Sense-Making and the Enactive Turn in Psychiatry: Sanneke de Haan, PhD

October 23, 2020
Awais Aftab, MD
Awais Aftab, MD

In this interview with Dr Aftab, Dr de Haan discusses her enactive approach to psychiatry which applies insights from enactivism to help conceptualize and navigate the immense complexity of factors that contribute to psychiatric disorders, and articulates the enactive view of psychiatric disorders as disorders of sense-making.

CONVERSATIONS IN CRITICAL PSYCHIATRY

Conversations in Critical Psychiatry is an interview series that explores critical and philosophical perspectives in psychiatry and engages with prominent commentators within and outside the profession who have made meaningful criticisms of the status quo.

Dr de Haan is a philosopher and postdoctoral researcher at Tilburg University, Netherlands, working in philosophy of psychiatry. Her main interests are the nature of psychiatric disorders, the existential dimension of psychiatry, and patients’ experiences and perspectives. She received her PhD in philosophy in 2015 from Heidelberg University. Her past research has included studies of phenomenological of experiences preceding the first episode of psychosis in individuals with schizophrenia and the effects of deep brain stimulation on patients with obsessive-compulsive disorder. Her current research is about self-illness ambiguity and relational authenticity in psychiatry. She is the author of Enactive Psychiatry (Cambridge University Press, 2020).

Enactivism is a theory of embodied cognition that characterizes the mind as Embodied, Embedded, Enacted, and Extended (described as 4E approach for that reason; or 3E if Extended is dropped from the list, as Dr. de Haan does). In her book Enactive Psychiatry, Sanneke de Haan applies insights from enactivism to conceptualize and navigate the immensely complicated factors that contribute to psychiatric disorders. According to the enactive view, psychiatric disorders are disorders of sense-making. Enactive Psychiatry is an impressive book, very well-written and remarkably accessible, and I reviewed it recently for Metapsychology (readers are encouraged to read my review here). Although some of the finest minds in philosophy of psychiatry have devoted themselves to integrating various perspectives and dimensions (such as neurobiological, phenomenological, socio-cultural, existential, etc. into a coherent whole, the problem has been hard to resolve satisfactorily without lapsing into covert reductionism, eclecticism, or pseudoscience. De Haan’s book is an admirable addition to this philosophical effort and has the potential, in my opinion, to dwarf all other competitor explanations. Given my admiration for and fascination with Dr de Haan’s work, I was delighted at the opportunity for this exchange.

Aftab: I hope that my review of your book Enactive Psychiatry can provide readers some context for this interview, but I think it will still be a good idea for us to start with an introduction to your enactive view of psychiatry. You describe psychiatric disorders as disorders of sense-making. Can you explain for the readers what you mean by that?

De Haan: A good place to start may be with my motivation to develop this enactive approach. I wanted to address psychiatry’s integration problem. It is among psychiatry’s main puzzles: how do the many factors that potentially contribute to the development of psychiatric disorders relate to and affect each other? This is particularly difficult because these factors are so heterogeneous, ranging from individual’s genes, neurotransmitters, and current stressors to childhood experiences and existential concerns. The integration problem forces us to get clear on the nature of psychiatric disorders. What does the “mental” in mental illness refer to and how does it relate to our bodies and our environments?

Reductionist accounts of psychiatric disorders solve the integration problem by assigning all causal power to 1 physiological factor, usually the brain or genes. This factor is assumed to underlie the others. Mental processes, for instance, are corollaries of neural processes. They do npt have any causal powers themselves. That is quite something to give up on. Also, this a priori singling out of the brain or genes as the only relevant causal power is a matter of a priori faith rather than empirical facts and does not seem to do justice to the complexity of psychiatric disorders. The biopsychosocial (BPS) model on the other hand has a clear holistic agenda but fails to deliver a proper account of how the bio, the psycho, and the social relate.

