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The promotional insert included in my review copy of David A. Kessler's Capture: Unraveling the Mystery of Mental Suffering, declares that it is "a book bolder than anything yet written on mental illness and suffering." Even by the standards of promotional hyperbole, this is a silly claim, and it takes only a little knowledge of the history of theory about mental disorder to see that it is plain false. The book's supposed boldness stems from its advocacy of a unified theory of mental disorder, one which claims that all psychiatric phenomena stem from a single type of cognitive cause. Kessler states the view as follows: "a stimulus -- a place, a thought, a memory, a person -- takes hold of our attention and shifts our perception. Once our attention becomes increasingly focused on this stimulus, the way we think and feel, and often what we do, may not be what we consciously want. I have termed this mechanism 'capture'" (7). There are two primary complaints to be made concerning the way the claim is presented. First, Kessler (along with the marketing team at Harper Wave, his publication house) seems to not know that the hypothesis that all madness is a form of monomania was quite popular among French physicians of the early 19th century (cf. Hacking 1990, chapter 8). He certainly never acknowledges that view or attempts to distinguish his own from it. Even so, this book is written for a popular audience and so it may be forgivable that his discussion of historical precursors is brief, confined to William James's account of attention and Freud's theory of drives. The second complaint is more consequential, for though he claims to offer a theory of mental disorder, one very quickly realizes that Kessler has no idea how to construct anything of the sort. Capture does not offer a theory of anything; it is a scattershot assemblage of anecdotes and case studies, with loose associations drawn between them and a dash of inconclusive neuroscience tossed in for good measure. This being the case, there is little to recommend in the book, either for those already familiar with the literature on the topic or those looking for an accessible introduction to it.
To explore the ways in which Capture fails to live to up to its billing, one must examine the conditions on its success, and so one should ask what a genuine theory of mental disorder ought to look like. A theory of a phenomenon does many things, but a minimal condition on the adequacy of any theory is that it explain why the phenomenon in question exists. On a view of explanation espoused by Van Fraassen (1980) and others, this entails contrasting that phenomenon to other relevant possibilities. So, for any phenomenon X that we wish to explain, it is not sufficient to merely give a causal account of X's origin; rather, the account must be such that it is clear why X obtained rather than some Y. Applying this insight to the explanation of psychopathology, it can be seen that to merely give a causal account of a disorder's characteristic symptom set is insufficient to explain the phenomenon. A true explanation of disorder will make clear that the causal agents appealed to had to (or at least were far more likely to) result in that disorder as opposed to some other, or, indeed, rather than some non-disordered psychological profile. This is not to say that one must draw an absolute, categorical distinction between mental health and mental disorder. The notion that there is a continuum between healthy and disordered psychology goes as far back as Freud (1901/1965) and has recently been taken up by new advocates (e.g. Bortolotti 2010). But the continuum view does not entail that there is no distinction at all to be drawn between the etiologies of individual disorders or between a disordered and a healthy mental life. It does say that the same behavioral or cognitive traits may be symptomatic of pathology in some contexts and relatively innocuous in others. And so a theory which posits a continuum between psychopathology and normal psychology had better give an account of the contextual factors which determine a trait's transition from personality quirk to symptom. A theory which cannot do that, or explain why symptom sets develop into characteristic groupings, is no theory at all. In order to be successful, Kessler would have to show that positing attentional capture as a common cause of all mental disorder is sufficient to explain the difference between disordered and healthy psychology, and to account for the array of distinct ways in which a person can be mentally disordered. Unfortunately, his theory is simply incapable of passing this test, as can be seen from examination of the case studies which constitute the vast majority of the evidence adduced in favor of his view.
