Psychopathy is often characterized in terms of what I call “the language of disorder.” I question whether such language is necessary for an accurate and precise characterization of psychopathy, and I consider the practical implications of how we characterize psychopathy—whether as a biological, or merely normative, disorder.

Psychopaths are agents who lack the normal capacity to feel moral emotions (e.g. guilt based on empathy with the victims of their actions). Evidence for attributing psychopathy at least in some cases to genetic or early childhood causes suggests that psychopaths lack free will. However, the paper defends a sense in which psychopaths still may be construed as responsible for their actions, even if their degree of responsibility is less than that of normal agents. Responsibility is understood in Strawsonian terms, (...) as a question of our appropriate reactive attitudes toward an agent for what she does, and as distinct from the question of the agent's own motivating attitudes, which lead him to do what he does. The latter is the question more directly relevant to free will, though moral motivation normally depends on the capacity in early childhood to pick up motivating attitudes from others' reactive attitudes. Reactive attitudes based on hatred rather than anger (e.g. disgust or contempt) count as alternative forms of blame that may be appropriately directed toward agents manifesting bad qualities of will, even as a matter of motivational impairment. So psychopaths may still be said to deserve blame, even if they are incapable of modifying their behavior in response to blame. (shrink)

This paper explores the phenomenology of the Capgras and Cotard delusions. The former is generally characterised as the belief that relatives or friends have been replaced by impostors, and the latter as the conviction that one is dead or has ceased to exist. A commonly reported feature of these delusions is an experienced ''defamiliarisation'' or even ''derealisation'' of things, which is associated with an absence or distortion of affect. I suggest that the importance attributed to affect by current explanations of (...) delusional experience can serve to make explicit the manner in which we ordinarily experience the world under a taken-for-granted aspect of affective familiarity. This implicit feeling is, I argue, partly constitutive of our sense of reality. However, so-called ''folk psychology,'' which is generally adopted by philosophers as an initial interpretive backdrop for delusional beliefs and for beliefs more generally, fails to accommodate it. As a consequence, some pervasive philosophical assumptions concerning the manner in which we experience and understand the world, ourselves, and each other are called into question. (shrink)

There are many interesting empirical and theoretical issues concerning the evolution of cognition. Despite this, recent books on the topic concentrate on two problems. One is mental modularity. The other is what distinguishes human from non-human minds. While it is easy to understand why people are interested in human uniqueness, it is not clear why modularity is the centre of attention. Fodor (2000) has a nice argument for why people _should_ be interested in modularity.

Though researchers working on congenital aphantasia (henceforth “aphantasia”) agree that this condition involves an impairment in the ability to voluntarily generate visual imagery, disagreement looms large as to which other impairments are exhibited by aphantasic subjects. This article offers the first extensive review of studies on aphantasia, and proposes that aphantasic subjects exhibit a cluster of impairments. It puts forward a novel cognitive theory of aphantasia, building on the constructive episodic simulation hypothesis of memory and imagination. It argues that aphantasia (...) is best explained as a malfunction of processes in the episodic system, and is therefore an episodic system condition. (shrink)

Jonathan Y. Tsou examines and defends positions on central issues in philosophy of psychiatry. The positions defended assume a naturalistic and realist perspective and are framed against skeptical perspectives on biological psychiatry. Issues addressed include the reality of mental disorders; mechanistic and disease explanations of abnormal behavior; definitions of mental disorder; natural and artificial kinds in psychiatry; biological essentialism and the projectability of psychiatric categories; looping effects and the stability of mental disorders; psychiatric classification; and the validity of the DSM's (...) diagnostic categories. The main argument defended by Tsou is that genuine mental disorders are biological kinds with harmful effects. This argument opposes the dogma that mental disorders are necessarily diseases that result from biological dysfunction. Tsou contends that the broader ideal of biological kinds offers a more promising and empirically ascertainable naturalistic standard for assessing the reality of mental disorders and the validity of psychiatric categories. (shrink)