This is where enactivism comes in. Enactivism offers a promising account of how body, mind, and world relate. Instead of assuming that the mind/cognition is best understood as (passive) information processing done by the brain, enactivism takes a more biological approach and argues that cognition is the embodied and embedded activity of an organism in interaction with its environment. As living beings, we have vulnerable bodies that require a constant exchange with our environment in order to stay alive. It is thus of vital importance to make some sense of one’s environment: to distinguish food, danger, shelter, etc. According to enactivism, mind/cognition is this embodied and embedded action of sense-making, of evaluatively interacting with one’s environment. All living beings engage in some basic form of sense-making, and although the sense-making of individuals is special in many regards, it remains an embodied and embedded capacity. In order to understand the mind, then, we should recognize its fundamental ties to both body and world.

Applied to psychiatry, we can regard psychiatric disorders as disorders of sense-making: disorders of the way that individuals make sense of themselves and the world around them. In particular, psychiatric disorders refer to structurally disordered patterns of sense-making: typically biased or stuck in a certain direction, such as overly anxious, overly meaningless, or overly meaningful. Following this enactive perspective, psychiatric disorders are not exclusively in the brain, but the proper unit of analysis is rather the individual interacting with her world, plus the history of these interactions. Starting from this enactive view on sense-making and its relation to body and world, we can proceed to develop a solid, integrative account of psychiatry’s diverse aspects, without succumbing to reductionism, dualism, or vagueness.

Aftab: One thing I have become very conscious of after reading your book is of the use of the word “underlying” when it is used to describing the causes or mechanisms of disorders, and how talking about “underlying causes” biases us toward a vertical hierarchy in which we privilege neurophysiological processes. You write: “The vertical hierarchy implied by underlying causes invites a physiological reductionism: after all we never hear of research that aims to find the experiences that underlie certain neural phenomena.” Can you talk more about the dangers of thinking vertically and how enactive psychiatry takes a different approach?

De Haan: Yes, the notion underlying mechanism is used so often that it seems to refer just to what cognitive neuroscience does. But “underlying” implies an asymmetry: what is underlying is more basic than whatever rests on it. Like in a pyramid (a common form of depicting vertical hierarchies) the higher levels rest on and depend on the stones beneath, but the stones beneath do not in turn depend on the stones above. Since such underlying mechanisms are practically always assumed to be physiological processes, this talk indeed invites physiological reductionism.

One of the corollaries could be that we start to assume that the best way to treat psychiatric disorders is to direct our interventions at these underlying mechanisms: after all, we want to get to the root of the problem and not merely treat symptoms. Who wants to treat symptoms when you can treat causes? Now if all the separate symptoms can indeed be traced back to 1 underlying cause, like in a bacterial infection, treating this cause is indeed the most sensible thing to do. But what if psychiatric disorders are more complex than bacterial infections, what if 1 symptom induces or worsens the other(s)? And what if what is happening in the brain is only 1 of the factors involved instead of the core of psychiatric disorders? We are often inclined to assume that the smaller parts of a system have more causal power than the larger ones: a prejudice that Wilson called “smallism.”1 Such prejudices nicely tie up with reductionist accounts, but it is still only a prejudice.

An enactive approach advocates a dynamical, systemic perspective. The image here is that of a network rather than a pyramid. We can still discern a hierarchy between the elements or nodes of the network in that some nodes are more connected than others and thus more central. We can also still differentiate between different strengths of the relations between nodes. But the hierarchy is horizontal: no part of the network can be said to underlie the other parts, as the nodes are all (more or less strongly and more or less directly) connected. In order to capture the difference between more local and more global processes of the system, we can think of rings, or networks within networks, where global processes consist of several local processes.

Aftab: Individuals often think that one cannot be a neuro-reductionist if one upholds the biopsychosocial model. Although the biopsychosocial model does not imply reductionism by itself, the model, as it is commonly understood, can nonetheless be compatible with certain forms of neuro-reductionism. This is because one can maintain that psychosocial factors are relevant, but they have causal efficacy only by virtue of the fact that they influence the brain, and the real causal work is still being done by those neural changes rather than the psychosocial factors themselves. I find this sort of thinking to be quite prevalent among my colleagues. Why is such a view mistaken from the perspective of enactivism?