Consider his example of manic psychosis, the American poet Robert Lowell (99-102). (Writers loom large in Kessler's case studies, with Kafka, Dostoyevsky, Plath, Sexton, Woolf, Hemingway, Robert Graves, Tennessee Williams, and William Styron also receiving cursory armchair analyses. David Foster Wallace -- American literature's tragic hero du jour -- earns a dedicated chapter and segments of others. By midway through Kessler's book, one might be surprised to hear of a distinguished writer from the past century who managed to make it through life untouched by the specter of psychopathology.) He suggests, without explicitly claiming it, that Lowell's mania was a function of the contents of his peculiar attentional fixation, specifically, absolute conviction in his own literary brilliance. Lowell, by his own account, had fallen under the spell of the delusion that he was recipient of a divinely ordained mission to rescue the United States from incipient degeneracy. Maybe it is true, then, that Lowell's inflated self-worth conditioned the contents of his delusion but his is still a classic case of grandiosity and not a particularly unique one. In fact, grandiose delusions manifest within a wide range of contexts that include mania like Lowell's, but also paranoid schizophrenia, a disorder with a much different affective profile. Nevertheless, Kessler writes as though conviction in one's status as redeemer of the union could not but fill one with such exuberant energy that one would necessarily go sprinting through the streets of Bloomington, Indiana, in the nude (99). If the causal account here seems spurious, that is because it should, but it is important to observe that it is the only one Kessler, having committed himself to the idea that attentional fixation is the ultimate cause of all mental disorder, could give to the question of why symptoms cluster together into the unique groups that they do. On his theory, every element of a disorder's characteristic symptom set must be seen as occurring after and because of attentional abnormality. Thus, his case studies are shot through with creative reinterpretation. He proposes that Anne Sexton's depression was the intermediate link between an unhealthy obsession with death and her eventual suicide (74-77), though it seems prima facie far more plausible that obsession with death was an effect of her depression which, in turn, helped bring about her suicide. Did Plath's obsession with her dead father (102-107) necessarily lead to her own depression and suicide? Kessler seems to think so, even though he expends several pages worth of words detailing Kafka's own paternal obsession, one which did not lead to suicide (48-51). Indeed, nowhere in his analysis is there any indication that Kafka was mentally ill at all, unless one counts as evidence the intuition that the mind which gave us such paranoid classics as The Metamorphosis and The Trial must have had something at least a little odd going on in it. Sure, the American painter Jay DeFeo spent eight years and nearly 2,000 gallons of paint on her masterpiece, The Rose (72-74), but so what? Did she at any point cross the threshold from good old-fashioned determination to realize her artistic vision into pathological fixation? Kessler gives us no clear indication that she did but he seems to think something unhealthy was up. What it was, we do not know. It is ironic that, when reading a book which presumes to shed light on a supposedly mysterious topic, one does not get very far before discovering that if Kessler is right then the phenomenon is far more mysterious -- and potentially intractably so -- than if he is wrong.
Again, it should be reiterated that I do not have a quarrel with the type of view that Kessler presents, but rather with the fact that he seems not to know what would counts as evidence in its favor. He can neither convincingly say how attentional abnormality characteristic of mental disorder is distinguished from the sort of monomania which is innocuous and perhaps even beneficial in the context of one's lifestyle, nor how symptom sets diverge across the spectrum of disorder. A similar problem is present on the few occasions when he takes a break from opining on the sad lives of the great writers -- or recounting the violent deeds of various religious fanatics, all of whom, alarmingly, have Middle Eastern-sounding names (184-204) -- to dabble in discussions of experimental evidence. Kessler seems to find it sufficient for his purpose to take notice of neurological similarities found across various different disorders. He observes that several are associated with dysregulated dopamine functionality and that dopamine has been hypothesized to underlie perception of environmental salience, which, in turn, can be understood as a key determinant of attentional direction (e.g. Kapur 2003; Howes and Kapur 2009). He is not on entirely shaky ground here; the connection between salience detection and motivational circuitry in addiction, for example, is well documented, and he is correct to point out that the most effective antipsychotic medications available work by modulating dopamine functionality. The problem with this evidence is that it is consistent with a vast array of roles for attentional abnormality in the etiology of mental disorder other than ultimate cause. Indeed, the very theory of psychosis he references for proof of the role of attention in the disorder postulates that delusions are formed rather late in its etiology, as a way for those who experience abnormal salience perception to understanding the resultant bizarre phenomenology. It is unclear whether Kessler does not notice that this way of conceptualizing the etiology of psychosis conflicts with his own view -- on which, to reiterate, any additional symptomatology must be "sequelae" to the contents of one's captured attention (118) -- or merely ignores the fact. Nevertheless, the conflict is there and provides ample reason to be skeptical of the view that he asserts.
