Madness Revisited: Replies to Contributors

1.1 Madness as conceptual genealogy

At the outset of my book, I rejected the idea that Madness is an exercise in either the history of science or “conceptual genealogy”, by which I meant a project that purports to answer empirical-historical questions (e.g., “When did madness-as-dysfunction originate? How did it come to dominate mental health thinking today?”). The primary goal of my book is not to provide a causal explanation, nor is it to explain how the dysfunction-centered perspective has become so entrenched in today’s mental health thinking and practice. It is an attempt to use historical texts to construct new concepts: madness-as-dysfunction and madness-as-strategy. Of course, once these concepts are available, a historian may wish to use them to frame a proper historical narrative.

Yet Khalidi argues that, understood in a specific way—namely, in the way Foucault (1977) characterizes genealogy—my book is an exemplar of genealogy. I agree entirely with Khalidi that I was too hasty in rejecting the idea that the book may be a genealogy in some sense of that term. In rejecting that my book is a “genealogy”, I wanted to distance myself from a certain mode of philosophizing that is primarily causal-explanatory in its intent, in a way that is perhaps closer to what Queloz (2021) calls “conceptual reverse-engineering”. This is the sense of genealogy that I had taken from Nietzsche’s 1877 On the Genealogy of Morals. A conventional way of understanding Nietzsche’s work is that it sketches a causal-historical explanation for the existence of a distinctive (and, he thinks, distinctively perverse) value system that, roughly, equates “good” with weakness and “evil” with strength. For Nietzsche, the existence of this value system requires a historical account, much like how one might give a historical account of World War II, or the Irish potato blight of 1845.

I agree with Khalidi that if we construe genealogy from the standpoint that Foucault describes in 1977—as, in a sense, the precise antithesis of a historical account—as an attempt to provide not an origin story, but to disrupt the possibility of origin stories, to find multiplicity rather than singularity, and to demonstrate discontinuity rather than continuity—then my work comes much closer to genealogy.

Yet there is one aspect of Foucault’s characterization of genealogy that I want to resist. In some ways, my goal is the opposite of the one Foucault describes. If Foucault wants us to dissolve the unity of an origin into a multiplicity of competing goals, desires and agendas, I, in contrast, want to retrieve a certain conceptual unity from that apparent multiplicity. I want to emphasize the extent to which these texts, produced in different eras and motivated by different worldviews, form a surprising unity, “a secret resonance, a spiritual brotherhood” (Garson 2022a, 3), but one that is not connected by chains of influence. Whether we think of madness as a divine punishment designed to redeem fallen humanity, or as a compromise between conscious and unconscious desires, or as the working out of the vis medicatrix naturae, or an evolved adaptation, we are seeing teleology rather than dysteleology. It is in this sense that I think the modern evolutionary theory that depression is a designed signal is far closer to Robert Burton’s theological view of melancholy as a divine intervention than it is to the chemical imbalance theory of depression of the 1980s and 1990s. The reason it is difficult to see the conceptual continuity between these various texts is because we simply lack the concepts to.

1.2 Fanon and the biopsychosocial paradigm

I now turn to Khalidi’s invocation of Fanon, which aligns neatly with the social and political aims of my work. What I want to highlight is Khalidi’s insightful observation that for Fanon, madness does not merely have a political cause (even the proponent of madness-as-dysfunction will happily acknowledge as much), but more deeply, it can arise as a strategic response to that political situation. Khalidi helpfully points out that for Fanon, madness can be adaptive, functional, and purposeful, rather than as a pathology that happens to be “triggered” by external forces.

The mere idea that madness has a social cause (as Khalidi notes) has indeed been a part of traditional discourse, even reaching back before Fanon. My favorite example comes from George Cheyne, whose The English Malady of 1818 depicts melancholy as a response to British imperialism and, strangely enough, to the international spice trade. As I summarize his view

God uses melancholy as a signal “to draw our attention to the rebelliousness of our hearts” (Ibid.). This idea that madness has social causes is also alluded to, as Khalidi notes, in the more contemporary notion of a “biopsychosocial” paradigm (Engel 1977).

Yet, I think Fanon is doing something quite distinctive in the texts at issue, and it is a virtue of Khalidi’s discussion to draw it out. There are two very different claims that need to be separated when we say, as many do, that we need to better “understand the social causes of mental illness”. I think by confusing these two claims under the rubric of the “biopsychosocial” view, it has become too easy for psychiatrists and other mental health professionals to present themselves as being far more progressive and politically attuned in making sense of mental health problems than they really are.

The first claim is that social factors, such as poverty, migration, or climate change, can initiate a causal sequence that culminates in some kind of internal pathology (e.g., Jester et al. 2023). This is still an instance of madness-as-dysfunction, despite the fact that seeks the ultimate causes of madness in the social world. (In the context of the French occupation of Algeria, one might imagine a doctor saying, “It is so unfortunate that colonialism has broken the minds of young Algerians, making them hallucinatory, delusional, and aggressive.”) The problem is that this seemingly inclusive viewpoint doesn’t succeed in moving beyond the internalizing, pathologizing tendency of the biomedical framework as whole (Read 2005).