De Haan: Yes, I hear that a lot too. But it is a kind of cheating, of trying to have one’s cake and eat it too. Neuro-reductionism is actually quite a demanding position, in the sense that it comes at the cost of giving up on psychosocial factors being causally effective. This is a way to sneak them the psychosocial factors in through the backdoor. The idea is that if patients get a job, or a relationship, or if they succeed in changing their ways through psychotherapy and they subsequently recover from their problems, the real causal force is in the brain. These psychosocial changes affect the brain, and it is these changes in the brain that are the cause of their recovery. In this way one can seemingly commit to neuro-reductionism while also acknowledging the importance of psychosocial factors.

But this reasoning is flawed. It is like saying that the real cause of being drunk is not the beers I have been drinking, but what is happening in my brain. Surely, the alcohol affects my brain – as well as the rest of my body. But the intervention here is my drinking, and what happens in my brain and body results from that intervention. To call what is happening in my brain the cause of my drunkenness is mistaking a (part of) the medium for a cause. Everything we do changes our brains in more or less relevant ways. But that does not make our brains the cause of everything we do. Our brains rather reflect what we do. If you get a job and you subsequently feel better—also because jobs typically include financial benefits, social interactions, daily structure, and contribute to one’s self-worth—this may well be reflected in certain changes in the brain. But the difference that made the difference was getting that job.

Aftab: Although you reject mind-body dualism, you nonetheless maintain a distinction between somatic and psychiatric disorders, as different kinds of disorders that affect the same undivided individual. You write, “Psychiatric disorders are disorders of sense-making, while in somatic disorders this sense-making is only secondarily involved—if it is involved at all.” This distinction between primary and secondary disorders of sense-making makes me somewhat uncomfortable. You are careful to state that the distinction is not a matter of causes vs reasons. However, when you discuss this idea in detail, you say that various symptoms in brain diseases can be linked to a neurological problem, such as diminished dopamine production in Parkinson disease (PD), and “No such disturbance in the brain has been found for psychiatric disorders, despite all the research that has been done to try to find such ‘underlying mechanisms.’ And if we were to find such a neuronal mechanism, this would mean that we had been wrong to think that here we had a psychiatric disorder.” That sounds awfully like the functional-organic distinction (possibly even like the Szaszian disease vs problems-in-living distinction) and even though you say that the distinction is not based on causes, you nonetheless seem to be making that distinction, at least partly, based on whether a disturbance in the brain has been identified yet or not. Consider persecutory delusions in an individual with Alzheimer dementia vs persecutory delusions in an individual with schizophrenia. From my perspective, both instances of delusions are disorders of global sense-making, and these disordered states of sense-making are products of different causal trajectories (we know much more about the former than the latter) but why should that imply that we have to regard these 2 instances as fundamentally different kinds of disorders. Why not say that different disorders of sense-making have different causal trajectories and just leave it at that?

De Haan: I can see the appeal of your suggestion, but giving up on the distinction between somatic (including neurological) and psychiatric disorders does not foster our understanding of either of them, while trying to get clear on their differences does. I think the distinction matters. Take Nietzsche, for example. At the end of his life, he went mad. Was his madness caused by untreated syphilis or not? This seems a relevant question to me: syphilis-caused madness seems different from non-syphilis-caused madness. Or suppose my partner would become selfish and indifferent towards me. If we would find out he had a brain tumor, that would put his whole behavior in a different light. But why would that be? Is not the behavior the same?

I think the different causal trajectories of primary (psychiatric) and secondary (neurological) sense-making problems reflect that we are dealing with different kinds of problems that potentially call for different kinds of interventions. The problem is how to respect the difference between somatic and psychiatric disorders without turning this difference into a problematic duality between body and mind. This is where my own uneasiness with the distinctions you mention comes from. They all more or less strongly echo body-mind dualism by suggesting that we are dealing with 2 fundamentally different realms: separating a meaningless, causally determined body from a meaningful, reason-governed mind. This dualism makes them unhelpful if you instead think that body and mind are fundamentally integrated. So how do we make sense of the idea that psychiatric disorders are different from somatic disorders without resorting to dualism or without thinking that the errors of dualism should make us lose the distinction?