Most mental disorders affect only a small segment of the population. On the reasonable assumption that minds or brains are prone to occasional malfunction, these disorders do not seem to pose distinctive explanatory problems. Depression, however, because it is so prevalent and costly, poses a conundrum that some try to explain by characterizing it as an adaptation—a trait that exists because it performed fitness-enhancing functions in ancestral populations. Heretofore, proposed evolutionary explanations of depression did not focus on thought processes; instead, (...) they emphasized that it facilitates navigation of adverse social circumstances or promotes immune response to infectious agents. According to a new hypothesis, the “analytical rumination hypothesis” (ARH), however, depression’s crucial adaptive trait is rumination—negative, intrusive thought. ARH holds that, (i) social dilemmas trigger depressed mood; (ii) depressed mood induces changes in body systems that facilitate ruminative analysis aimed at solving dilemmas; and, (iii) depressive rumination is a fitness-enhancing trait that was selected for in evolutionary time. Jointly, (i)~(iii) imply that we should not think of rumination as a disorder; instead, it is a trade-off, an eminently rational one. In the same way that fever solves a problem—coordination of the immune system in response to infection—so too does depressive rumination solve a problem, a social dilemma, albeit at the cost of inducing anhedonia and other maladies. But they argue that the cost is worthwhile, something that should be endured “until the problem is solved.” First, we argue that there are two distinct types of rumination, brooding and pondering; the former is associated with a disposition for depression, not the latter. But only the latter has the problem-solving capabilities that ARH requires. Second, recent brain imaging studies of depression reveal resting state hypoactivity in lateral regions and hyperactivity in paralimbic regions; this asymmetric pattern correlates with heightened levels of brooding, self-focused rumination. In other words, on the personal level, patients are trapped within self, isolated from the external world and suffused with negative affect; on the subpersonal level, this pattern is reflected by an asymmetric pattern of lateral vs. paralimbic resting state activity. Third, we proceed to conjecture that rational responses (e.g., pondering) to social dilemmas are those that strike a balance between internal and external considerations in the process of belief formation. Fourth, because the asymmetric resting state activity blocks those who suffer with depression from accessing and processing potentially positive stimuli from the external world, the capacity for rational, analytic response—hence, problem-solving—is constrained. Fifth, it follows that, although there might be conditions for which suffering should be endured rather than pharmacologically alleviated, depression is not one of those. Indeed, in view of the effects of the asymmetric resting state pattern, it is unlikely that depressive rumination would have been useful even for ancestral populations. (shrink)

In the last few decades, there has been a genuine ‘adaptive turn’ in psychiatry, resulting in evolutionary accounts for an increasing number of psychopathologies. In this paper, I explore the advantages and problems with the two main evolutionary approaches to depression, namely the mismatch and persistence accounts . I will argue that while both evolutionary theories of depression might provide some helpful perspectives, the accounts also harbor significant flaws that might question their authority and usefulness as explanations.

The concept of mental disorder is often defined by reference to the notion of mental dysfunction, which is in line with how the concept of disease in somatic medicine is often defined. However, the notions of mental function and dysfunction seem to suffer from some problems that do not affect models of physiological function. Functions in general have a teleological structure; they are effects of traits that are supposed to have a particular purpose, such that, for example, the heart serves (...) the goal of pumping blood. But can we single out mental functions in the same way? Can we identify mental functions scientifically, for instance, by applying evolutionary theory? Or are models of mental functions necessarily value-laden? I want to identify several philosophical problems regarding the notion of mental function and dysfunction and point out some possible solutions. As long as these questions remain unanswered, definitions of mental disorder that rest upon the concept of mental dysfunction will lack a secure foundation. (shrink)

I distinguish three evolutionary explanations of mental illness: first, breakdowns in evolved computational systems; second, evolved systems performing their evolutionary function in a novel environment; third, evolved personality structures. I concentrate on the second and third explanations, as these are distinctive of an evolutionary psychopathology, with progressively less credulity in the light of the empirical evidence. General morals are drawn for evolutionary psychiatry.

"Rationality: Contexts and Constraints" is an interdisciplinary reappraisal of the nature of rationality. In method, it is pluralistic, drawing upon the analytic approaches of philosophy, linguistics, neuroscience, and more. These methods guide exploration of the intersection between traditional scholarship and cutting-edge philosophical or scientific research. In this way, the book contributes to development of a suitably revised, comprehensive understanding of rationality, one that befits the 21st century, one that is adequately informed by recent investigations of science, pathology, non-human thought, emotion, (...) and even enigmatic Chinese texts that might previously have seemed to be expressions of irrationalism. Addresses recent challenges and Identifies a direction for future research on rationalityInvestigates the relationship between rationality and mental disorders, such as delusion and depressionAssesses reasoning in artificial intelligence and nonhuman animalsReflects on ancient Chinese Philosophy and possible cultural differences in human psychology Employs philosophical reflection, along with linguistic, probabilistic, and logical techniques. (shrink)