The second claim is that the symptoms of disorder—hallucinations, delusions, aggressiveness, paranoia, anxiety, and suicidal ideation—can be, in a sense, strategic responses to political situations. These are survival strategies, not brain defects—much less brain defects “triggered” by social causes. It seems to me that this is precisely what distinguishes Fanon’s vision from modern invocations of the “biopsychosocial” model. As Khalidi observes

What Khalidi articulates is not merely a recognition of the social dimension of mental health problems but an acknowledgment that these problems may be functional responses to the social situation, or, as Laing memorably put it, a “sane response to an insane world”. This is where we gain the full benefit of moving away from the individual pathologizing perspective toward sociocultural critique. You could say that both perspectives draw attention to social causation, but one still maintains a pathologizing tendency that the other abandons.

1.3 The (dis)unity of mental illness

I have less to say about Khalidi’s provocative suggestion that if we accept that some forms of madness (or, equivalently, “psychiatric condition”, “mental illness”, “mental disorder”) are in some sense “by design”, then that would fragment the very concept of madness. After all, many theorists, such as Boorse and Wakefield, have argued that the chief factor that unifies all of the diverse conditions we characterize as mental illness is that they stem from an underlying dysfunction, or a failure of something in the individual to “do what it is supposed to do”. This consideration leads Khalidi to suggest that, if some forms of madness are truly by design, we appear to abolish the very category of madness (“mental illness”, “mental disorder”, etc.) as a natural kind or even as a unified field of study. That, in turn, would raise a challenge to the very status of psychiatry as a branch of medicine: if mental illness is not a single kind, but a hodge-podge of conditions marked by vague intuitions about suffering, social deviance, or abnormality, then psychiatry has no proper object. (By the same token, there’s no such thing as a science of weeds.) And without a proper object, critics have no basis for reprimanding psychiatry for “overreach”. Psychiatry could neither succeed nor fail to stay within its bounds.

It’s worth noting that, in some ways, these provocative implications echo those raised by Thomas Szasz (1960). One way of reading his complex article is to see it as arguing that mental illness does not exist as a natural kind. Instead, “mental illness” is similar to “jade”, which refers to the disjunctive kind jadeite-or-nephrite. For Szasz, “mental illness”, similarly, lumps together two quite different categories. There are brain disorders, such as Alzheimer’s, which fall under the purview of neurology, and there are problems of living, which fall under the purview of psychotherapy. Lacking a unified domain, psychiatry dissolves.

Khalidi argues that we can rescue psychiatry from this unhappy fate. He points out that there are other domains of medicine that study diverse sets of phenomena, such as pediatrics. Yet perhaps I betray my Szaszian leanings by welcoming the conclusion that perhaps psychiatry should dissolve and be replaced by an array of specific mental health practices and interventions, such as peer support, psychotherapy, neurology, social work, and so on. If, as I argue (Garson forthcoming), psychiatry is essentially wedded to a dysfunction-centered framework—that is, if part of what makes psychiatry, psychiatry, is that it depicts mental health challenges as symptoms of disorders—then perhaps the needs of troubled people would be better supported by alternative interventions.

2.1 Points of Convergence

I want to applaud Palafox-Harris and Sullivan-Bissett for wading through the complex morass of terminology and concepts that have arisen regarding the understanding of function, dysfunction, and delusion. Not only do we have the distinction between madness-as-dysfunction and madness-as-strategy, but within strategy models, we also encounter the important distinctions between adaptation (evolutionary vs. ontogenetic, which can clash), adaptive (psychological vs. biological, which can also clash), and hybrid dysfunction/strategy models (such as a standard explanation for Capgras syndrome as involving a “functional” response to a perceptual “dysfunction”). To this complex landscape, Palafox-Harris and Sullivan-Bissett add a new distinction between “abnormal dysfunction” and “everyday dysfunction”.

The conceptual and terminological difficulties multiply when we consider the range of models of delusion, including predictive coding frameworks (of both dysfunction and hybrid dysfunction/strategy varieties), explanationist approaches (including one-factor and two-factor theories), traditional psychodynamic approaches, and phenomenological approaches. It’s not always clear how one ought to situate these theories in relation to one another.

Given the conceptual and empirical complexities we are navigating, I want to take a moment to step back and summarize the points of agreement between myself and Palafox-Harris and Sullivan-Bissett. This is crucial because it highlights what we all take to be the most important problem: how to ethically engage with those whose beliefs are labeled “delusional”, or, more tellingly, who are simply labeled “delusional” as persons.