The central tenet of enactivism is the fundamental intertwinement of body, mind, and world. I am not suggesting that we can understand either the mind or the body in isolation from each other (nor from the interactions with the world). Somatic problems affect whole individuals, who feel and think and interact—just like psychiatric problems. Just like psychiatric problems, somatic problems often require a systemic approach that takes into account the individual in her world. I am all in favor of an enactive approach to general medicine too! Yet psychiatric and somatic disorders are different in that they refer to different types of problems of this single individual-world system. This system can be affected in different ways.

Psychiatric disorders are disorders of sense-making. They take place at the level of the individual interacting with her world. Psychiatric problems result from the difficulties that being an individual in the world imposes on us, and the self-preservation strategies we use in order to deal with these difficulties. Take your example of persecutory delusions. Speaking in very general terms, I would say that for someone who has schizophrenia, the pressure, the anguish of being an individual in the world, of trying to maintain themselves in their current situation, becomes so great that it induces a disruption of reality contact. Reality has become unbearable. For a patient with Alzheimer disease (AD), it is the dementia that has disrupted their contact with reality, and this in turn is the cause of their anxiety. Although they may both have persecutory delusions, the causal trajectories of their problem are different. In the case of AD or other neurological disorders, the sense-making problems arise from (local) brain problems, whereas in the case of psychiatric disorders the problems concern this global level of sense-making directly (typically including certain local effects too). Another way of putting this may be to say that while other disorders may have an effect on the mind, psychiatric disorders are disorders of the mind.

Psychiatric disorders are motivationally intelligible in a way that sense-making problems due to syphilis, AD, or brain tumors are not. By motivational I do not mean that patients act from deliberate, intentional, or even shrewd considerations. I just mean that the kind of troubles psychiatry deals with can at least partly be understood from the assumption that individuals are trying to somehow preserve themselves and may get stuck in rigid, often counterproductive, ways of interacting with themselves and/or their environment.

This difference between primary and secondary sense-making problems matters, not only for our (self) understanding, but also for our course of action. If someone has a psychiatric disorder, the problem is solved if they manage to rid themselves of their rigid patterns, if they manage to make sense of themselves, others, and the world around them in a more differentiated and flexibly attuned way. I am not saying it is easy, but practicing different sense-making is solving the problem. Using medication may be helpful, too, if individuals are too anxious to engage in therapy and practice different forms of sense-making this entails. If, however, someone turns out to have a brain tumor, he can try acting differently and engage in psychotherapy, but it will not solve the problem (even though it may still be beneficial in terms of insight and ways of coping).

Aftab: You say that neurological/somatic disorders consist of local disturbances that can add up to global sense-making problems, while psychiatric disorders are problems of global sense-making which also involve certain local neurological processes but are not really products of local brain disturbances. However, there is also a third possibility: local somatic disturbances might predispose an individual to global sense-making problems. These disturbances may increase the risk that one will develop a disorder, but they may be neither sufficient nor necessary to cause the disorder. For instance, functioning of thyroid gland in the subclinical or even lower normal range increases the probability that an individual will experience depressive illness, but this is neither necessary nor sufficient. Major psychiatric disorders can involve local as well as global disturbances in ways that seem to defy their simple categorization as somatic or psychiatric. This is also consistent with Ken Kendler’s view of psychiatric disorders as having a dappled distribution of causal risk factors across multiple levels of analysis.2 What are your thoughts on this?

De Haan: The crux here is that we are talking about physiological factors that may contribute to or play a role in the development of psychiatric disorders, but that are neither necessary nor sufficient causes. If these physiological disturbances were the necessary and sufficient causes of the sense-making problems, we would not be dealing with psychiatric disorders of sense-making, but with the secondary sense-making problems of a somatic disorder.

On the enactive view I am advocating, psychiatric disorders have 4 main dimensions: the physiological, experiential, socio-cultural, and existential. Physiological processes are clearly involved. The crucial question, however, is how they are involved. From an enactive perspective, psychiatric disorders cannot be reduced to any of these 4 dimensions: none of these dimensions can be understood in isolation from the other 3. Physiological processes can certainly play a role in the development and persistence of psychiatric disorders, but they are not the “core” or the “foundation”: psychiatric problems cannot be reduced to them. That is because the mind or sense-making is the capacity of an individual interacting with her world. Sense-making and its problems take place at a more global level than local physiological disturbances, even though they can obviously include such disturbances.