Even if one is charitable to Kessler, acknowledging that he is right about the role of salience in psychosis -- he is -- and merely understands it in a naïve way -- he does -- there is still the problem of generality. Kessler claims that all mental disorder can be explained by capture, and this entails that all mental disorder ought to be equally receptive to the same sorts of treatment. Thus, having decided that salience detection and attention capture are the same thing, he claims, without citation, that anxiety and depressive disorders respond "equally well" to antipsychotic medications. This is followed with a recitation of the litany of conditions for which antidepressants have been approved. He does not mention that many therapies for mental disorder are more efficacious than medication and some of them are based on theories which place attention later in the etiological chain than his does. Consider exposure therapy for anxiety, which is based upon the idea that disordered anxiety results from learned fear responses and that such learning can be undone by new experience with the stimulus (cf. LeDoux 2015, chapter 11). Attention is, of course, involved in disordered anxiety, for once a person has been conditioned to perceive a stimulus as threatening, the reflexive anxiety response attendant to that stimulus will monopolize the person's attention. But this model posits heightened attention as an aftereffect of anxiety rather than its cause. One can put further pressure on Kessler's attempt at causal unification by observing that one would not prescribe exposure therapy to a person with depression. There the problem is not what associations one has learned for a stimulus, but the emotional valence with which it is perceived in the first place. Kessler is correct to point out the tendency among individuals with depression to ruminate on negative stimuli, but it is also true that they tend to interpret as negatively valenced stimuli which non-depressive people would consider neutral or even positive, and it is not obvious which of these phenomena, if either, has priority in the etiology of the symptom set. So, even if we could say for certain that the neural correlates of attention behave peculiarly in depressed people, this still would not be enough to show that attentional abnormality causes whatever symptoms follow. This is precisely the case for anxiety disorder. Considered out of context, we might find heightened activity in the neural circuitry of attention surprising and afford it a causal role in our theory of anxiety, but taken in the context of what we know from other avenues of research into the phenomenon, it is not surprising at all. Indeed, the evidence from exposure therapy tells us that even when we do correlate anxiety with the neural signature of attention, it will be a mistake to infer that such activity is the ultimate cause of the disorder.
It is a trope in books written for the popular science market, as this one was, to propose (or evangelize for) a unified theory of some phenomena previously believed to be disparate or irreconcilable. Sometimes such books are written by disciplinary insiders as primers on the current state of thought in their fields. Brian Greene's popular series on string theory is a case in point. David A. Kessler is not a psychiatric insider and, if anything, his overreliance on hastily interpreted anecdotal evidence suggests that he has little grounding in current research into mental disorder. Perhaps, though, the evidential problems of Capture can be forgiven and a broader lesson about theory building (in any area of science) can be taken from the book's failure. Unified theories are popular because they are elegant and reduce complex phenomena down to a manageable set of fundamental principles. But sometimes phenomena really are complex, and sometimes they are intractably so. For such phenomena, demystification depends upon acknowledgement of their intrinsic complexity, rather than manipulating them into prefabricated theoretical frameworks. Artificial simplification will simply serve to obscure their true natures. I suspect that this is the case for mental disorder, a broad category which includes a large array of psychological phenomena, some of which have common features and causes and some of which are quite distinct from one another. The threat of obfuscation is particularly dangerous for psychiatric phenomena because they cause pain, suffering, and, indeed, death. To effectively deal with mental disorder, it is necessary to have a clear understanding of its nature and causes. Books such as Kessler's, which are ill-informed and poorly conceived only detract from that aim.
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Howes, O. D., & Kapur, S. (2009). The dopamine hypothesis of schizophrenia: version III--the final common pathway. Schizophrenia Bulletin, 35(3), 549--562.
Kapur, S. (2003). Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia. The American Journal of Psychiatry, 160(1), 13--23.
Kessler, D. A., M. D. (2016). Capture: Unraveling the Mystery of Mental Suffering. New York: Harper Wave.
LeDoux, J. (2016). Anxious: Using the Brain to Understand and Treat Fear and Anxiety. New York: Penguin Books.
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© 2016 Christopher Parker
Christopher Parker, University of Cincinnati