I see three key points of agreement between Palafox-Harris and Sullivan-Bissett and myself. First, we agree that the paradigm I describe as madness-as-dysfunction, and what they describe as the “mere dysfunction” model, is deeply entrenched in current mental health orthodoxy. Despite the fact that for over two centuries, clinicians have regularly observed that delusions might, in some ways, be beneficial or even “designed”, psychiatry, and the mental health professions more generally, remain dominated by the dysfunction model. While there are a handful of voices emphasizing “strategy” approaches to delusions, including Fineberg and Corlett (2016), Sullivan-Bissett (2022), Isham et al. (2022), Ritunnano et al. (2022), López-Silva (2023), Bortolotti (2023), and Garson (2024a), they remain in the slim minority. When it comes to the issue of theory evaluation in the sciences, it is important not to pretend that strategy and dysfunction approaches to delusions are on a “level playing field”.

Secondly, we agree that delusions are functional in some clinically meaningful sense, and that this fact must be central to mental health practice. (What are the delusions “doing” for the patient? How can we take this “function” into account when crafting a treatment plan?) What we primarily disagree about is whether delusions are functional in the sense of being adaptations—a matter of biological design, or as I put it, the output of “mechanisms that are performing their evolved functions perfectly well”. They think the evidence against the adaptationist view is far stronger than I think it is.

Third, despite these conceptual and empirical puzzles of delusion, our primary mission is a moral one: how can we best avoid the systematic epistemic injustice that people labeled “delusional” are routinely subjected to? We must not only conceptualize delusions in a way that is empirically accurate, but also deeply respectful of the agency, humanity, and reasonableness of people who are ordinarily dismissed as “irrational”, “crazy”, or “not worth listening to” (Garson 2024c). In this connection, it’s noteworthy that in these scholarly discussions, such as the one we are engaged in here, people with delusions are generally the them (the object under discussion) in contrast to the us (we who are presumptively non-delusional, and thus possess enough sense to talk cogently about them).

My aims here are limited: I simply want to elaborate on my claim that delusions “could stem from mechanisms that are, in fact, performing their evolved functions perfectly well”. Despite their objections, I continue to think that, when properly articulated, this remains a viable starting point for approaching delusions. To properly articulate it, though, I must sketch the underlying theory of biological function that my work is rooted in. Because of space limitations, I won’t address Palafox-Harris and Sullivan-Bissett’s illuminating discussion of epistemic justice, except to note that I strongly agree that theorists have a deep ethical imperative to minimize epistemic injustice in all of its forms.

2.2 The prediction error model

Palafox-Harris and Sullivan-Bissett agree that there is some limited sense in which we can see delusions as “strategic”, but they believe we can acknowledge this without going so far as to say that delusions are a matter of biological design. Put differently, they wish to problematize the inference from strategy to adaptation. I agree that there is no easy inference from “delusions may benefit people in some way or another” to “delusions are adaptations, specifically shaped by natural selection to deliver a benefit”, or, even more weakly (and closer to my own view), that “delusions are the outputs of a cognitive mechanism functioning exactly as designed”. Adaptationist inferences are always risky in multiple ways (Garson 2022b, Chapters 3 and 4). But I don’t see any compelling theoretical or empirical reasons to take the adaptationist view off the table—for example, as suggested by Lancellotta (2022) in an essay entitled “Is the biological adaptiveness of delusions doomed?”

To survey the problems with adaptationist views, Palafox-Harris and Sullivan-Bissett consider two different approaches to delusion, the prediction error approach, and the explanationist approach. (While some might see the prediction error approach as a form of explanationism, they keep the two approaches separate.) The prediction error approach holds that delusions stem from some disruption to the “prediction error” signal, the signal that’s supposed to tell us whether our perceptual inputs conform to our top-down expectations about the way the world should be. The specific version of the prediction error approach endorsed by Fineberg and Corlett (2016), however, is quite complex. It depicts delusions both as a product of a dysfunctional prediction error, and also as performing a function—namely, the function of helping the individual conserve cognitive resources in a profoundly disorienting situation. In this way, their view embodies an intriguing mixture of dysfunction and strategy approaches.

Lancellotta (2022) has objected to their hybrid function-dysfunction model on the grounds that it is unnecessarily complex relative to mere dysfunction models, and Palafox-Harris and Sullivan-Bissett agree with her assessment. In Lancellotta’s view, a theory that accounts for delusions merely in terms of a dysfunction is simpler, and therefore preferable, to one that depicts delusions both in terms of a dysfunction and a function.

I found Lancellotta’s argument less than persuasive, for three reasons. First, Fineberg and Corlett are trying to reconcile over two centuries of clinical data (see references above) as well as their own empirical research, that shows that delusions benefit people in certain ways, and that these benefits seem to play some role in their “fixity”, that is, their resistance to counterevidence. Their hybrid dysfunction/strategy model is one way to reconcile this complex data. To get a parsimony argument off the ground, Lancelotta would have to show that the “mere dysfunction” model explains that data equally well, which I don’t think she does. (Incidentally, parsimony arguments are notoriously difficult to apply—see Sober and Wilson 1998, 291-295. Researchers who hold competing theories rarely agree on which is the simpler theory, which data those competing theories are meant to account for, and how to spell out the tacit ceteris paribus conditions.)