But should not such physiological predispositions be granted a bigger role than just being included as 1 of the dimensions of the problem involved? Does not this make psychiatric disorders a bit more like somatic disorders? I do not think so. The term “predisposition” has a bit of a deterministic tone to it, but, like you said, physiological vulnerabilities in themselves are not enough to explain the occurrence of psychiatric disorders. Besides, such vulnerabilities can of course be random bad luck, like a fault in one’s genes. But they may also themselves be the result of that individual’s previous interactions with their environment. A more strongly reactive amygdala can for example increase the risk of developing PTSD, but this may itself be the result of prolonged experiences of stress. Both the study of epigenetics as well as the brain’s plasticity force us to include interactions with the environment in the picture. On a developmental picture then, a (local) vulnerability may be the result of a (global) history of interactions. Besides, I do not see why physiological risk factors should have a special status compared to other risk factors: being poor, for instance, is also a predisposition to all sorts of psychiatric (and somatic) problems, and that does not make them purely socio-economic problems either. It is the (potential) interplay of factors from all 4 dimensions that characterizes psychiatric disorders.

Aftab: In the real world, the distinction between neurology and psychiatry is not based on some theoretical philosophical principle, but rather it is much more pragmatic and historically contingent, based on considerations such as the nature of symptoms, settings in which patients present for help, interventions available, and the necessary expertise needed to address the problem. That is why the DSM considers a diverse range of conditions, including substance use disorders, neurodegenerative conditions, and mechanical respiratory disturbances (such as obstructive sleep apnea) to be psychiatric disorders. When you distinguish between neurological and psychiatric disorders based on certain philosophical considerations, do you also intend to suggest that those philosophical considerations should override the pragmatic considerations that currently determine the separation and identity of neurology and psychiatry as 2 medical specialties?

De Haan: I am all in favor of pragmatic considerations: after all, we just want individuals to get the best treatment for their particular problems, in their particular situations. I do think, however, that our (often unarticulated) philosophical/theoretical assumptions inform our pragmatic considerations. Therefore, I think it is useful to be aware of one’s tacit assumptions as much as possible. This can also be helpful in collaborations, especially when the pragmatic considerations of those involved go into different directions.

Aftab: You write, “Psychiatric disorders are enacted: they dissolve if one succeeds in changing one’s way of interacting with the world, opening up one’s struck pattern of sense-making.” I see what you are saying, and it makes sense in a certain way. However, when it comes to chronic psychotic disorders such as bipolar disorder, it appears to me that one can successfully change one’s way of interacting with the world (ie, achieve remission from a manic or depressive mood episode) yet still continue to have the disorder in the sense that they remain at high risk of recurrence of future mood episodes and hence may require maintenance treatment. It would be odd to say that bipolar disorder has dissolved just because one is no longer experiencing active mood symptoms. What would you say to that?

De Haan: I see your point and I see why you would say “I have bipolar disorder” or “I have depression,” even if you are currently doing well. But it is important to acknowledge that at times of “remission” (a word that already implies there will be another depressive or manic episode in the future) you are not disordered: you are just like anyone else (who might also have 1 or more depressive or manic episodes waiting for them in the future). Your testimonial in court would be just as trustworthy, for example, and you are just as accountable for your actions. You just know that you are vulnerable. Knowing this has all sorts of implications, of course, but you are not at this very moment impaired in your sense-making.

Chronicity is a difficult issue in psychiatry. Unlike some chronic somatic conditions such as ALS or PD, for most psychiatric disorders one does not know at the outset if the condition will be chronic, if more depressive or manic or psychotic episodes will follow, or how long the obsessive-compulsive symptoms will remain. We call a disorder chronic if these episodes prove to be recurring, or if the problems remain for a long time. So, it is by looking back and being realistic about the future that we typically determine chronicity in psychiatry. I think it is important to be clear that by “chronic” in this context we mean being vulnerable and having a high risk, and to still differentiate between depressive or manic periods and the periods in which you are doing well.

