wish I were dead

• I want to kill myself

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

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

• (dead)

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

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

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

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

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

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

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

How did it get there?

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

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

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

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

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

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

A taxonomy of post-discontinuation and withdrawal phenomena

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The withdrawal intellectuals

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

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

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

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

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

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

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

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

What do we really know?

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

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

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

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

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

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

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

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

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

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

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

The implausibility problem

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

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

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

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

The dogmas and unknowns of hyperbolic tapering

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

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

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

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

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

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

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

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

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

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

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

Some predictions, frankly speculative

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

There are two headline results:

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

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

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

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

The B-SNIP Project

Three methodological choices are key to B-SNIP.

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

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

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

• Stop Signal Task for motor inhibition;

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

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

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

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

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

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

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

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

B-SNIP and DSM Diagnoses

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

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

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

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

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

B-SNIP Biotypes

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

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

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

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

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

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

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

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

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

External Validation

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

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

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

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

Stability Over Time, and the Signal in Relatives

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

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

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

Clinical Recognition of Biotypes

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

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

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

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

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

Treatment Implications

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

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

An Analogy: Kidney Function and Insulin Resistance

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

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

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

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

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

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

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

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

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

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

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

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

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

The two key reference papers for my discussion are:

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

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

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

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

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

Book: Dad Brain

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

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

Concept: Facultative adaptation

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

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

Person: Sarah Hrdy

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

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

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

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

Surprise item: The prairie vole

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

See previous posts in the “Mixed Bag” series.

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

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

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

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

Getting the Order of Things Right

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

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

Clinical and Pragmatic Justification

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

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

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

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

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

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

The Scope of Institutions

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

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

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

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

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

Contingency Without Catastrophe

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

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

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

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

Communities as Justification

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

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

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

Pluralism

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

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

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

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

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

Where Things Go Wrong

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

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

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

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

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