Second, there is nothing particularly surprising about the idea that the mind is replete with mechanisms that are, to put it colorfully, designed to fail. This is, of course, the chief theoretical innovation of Freud’s The Psychopathology of Everyday Life. There, Freud points to a wide range of such “designed failures”: forgetting, misplacing items, slips of the tongue. He calls all of them aptly Fehlleistung, a term that his biographer Ernest Jones unfortunately translated as “parapraxis”, but would be more accurately translated as “faulty performance”. Forgetting the name of an ex-lover can be seen as a minor breakdown of memory—after all, the whole purpose of memory is to retrieve facts and present them to consciousness. Yet, in another sense, it’s a designed breakdown. It’s a way of managing anxiety or grief. Self-deception, as Trivers (2011) famously argued, is another example of such a designed failure. True, it pays, evolutionarily, to have an accurate representation of your own abilities (for example, if you’re wandering into combat unprepared). But it also pays, evolutionarily, to have an inflated sense of your own capacities (for example, when it comes to taking on challenges that you would have otherwise avoided). There’s nothing ontologically profligate about seeing delusions as one more example of a “designed failure”.

Finally, I worry that Lancellotta overstates the distinction between psychological adaptiveness and biological adaptiveness. She points out correctly that even if delusions can improve one’s self-image, that doesn’t mean that they have fitness advantages that can be cashed out in terms of survival or reproduction—the only criterion that evolution really cares about. But on this score, I agree entirely with López-Silva’s (2023) recent observation that disentangling biological and psychological adaptiveness is actually quite difficult. This is because, as he points out (echoing Fineberg and Corlett 2016), delusions in the context of schizophrenia are often preceded by a “prodromal” period marked by an intense sense of disorientation. The delusion doesn’t just explain something that I’d otherwise find puzzling; it brings a kind of stability into my world that enables me to function well enough to meet my basic survival needs.

There is a second reason that it’s quite difficult to disentangle biological and psychological adaptiveness: one benefit of achieving psychological well-being, quite generally (that is, even outside the context of mental illness) is that it makes us less likely to commit suicide. Swanepoel and Soper (2025), building on Soper (2018), recently argued that suicide is a much more serious danger for our species than we typically realize. They think that any organism that possesses both the capacity to suffer, and the cognitive capacity to understand its own mortality, would consider hastening its own death as a solution to suffering. Consequently, they conjecture that evolution likely equipped us with a host of “anti-suicide” devices—cognitive quirks that prevent us from taking our own lives. Delusions, they conjecture, are just one of those designed “quirks”. By giving us a sense of understanding, self-worth, or purpose, they argue, delusions literally give us a reason for living.

2.3 The explanationist model

In explanationist models, delusions are considered to be explanations for anomalous perceptual experiences. Capgras delusion, for example, describes the belief that a loved one has been replaced by a perfect imposter. One prominent theory of Capgras is that there’s a dysfunctional communication failure between the perceptual and affective parts of my brain. That leads to an absence of an emotional response upon seeing my loved one. The patient then begins looking for explanations for this disorienting experience. The explanation that they arrive at: my loved one must’ve been replaced by a perfect imposter.

Explanationist models split into two-factor approaches, which depict delusions as resulting from both a perceptual dysfunction and a cognitive dysfunction, and one-factor approaches, which depict delusions as the output of a cognitive mechanism functioning fairly “normally” in the face of a perceptual dysfunction. Put differently, according to the one-factor approach, we don’t need to postulate any distinctive cognitive malfunction in order to understand why somebody would arrive at such an unusual belief. I had one-factor theories in mind when I wrote that delusions “could stem from [cognitive] mechanisms that are performing their evolved functions perfectly well [when confronted with such unusual perceptual data]”.

Palafox-Harris and Sullivan-Bissett still object to my way of putting things. Clearly, the delusional mind is not working “perfectly well”, cognitively speaking. If it were working perfectly well, then when faced with this perceptual anomaly, you would imagine the sufferer thinking something like this: That’s funny—I suddenly feel perfectly cold toward my wife. Perhaps there’s something wrong with my brain. Or perhaps I’m more ambivalent about our relationship than I was willing to acknowledge. Or perhaps she’s not actually my wife but a cleverly-designed impostor. At any rate, I should probably go see a neurologist or therapist before exploring this rather far-fetched theory.

I agree that such an inner monologue would be more epistemically ideal. But there’s a sharp distinction between the norms that govern our epistemic ideals, and the norms that govern (biologically) proper functioning. Perhaps the reasoning powers in the Capgras sufferer are less than “ideal” in some human sense. But that doesn’t mean they’re not functioning exactly as designed by evolution. In fact, I think one of the most striking findings of modern evolutionary theorizing, particularly as its embodied in the movement known as Darwinian medicine (Gluckman et al. 2009), and equally, the movement known as evolutionary psychiatry (Abed and St. John-Smith 2022), mechanisms operating “perfectly well” according to evolved norms of proper functioning can fall far short of what we might consider “ideal” in the modern world: a canonical example is our human proclivity toward sugary and fatty foods. A standard explanation for this contemporary ailment is that it represents the outcome of cognitive mechanisms functioning exactly as they are (evolutionarily) meant to despite the fact that, given that our modern environments are replete with such foods, that proclivity leads to suboptimal health outcomes.