Enactivists use a nice metaphor for what it means to enact something: they say you “lay down a path in walking.” Something becomes a habit or a pattern by repeatedly doing it, and once there is this path it is so much easier to walk that road again rather than go through all the trouble and hard work of making a new path. We slip into old patterns because they have become so engrained and come so naturally. Vulnerability is like having deeply engrained paths, making relapse probable, yet we are not destined to walk them.

Aftab: I really like your discussion of how “a cause is only a cause in a certain context.” The way we currently design intervention trials in psychiatry, for instance randomized clinical trials for psychotropics, there is a presumption that the therapeutic effect of the intervention is independent of the context of the patient. From an enactive perspective, how should we approach intervention trials differently so that we also take into account the role of the context? I understand you have been involved with clinical trials of deep brain stimulation (DBS). What have your observations been in this regard?

De Haan: There are many examples of the context-relativity of causes, both when it comes to causes for the development of psychiatric disorders (not all traumatic experiences lead to posttraumatic stress disorder [PTSD], for instance) and when it comes to treatment as well. DBS is indeed a good example of this. If we think of the effects of DBS treatment, we are inclined to give all merits to the electrical stimulation of a part of the brain. But DBS treatment consists of more than that: there is the context of being selected for an experimental treatment and of being closely monitored in weekly meetings. A randomized, controlled study by Dougherty and colleagues3 suggests an important placebo effect, as such contextual factors are typically called. Depending on the clinic, patients may also engage in some form of psychotherapy, which seems to have beneficial effects too.4 The DBS appeared to lower patients’ anxiety, which in turn allowed them to fight their compulsions with the help of therapy.5 Another interesting clinical impression was that patients who had more social support seemed to profit more from treatment than patients with less social support. I do not know if this has since been investigated, but these sorts of contextual factors may help to distinguish between the patients who profit from DBS and the patients who do not. It is a very common problem: how could we distinguish beforehand between the patients for whom intervention X works and those for whom it does not? Any kind of marker would be most welcome. Some such markers might be part of what we now summarize as the patient’s “context.”

Important as the context is, it will be very difficult to design intervention trials that take its role into account, as context is not a monochrome thing. For each patient, their context will be different, and different aspects of their context may be relevant to them. Still, it is important to try to get a better overview of relevant contextual factors. One way to do this would be to add a qualitative study to the protocol. For instance, by conducting in-depth interviews with a selected subset of the participants in order to detail some of the individual experiences behind the numbers. Qualitative research can provide context for the trial’s outcomes and help us understand the ways in which aspects that are not measured nonetheless potentially affect participants. Based on these findings, subsequent intervention trials could include the main relevant contextual aspects that emerged from these qualitative data. In DBS trials, for instance, a measure of (experienced) social support could be added, based on the clinical impression of its relevance for treatment outcome.

There is a limit to how many factors you can reasonably include in a trial, though, and individualsand their circumstances are different in so many ways that to some extent it will be unavoidable that treatment will have to include a kind of “individual trial,” set up by the individual patient and professional to find out what does and does not work for this particular individual in this particular situation. General findings remain important to feed into such personalized models, but I suspect there will always remain a gap between general knowledge and the idiosyncrasies of concrete individuals.

Aftab: You introduce the wonderfully illustrative analogy of a cake to explain organizational causality (readers can find a brief description of it in my book review). In a recent article for Philosophy, Psychiatry, & Psychology6, you contrast that with the analogy of a clock to represent linear causality. You argue that when we think of minds, we should think cakes, not clockworks. It is an appealing and elegant analogy. However, as you say in the book yourself, metaphors are never innocent and require eternal vigilance. What if the reality is more complicated than our choice of metaphors? What if the mind-brain system operates by more than a single form of causality and what if the reality is that it is like a cake in some respects and like a clock in other respects?