Mental disorders are often thought to be harmful dysfunctions. Jerome Wakefield has argued that such dysfunctions should be understood as failures of naturally selected functions. This suggests, implicitly, that evolutionary biology and other Darwinian disciplines hold important information for anyone working on answering the philosophical question, 'what is a mental disorder?'. In this article, the author argues that Darwinian theory is not only relevant to the understanding of the disrupted functions, but it also sheds light on the disruption itself, as (...) well as on the harm that attends the disruption. The arguments advanced here are partially based on the view that a core feature of Darwinism is that it stresses the environmental relativity of functions and dysfunctions. These arguments show a very close empirical connection between social judgments and dysfunctions, which is of interest for psychiatric theory. Philosophically, they lead to the conclusion that the concept of mental disorder is identical to the concept of mental dysfunction. Consequently, it is both misleading and redundant to conceptualize mental disorders as 'harmful dysfunctions', and not simply as 'mental dysfunctions'. (shrink)

Mental disorders are often thought to be harmful dysfunctions. Jerome Wakefield has argued that such dysfunctions should be understood as failures of naturally selected functions. This suggests, implicitly, that evolutionary biology and other Darwinian disciplines hold important information for anyone working on answering the philosophical question, ‘what is a mental disorder?’. In this article, the author argues that Darwinian theory is not only relevant to the understanding of the disrupted functions, but it also sheds light on the disruption itself, as (...) well as on the harm that attends the disruption. The arguments advanced here are partially based on the view that a core feature of Darwinism is that it stresses the environmental relativity of functions and dysfunctions. These arguments show a very close empirical connection between social judgments and dysfunctions , which is of interest for psychiatric theory. Philosophically, they lead to the conclusion that the concept of mental disorder is identical to the concept of mental dysfunction. Consequently, it is both misleading and redundant to conceptualize mental disorders as ‘harmful dysfunctions’, and not simply as ‘mental dysfunctions’. (shrink)

In this paper, I explain why evolutionary psychiatry is not where the next revolution in psychiatry will come from. I will proceed as follows. Firstly, I will review some of the problems commonly attributed to current nosologies, more specifically to the DSM. One of these problems is the lack of a clear and consensual definition of mental disorder; I will then examine specific attempts to spell out such a definition that use the evolutionary framework. One definition that deserves particular attention, (...) is one put forward by Jerome Wakefield. Despite my sympathy for his position, I must indicate a few reasons why I think his attempt might not be able to resolve the problems related to current nosologies. I suggest that it might be wiser for an evolutionary psychiatrist to adopt the more integrative framework of “treatable conditions”. As it is thought that an evolutionary approach can contribute to transforming the way we look at mental disorders, I will provide the reader with a brief sketch of the basic tenets of evolutionary psychology. The picture of the architecture of the human mind that emerges from evolutionary psychology is thought by some to be the crucial backdrop to identifying specific mental disorders and distinguishing them from normal conditions. I will also provide two examples of how evolutionary thinking is supposed to change our thinking about some disorders. Using the case of depression, I will then show what kind of problems evolutionary explanations of particular psychopathologies encounter. In conclusion, I will evaluate where evolutionary thinking leaves us in regard to what I identify as the main problems of our current nosologies. I’ll then argue that the prospects of evolutionary psychiatry are not good. (shrink)

The neurosciences are generating new findings regarding genetic and neurobiological aspects of the pathophysiology of mental disorders. Especially, certain genetic risk factors like neuregulin-1 seem to predispose individuals to a psychotic phenotype beyond the limits of traditional classificatory boundaries between organic psychoses in Alzheimer’s disease, bipolar affective disorder and schizophrenia. Little, however, is known about how such genetic risk factors actually confer an increased risk for psychosis in an individual patient. A gap between neuroscientific findings and psychopathological phenomena exists. The (...) main hypothesis how this gap may be bridged is that mental disorders arise as a consequence of dysfunctions of normal mental functions. Modularity may provide a useful conceptual framework in that temporally and/or spatially stable neural circuits subserve certain physiological functions of the human brain, which become the target of pathophysiological effectors. The idea of a modular construction of the human brain is based on neurobiological evidence regarding the columnar architecture of the cerebral cortex, which provides certain elementary analytical functions. Modular dysfunctions may be assessed with methods of experimental psychopathology, in which subsystems of brain functions are tested with standardized experimental psychological techniques (functional psychopathology). The main questions here are how to define a module, and whether the classical neuroscientific definitions can be used to characterize higher integrative functions of the human brain. (shrink)

In a series of recent works, Ian Hacking has produced a model of social causation in mental illness and begun to sketch in outline how this might be integrated with the medical model of psychiatry. This article elaborates and revises Hacking 's model of social forces, criticizes him for attempting a merely semantic resolution of the tension between the social and the biological, and sketches an alternative approach that builds upon his substantial insights.