For a more extreme and unusual example, consider the case of “imprinting gone awry”, a thought experiment devised by Jerome Wakefield (1999), which Fagerberg and Garson (2024) discuss at length. At birth, goslings have an imprinting mechanism—a neural device that’s meant to “imprint” upon the first large moving object the gosling sees. In the (statistically) ordinary case, the first large moving object the gosling sees will be its own mother. But if, by chance, a porcupine wanders through the gosling’s visual field during the imprinting period, the gosling will imprint on the porcupine. In this case, we insist, the imprinting mechanism is working exactly as designed, since it’s designed to imprint on the first large moving object you see. True, something isn’t going according to evolution’s plan, but we shouldn’t use the term “dysfunction” to describe that sort of wrong, as it would confuse many issues that deserve to be kept separate.

In sum, I’m happy to acknowledge that the move from seeing delusions as psychologically beneficial in some way, to the conclusion that they are evolutionary adaptations—either products of biological design, or outputs of systems working just as designed—is not beyond dispute. But I think it would be quite premature to take the adaptationist view off the table.

3.1 A scaffolding for Mad Pride

Núñez de Prado Gordillo centers his commentary on the political dimension of my book, particularly on the connections between madness-as-strategy and Mad Pride. I am grateful for the opportunity to expand my view slightly, as I only touch upon it in passing in the book. As I note there, there are four ways in which the dysfunction/strategy distinction can be useful: in its implications for history, philosophy, treatment, and Mad Pride:

I also write that, in the view of madness I endorse, “madness is not always a disease to be cured but a force of disruption to be reckoned with”.

I agree that these remarks are cryptic at best, and I sought to elaborate on them in another paper, “Madness and Idiocy” (Garson 2023). I’ll recapitulate the core idea here. My view is that, to the extent that Mad Pride takes inspiration from movements like Gay Pride, Black Pride, or Deaf Pride, it must start by rejecting a dominant cultural narrative about what it means to be gay, Black, or deaf. The very idea of Gay Pride makes little sense if one really thinks that being gay amounts to having a pathology of sexual orientation. Similarly, Deaf Pride makes little sense if one thinks that being deaf is merely a disease that the world would be better off without. The most obvious way to dislodge such pathologizing paradigms would be to replace them with an alternative paradigm that frames the issue in a more positive, empowering way. For example, one might say that being gay is just a variation in sexual orientation, like having freckles or a chin cleft, and variation is something to be celebrated rather than eliminated. Similarly, one might emphasize the way in which being deaf involves not (merely) a dysfunction, but an entirely different mode of engaging with the world that has value in its own right.

By the same token, if we want to promote Mad Pride, we must begin with rejecting the dominant cultural narrative that holds that the mad mind is a broken mind—a mind that fails to work as it should. That medical framing invites us to see madness—or its medically sanitized cousin, “mental disorder”—as a disease to be treated. At most, that framing gives us “mental health advocacy”, but falls short of Mad Pride. One way to shift the conversation away from pathologizing framings is simply to offer an alternative framing, one that’s more positive and empowering. Madness-as-strategy provides one such framing. As I put it, once we have the concept of madness-as-strategy at our disposal, “madness-as-dysfunction can no longer be a silent default in approaching the mad” (Garson 2022a, 260). For this reason, I called madness-as-strategy part of the “intellectual scaffolding” of Mad Pride.

I still agree with my assessment. But in retrospect, I think “scaffolding” is not an entirely apt metaphor, for two reasons. First, “scaffolding” is a temporary affair. It’s not a permanent part of the foundation of the building, but something to be thrown out after it has served its function. But I think of madness-as-strategy as a resource that we can draw on permanently, not merely as a conceptual tool to get us from one place to another, intellectually speaking. (It is not in that respect like Wittgenstein’s ladder, to be “thrown away” after it does its job.) In another way, however, “scaffolding” is too ambitious. Scaffolding is indispensable for constructing a building, like flour is indispensable for baking a cake. But I’m open to the possibility that there may be other empowering alternatives to the standard pathologizing framework. Perhaps a better way to describe madness-as-strategy is as a support beam for Mad Pride. It is part of the foundation of a building, but not the only thing that keeps the building up.

Of course, to depict madness-as-strategy as a support beam for Mad Pride raises the question of what other cogent alternatives there are for thinking about madness in a more empowering and positive way. What are some other “support beams”? Núñez de Prado Gordillo suggests that the emerging neurodiversity paradigm is a valuable alternative support beam. (He also sketches an alternative view, madness-as-right. Intriguing as it is, I will not have space to explore it here.) To suggest that madness-as-strategy and the neurodiversity paradigm are different, non-pathologizing alternatives to the default medical model, however, invites us to look more closely at how they relate to one another.