De Haan: Ha, good point! Your question has an empirical and a theoretical side to it, I think. But let me first say something about the metaphor and what work it does. Yes, metaphors are both important and dangerous because they shape what we see and what we go looking for in the first place. What I like about the cake analogy is that it provides an accessible way to understand the kind of non-linear causality that is at stake in mind-body causality. By adopting the kind of non-linear causality that characterizes complex, dynamical systems we can capture how the mind can affect the body (including the brain) and how the body (including the brain) can affect the mind and we can also explain the differences between these causal trajectories – all without relapsing into a mysterious dualism.

Now, linear causality is easy to understand. One thing works on the other (dominos, billiard balls, cogs) setting the other in motion in a linear sequence. But if we think of mind-body causality, we get confused about how a mental domino (a process in the mental realm) could possibly hit a physiological domino and vice versa. The assumption of crossing these different realms is so mind-boggling that it makes reductionism a more attractive option for many individuals. But, of course, reductionism has to sacrifice mind-to-body causality.

Non-linear causality on the other hand is much harder to grasp. Baking a cake is a good example though. As a fan of the Great British Bake Off show, I learned a lot about the intricacies of pastry and dough, the horror of soggy bottoms, and the complex interactions between the cake’s ingredients and such matters as kneading time and oven temperature. The cake’s ingredients (the amounts of flour, fat, sugar, eggs, moist, etc) affect the pastry and the eventual taste of the cake after baking. But these ingredients do not work on the cake like a domino hitting the next: they affect the cake by being part of it. A change in the amount of sugar for instance is a change of the cake as a whole. This is an example of what we could call a local-to-global effect. Such effects typically have thresholds: adding a grain of sugar will not be noticeable in how the cake tastes, but adding an extra cup definitely will. Similarly, when we put the pastry in the oven, it is not as if the heat changes the cake and this in turn affects the ingredients it has been made from. The heat rather affects the cake as a whole. Such global-to-local effects may also differ depending on the parts involved: the cake can be burned before it is cooked.

I think we can understand the relation between mind and body in a similar way. This starts with a shift in thinking from mental and physiological processes as different realms or systems to taking the unitary system of an individual-interacting-with-her-world as central. Physiological and mental processes refer to different excerpts of this single system, more local or more global processes of this system (typically also operating at different timescales). A change in one’s serotonin level for instance can affect one’s mood, in a similar way as a change in the amount of sugar can affect the taste of the cake. A change in one’s mood includes certain physiological changes, like the temperature of the oven affecting the pastry and the ingredients it is made of. There is a difference between local-to-global and global-to-local organizational causality, these are different causal trajectories, and yet no mysterious connection point between different realms has to be assumed.

To get back to your question: the theoretical issue at stake is whether it makes sense to assume some form of linear causality between mental and physiological processes. I do not think it does, simply because I do not think mental and physiological processes can be opposed in this way. Instead of assuming a “mind-brain system” as you call it, I would say there is an individual-in-her-world system, of which the brain is a local part, while the mind is a global property of the individual.

Still, this leaves open the possibility that some aspects of this single person-in-her-world system, some isolated physiological processes for instance, may well work in a linearly causal way. That is the empirical matter. It will depend on the kind of issue you are interested in and the level of analysis that best corresponds with that issue. To what extent is it useful to look at such local physiological processes in isolation from the global processes in which they are embedded?

Aftab: According to your enactive view, none of the 4 dimensions of sense-making is more fundamental than any of the others, since they refer to different excerpts of the same system. However, there may be a sense in which the physiological may be more fundamental than the experiential. I’m referring to Jonathan Schaffer’s notion of “metaphysical grounding”7, which conceptualizes dependence claims in the form of X grounds Y. One could argue that the mental depends on the physical, ie the physical grounds the mental. Does the metaphysical dependence of the experiential on the physiological pose any challenge to your view that no dimension is more fundamental than any of the other?

De Haan: There is no such metaphysical grounding of the experiential on the physiological! In fact, the enactive view poses a challenge to exactly that assumption. Physiological processes depend just as much on experiential processes as the other way around. That is the main point of the enactive life-mind continuity thesis.