3.2 Madness-as-strategy and the neurodiversity paradigm

The rest of Núñez de Prado Gordillo’s commentary explores points of convergence and divergence between madness-as-strategy and the neurodiversity paradigm. I think he highlights real points of intersection and tensions between the two views. But before diving into these, I feel the need to clarify, a bit more rigorously, what I mean by madness-as-strategy and to highlight the diversity of specific approaches that fall under that general framework, as I believe he may be construing it too narrowly. This narrow construal is partly responsible for the appearance of tension.

Núñez de Prado Gordillo suggests that madness-as-strategy is equivalent to the idea that madness is a “natural reaction” to adversity, as memorably described by Shaughnessy, or as a “sane response to an insane society”, as Laing put it. He’s correct that those are the primary contemporary examples I focus on in my book. But the idea of madness as a “natural reaction” is merely one expression of madness-as-strategy among others. (For example, for Robert Burton, melancholy is a strategy, but it is not clearly a “natural response” to the trials of life, but a divine wake-up call.) In other places, I elaborate this point in more detail (Garson 2024b), where I envision three main expressions of this view in contemporary mental health:

The last of these three dovetails neatly, I think, with what Núñez de Prado Gordillo calls the “relational-ecological” model of neurodiversity, in which conditions like ADHD are construed as forms of cognitive diversity that “might be an adaptive feature for maximizing collective thriving and fitness”. So construed, there’s no discrepancy between madness-as-strategy and neurodiversity. This relational-ecological approach to neurodiversity can be seen as one expression of madness-as-strategy.

3.3 Does madness-as-strategy support the “normalcy” paradigm?

So far, Núñez de Prado Gordillo and I seem to agree. But he rightly identifies tensions between madness-as-strategy and certain formulations of neurodiversity. In particular, he raises the question of whether madness-as-strategy subtly reinforces the normalcy paradigm that the neurodiversity paradigm seeks to dismantle. As he puts it, madness-as-strategy seems to assume that there is

This is a complex question, and I don’t hope to entangle all its threads here. My current view is that there is a thick sense of normalcy that I reject, and a thin sense of normalcy that I accept. Put differently, I agree that my view could probably ground a rather thin sense of normalcy—but I do not think that is a bad thing.

Let me try to elaborate on what I take to be the core objection. We have a culturally-conditioned idea that certain ways of being or acting are normal (natural, good), while others are abnormal (unnatural, bad). For example, we tend to think that experiencing a moderate degree of low mood after losing a job is normal, but that experiencing incapacitating depression as a result of the same loss is abnormal. Moreover, the idea goes, medicine has a special responsibility to help people achieve normalcy.

Given all this, one might argue that the idea of normalcy is harmful, particularly for those who, by current social standards, are deemed “abnormal”. We might be better off without this idea and ought to be wary of philosophical attempts to reinstate it. Amundson (2000) articulates this line of thought quite elegantly.

With these ideas in mind, one might worry that madness-as-strategy is not a way of challenging normalcy but of reinstating it, and perhaps even giving it a solid philosophical foundation. To get there, I’ll use the example of depression and give a bit of background. I have argued that we should begin to see depression not as a pathology, but as a functional, adaptive, and perhaps even evolved response to adversity—something like the brain’s designed signal that something in the environment isn’t going well and needs more attention. I believe this paradigm shift is incredibly beneficial for both treatment and stigma (Garson 2024b). First, it helps us reorient treatment. If depression is a designed signal that something in one’s life isn’t going well, then it stands to reason that we should listen to what it’s trying to say, rather than bombard it with antidepressant drugs. Second, there’s emerging evidence that simply framing depression as a designed signal (rather than a chemical imbalance) benefits patients, as it gives them a greater sense of optimism about recovery (Kneeland, Schroder, and Garson in prep). Given these benefits, I actually think it would be morally pernicious for mental health providers not to make patients aware of this perspective (Garson forthcoming).

Of course, if there are functional forms of depression, then there may be dysfunctional forms as well—and indeed, they do seem to exist. Depression can arise not as a designed signal that something is wrong in one’s life, but as a consequence of a brain tumor or neurodegenerative disease. In these cases, depression may still have some value—for instance, as a diagnostic indicator or as an opportunity for personal reflection—but it doesn’t have the same sort of value that the functional kind has. (Recall that I do not entirely reject madness-as-dysfunction, and as I state in my book, I think there are likely cases in which this concept deserves to be applied—see Garson 2022a, 2).

Now, back to normalcy: I wouldn’t object if someone wanted to use the term “normal” for what I describe as functional. Millikan (1984) sometimes uses the term in this way. For her, the “normal” (or “proper”) function of, say, the kidney is to eliminate waste. Along those lines, I wouldn’t object if someone wished to describe depression as a “normal response” to certain kinds of adversity, such as social humiliation, if what they mean is that it is functional, i.e., it represents everything in the cognitive system working as designed. Using “normal” in this sense, we might also say that ADHD is an example of normal cognitive variation—it represents one way that the mind is designed to work, rather than a deviation from design. In contrast, a neurodegenerative disease like Alzheimer’s isn’t an example of “normal cognitive variation”; instead, it represents dysfunctional or pathological variation. Not only do I find this notion of normalcy unproblematic, but it’s hard for me to even imagine what biomedicine or psychiatry would look like if it tried to do without it.

Of course, sometimes the notion of “normalcy” is used in a much thicker, metaphysically and ethically inflated sense—to denote a property that is meant to be at once universal, natural, and inherently good. For example, if someone says that same-sex sexual attraction is “unnatural”, they presumably mean it in this thicker sense. I don’t believe in normalcy in that sense. Tumors, for example, are perfectly “natural”, in that they arise through the same natural processes as any other biological development. Moreover, there is nothing inherently good about a trait performing its function. Teen pregnancy, for instance, represents normal reproductive function, but it’s still something society might wish to discourage.

In short, I believe that there is a thin notion of normalcy, which is pretty much synonymous with proper function—a concept that is relatively unproblematic and may even be central to the aims of biomedicine and psychiatry. In contrast, the thicker, metaphysically and ethically inflated notion of normalcy does not correspond to anything real, and society would likely be better off without it. But it would not be fair to try to saddle madness-as-strategy with this thicker notion of normalcy.

4.1 The allure of madness

I’m incredibly grateful to Jeppsson and Lodge for their unique contributions to this symposium. Starting with the idea that madness can be a strategy—the mind’s wake-up call, a coping mechanism, and so on—they raise an important question: why couldn’t a mad person consciously choose to implement various strategies for dealing with their madness? In other words, once we consider that madness may be a strategy, it makes perfect sense to begin discussing the strategies we can consciously adopt to navigate mad experiences.

The theme that struck me most from their piece, particularly in their personal testimonies of madness, is the theme of madness’s allure—a theme I will briefly develop before addressing their individual narratives. Madness, when presented to us in the medically sanitized and safe guise of “mental disorder”, is almost universally framed in biomedical literature as something that happens to us. As I put it in the book, it is “an accident that happens from time to time and that tragically befalls an otherwise healthy person, a promising young man or woman” (Garson 2022a, 263). Arguably, this idea of passivity in relation to madness has been a cornerstone of the biomedical movement since its emergence in the 1980s, which became solidified in the 1990s, the so-called “Decade of the Brain”. One popular slogan at the time held that “depression is just like diabetes” or “schizophrenia is just like cancer”. Nobody chooses cancer or diabetes; they happen to us. This idea that we are passive in relation to madness remains central to many advocacy movements. For example, the National Alliance on Mental Illness (NAMI), in their anti-stigma tips, tell us that we should “encourage equality between physical and mental illness”.2 And as a recent billboard campaign sponsored by a mental health advocacy group, Bring Change 2 Mind, reminds us: “Imagine if you got blamed for having cancer”.

Within this political context, discussing the allure of madness is provocative, to say the very least. Some might even call it dangerous. After all, describing madness as alluring suggests we have a choice in relation to it. To depict madness as a temptation insinuates that we might have some capacity to choose—that we may have a certain degree of freedom with respect to our madness. Will we resist the temptation of madness or succumb to it? As Jeppsson and Lodge emphasize, many mad people confront this dilemma in a concrete way—for example, when considering whether to continue taking antipsychotic or mood-stabilizing medications, or to stop. This raises the prospect that the mad person could, in some sense, be morally accountable for their madness. Hence the risk.

Along with the risk, however, there is tremendous opportunity: by depicting madness as a temptation and foregrounding the role of choice, we highlight the role of agency, which some might read as empowering. The mad person is no longer the passive subject of their madness but rather has an opportunity to exercise agency in relation to it, and to select new strategies for navigating it.

I don’t have particularly insightful suggestions for steering through this fraught set of concepts: agency, blame, madness. However, I do believe that this is among the most urgent tasks confronting philosophers of psychiatry and madness, and I applaud Jeppsson and Lodge for bringing this to our attention.

I want to spend time reflecting on Lodge’s and Jeppsson’s accounts of their own madness, which I found rich and philosophically fruitful. This is not a matter of critique but of extending the conversation. My own view, which aligns with theirs, is that the exclusion of mad narratives from the discipline of philosophy—a discipline that always seems to exist at the precipice of madness—has deeply impoverished our field (Kusters 2020 develops this theme at length). I hope these brief comments will serve as a continued stimulus for new growth.

4.2 Manic subjectivity and hermeneutic injustice

Lodge uses his own experience of mania to home in on two aspects of mania that clinical classifications typically exclude. The first is what he describes as the expansion of manic subjectivity. This, he notes, can be read as a philosophical redescription of what’s colloquially described as an “inflated sense of self”—a sense of being confronted with more stimuli and ideas than one could possibly attend to. The expansion of manic subjectivity leads to the second aspect of mania: the individual seeks to render this enriched state of consciousness intelligible by drawing upon their existing, albeit crude, conceptual toolkit. Because our culture does not provide us with a sufficiently expansive toolkit for making sense these experiences, people often turn to conceptualizations deemed strange, bizarre, mystical, or even “delusional”.