It is important to distinguish between the physical and the physiological. Physical stuff was there first, and physical stuff is everywhere. There must be physical stuff for there to be living beings. Conversely, physical stuff does not require living beings to be there. So there is an asymmetry between physical stuff and living beings. (I am reluctant to use the grounding metaphor here, as it may bring along all sorts of connotations that I would like to avoid.) Yet the mere existence of physical stuff alone is not sufficient for life to emerge. According to enactivism, living beings are characterized by a specific organization of matter: they are self-organizing unities in that they actively maintain their own boundaries by interacting with their environment. In contrast to physical stuff, living beings rely on a constant exchange with their environment in order to maintain themselves. So, while physical refers to stuff in general, physiological refers to matter in the specific organization of living beings. Because living beings depend on interactions with their environment in order to keep existing (by feeding, breathing, disposing of waste, etc.) they need to make some sort of basic sense of their environment to distinguish what is eatable and what is dangerous, for instance. Without such basic sense-making of their environment, organisms would die. In other words, because living requires interacting with an environment, it requires sense-making. There is no life without mind: living beings are sense-making beings, minded, or minding beings. None of the 3 elements involved is more fundamental than the others. A living being depends on its body, mind, and interactions with the world.

While the existence of living beings depends on the existence of physical stuff, the matter of living being, physiological processes, depends just as much on sense-making or mind as the other way around. Flour alone does not make a cake. Sure, there are moments at which we are alive without experiencing something, because we sleep or fainted or are unconscious. But at some point, we need to get up and eat and drink something in order to stay alive.

The assumption that physiological processes are somehow more fundamental than experiential (mental, psychological) processes is deeply entrenched in our thinking. But as long as you hold on to this assumption, you will be stuck with a reductionist picture of reality, with all the downsides and unsolved mysteries that picture brings along. Solving the mind-body problems without resorting to either reductionism or dualism requires us to shift from a 2-place relation to a 3-place relation and to acknowledge that the body depends on mind and world, and the mind depends on body and world.

Aftab: Thank you!

This interview is first of a pair of interviews on the topic of enactive psychiatry; you can read the companion interview with Kristopher Nielsen, PhD, here.

The opinions expressed in the interviews are those of the participants and do not necessarily reflect the opinions of Psychiatric Times.

Dr Aftab is a psychiatrist in Cleveland, Ohio, and clinical assistant professor of psychiatry at Case Western Reserve University. He is a member of the executive council of Association for the Advancement of Philosophy and Psychiatry and has been actively involved in initiatives to educate psychiatrists and trainees on the intersection of philosophy and psychiatry. He is also a member of the Psychiatric Times Advisory Board. He can be reached at awaisaftab@gmail.com or on twitter @awaisaftab.

Dr Aftab and Dr de Haan have no relevant financial disclosures or conflicts of interest.

References:

1. Wilson, R. Boundaries of the Mind. Cambridge University Press; 2004.

2. Kendler KS. The dappled nature of causes of psychiatric illness: replacing the organic-functional/hardware-software dichotomy with empirically based pluralism. Mol Psychiatry. 2012;17(4):377-388.

3. Dougherty DD, Rezai AR, Carpenter LL, et al. A randomized sham-controlled trial of deep brain stimulation of the ventral capsule/ventral striatum for chronic treatment-resistant depression. Biol Psychiatry. 2015;78(4):240-248.

4. Mantione M, Nieman DH, Figee M, Denys D. Cognitive-behavioural therapy augments the effects of deep brain stimulation in obsessive-compulsive disorder. Psychol Med. 2014;44(16):3515-3522.

5. de Haan S, Rietveld E, Stokhof M, Denys D. Effects of deep brain stimulation on the lived experience of obsessive-compulsive disorder patients: in-depth interviews with 18 Patients. PLoS One. 2015;10(8):e0135524.

6. de Haan, S. Enactive causality: interventions, cakes, and clockworks: a reply to allagher and Donovan and Murphy. Philos Psychiatr Psychol. 2020;27(1):31-33.

7. Schaffer J. Grounding, transitivity, and contrastivity. In: Correia F, Schneider B, eds. Metaphysical Grounding: Understanding the Structure of Reality. Cambridge University Press; 2012:122-138.