For example, one rather obvious concept within our culturally-conditioned toolkit is messianism. Perhaps “manic subjectivity” describes what Jesus felt in the aftermath of his baptism by John, or during the Transfiguration, when Moses and Elijah themselves appeared in their glory to provide a cosmic download of information. (Richard Saville-Smith (2023) develops these religious themes brilliantly.) The notion that the interpretation of one’s manic subjectivity is somehow limited by one’s impoverished conceptual toolkit also echoes Sullivan-Bissett’s (2018) discussion of “one-factor” theories of delusions (much as I hesitate to use the term “delusion” to describe such exalted states of mind).

This idea that manic subjectivity must be articulated, however imperfectly, through a limited conceptual toolkit also offers a novel way of considering epistemic injustice—particularly the form of epistemic injustice that Fricker (2007) calls “hermeneutic injustice”, in contrast to testimonial injustice. Whereas testimonial injustice occurs when someone’s status as a knower is denigrated, hermeneutic injustice arises when someone is unfairly deprived of the concepts necessary to articulate their experiences. (Fricker’s primary example is the absence of the concept of sexual harassment in the 1950s and 1960s, which left victims without a way to accurately identify the specific wrong inflicted upon them.)

Viewed in this light, the connection between madness-as-dysfunction and hermeneutic injustice becomes apparent. By offering only a single dominant narrative to make sense of manic experiences—dysfunction, or “something seriously wrong in the mind”—we unfairly deprive people of alternative conceptualizations that might better serve their needs, both psychologically and existentially. (I explore these in Garson 2025c). These alternatives include trauma-centered explanations, internal family systems (IFS) models, spiritual paradigms, and others. Not only does the predominance of dysfunction-centered framings in psychiatry deprive us of these meaning-making alternatives, but it actively discourages them.

Finally, I want to highlight a connection that I’m sure Lodge has already considered, between the kind of crisis induced by a manic experience and the sense of forlornness that follows an LSD trip or other powerful psychedelic experience. How does one come to terms with that experience? How does one construct a metaphysical and ethical worldview adequate to it? Similar conversations took place in the United States during the height of LSD culture in the early 1960s (e.g., Lee and Shlain 1992; also see Kusters 2020).

4.3 Back to madness’s allure

Jeppsson has used her experiences to reflect on basic questions of epistemology, particularly the problem of external world skepticism (2022a; 2022b). How can we know that the external world—the mainstream world with its trees, houses, cows, grass, and the like—is real? Philosophers have invented a whole range of strategies to reassure themselves that the external world is, in fact, real, solid, and substantial, just as it appears to be.

I have learned quite a lot from Jeppsson’s work about the various strategies—no pun intended—that philosophers have employed to achieve such reassurance. One such approach, the Wittgensteinian strategy, posits that belief in the external world is not something that can be logically demonstrated but rather serves as a foundation for reasoning itself. Some epistemologists describe belief in the external world as a “hinge belief”, a special kind of belief that makes reasoning about anything possible (Pritchard 2021). To put this hinge belief into question is either incoherent (as Wittgenstein 1969 suggests in On Certainty) or self-defeating. Jeppsson has performed an invaluable service for philosophy by illustrating, through her experience of the demon world, that questioning the existence of the external world is neither incoherent nor self-defeating for reason. Moreover, I believe she has successfully argued that most attempts to respond to external world skepticism are, in one way or another, question-begging, in the sense that they rely on assumptions that the skeptic couldn’t reasonably accept.

What was particularly striking to me about Jeppsson’s testimony here, however, is the way she ties her reflections to the problem of madness’s allure. As she notes, unlike the delusional belief that a famous actress is in love with me, there doesn’t seem to be anything particularly alluring about the prospect that I’m living in a demon world. I think most of us, if presented with that possibility in the abstract (“If you take the red pill, you’ll live under the conviction that murderous demons are persecuting you”) would choose not to.

Yet, behind this initial revulsion lies a deeper allure. Who doesn’t want to be the main character in a cosmic drama? To occupy the center of a persecution narrative is to be somebody, and for many, being somebody is better than being nobody. Jeppsson’s insight, I suspect, could prove fruitful in helping us understand why so many people, when confronted with the following two possibilities—(1) nobody is after you; you simply have a brain disorder that makes you think people are after you versus (2) everybody is actually after you, and the sooner you embrace this truth, the more likely you are to survive—choose the second option. I am thinking here primarily about targeted individuals, that is, people who believe themselves to be victims of gang stalking or electronic harassment (e.g., Garson 2024a, Garson 2024c). In 2016, The New York Times estimated that there are about 10,000 people who identify as targeted individuals, but the number now is probably much higher. I believe we cannot entirely understand this puzzling sociological phenomenon without drawing upon Jeppsson’s and Lodge’s notion of allure.

Ultimately, what I want to emphasize about Jeppsson’s and Lodge’s insightful paper is that they truly demonstrate the payoff of mad philosophy. They illustrate how madness can serve as a disruptive force for philosophy. This is simply a more roundabout way of affirming that madness, indeed, has its benefits.