Evolutionary psychiatrists invariably consider schizophrenia to be a paradox: how come natural selection has not yet eliminated the infamous ‘genes for schizophrenia’ if the disorder simply crushes the reproductive success of its carriers, if it has been around for thousands of years already, and if it has a uniform prevalence throughout the world? Usually, the answer is that the schizophrenic genotype is subject to some kind of balancing selection: the benefits it confers would then outbalance the obvious damage it does. (...) In this paper, however, I will show that the assumptions underlying such evolutionary accounts of schizophrenia are at least implausible, and sometimes even erroneous. First of all, I will examine some factual assumptions, in particular about schizophrenia’s impact on reproductive success, its genetics, its history, and its epidemiology. Secondly, I will take a critical look at a major philosophical assumption in evolutionary psychiatric explanations of schizophrenia. Indeed, evolutionary psychiatrists take it for granted that schizophrenia is a natural kind, i.e. a bounded and objectively real entity with discrete biological causes. My refutation of this natural kind view suggests that schizophrenia is in fact a reified umbrella concept, covering a heterogeneous group of disorders. Therefore, schizophrenia, as we now know it, simply doesn’t have an evolutionary history. (shrink)

I defend the historical definition of "function" originally given in my Language, Thought and Other Biological Categories (1984a). The definition was not offered in the spirit of conceptual analysis but is more akin to a theoretical definition of "function". A major theme is that nonhistorical analyses of "function" fail to deal adequately with items that are not capable of performing their functions.

In the first part of this article, I argue that Christopher Megone's natural-kind interpretation of Aristotle's argument that "the function of a human being is reason" does not resolve major puzzles about the argument, specifically the puzzles of why a human being has a function and why reason is that function. I attempt to resolve these puzzles by supplementing the natural-kind account with the doctrine that reason is the master regulatory natural function by which individuals enter into social life. In (...) the second half, I critique Megone's value account of function and argue for a nonevaluative, causal-explanatory account of function and teleological explanation. (shrink)

Emotions can be explained as specialized states, shaped by natural selection, that increase fitness in specific situations. The physiological, psychological, and behavioral characteristics of a specific emotion can be analyzed as possible design features that increase the ability to cope with the threats and opportunities present in the corresponding situation. This approach to understanding the evolutionary functions of emotions is illustrated by the correspondence between (a) the subtypes of fear and the different kinds of threat; (b) the attributes of happiness (...) and sadness and the changes that would be advantageous in propitious and unpropitious situations; and (c) the social emotions and the adaptive challenges of reciprocity relationships. In addition to addressing a core theoretical problem shared by evolutionary and cognitive psychology, explicit formulations of the evolutionary functions of specific emotions are of practical importance for understanding and treating emotional disorders. (shrink)

Sociopaths are “outstanding” members of society in two senses: politically, they draw our attention because of the inordinate amount of crime they commit, and psychologically, they hold our fascination because most ofus cannot fathom the cold, detached way they repeatedly harm and manipulate others. Proximate explanations from behavior genetics, child development, personality theory, learning theory, and social psychology describe a complex interaction of genetic and physiological risk factors with demographic and micro environmental variables that predispose a portion of the population (...) to chronic antisocial behavior. More recent, evolutionary and game theoretic models have tried to present an ultimate explanation of sociopathy as the expression of a frequency-dependent life strategy which is selected, in dynamic equilibrium, in response to certain varying environmental circumstances. This paper tries to integrate the proximate, developmental models with the ultimate, evolutionary ones, suggesting that two developmentally different etiologies of sociopathy emerge from two different evolutionary mechanisms. Social strategies for minimizing the incidence of sociopathic behavior in modern society should consider the two different etiologies and the factors that contribute to them. (shrink)

Most attempts to craft a definition of disease seem to have tackled two tasks simultaneously: 1) trying to create a series of inclusion and exclusion criteria that correspond to medical usage of the word disease and 2) using this definition to understand the essence of what disease is. The first task has been somewhat accomplished, but cannot reach closure because the concept of “disease” is based on a prototype, not a logical category. The second task cannot be accomplished by deduction, (...) but only by understanding how the body works and what each component is for, in evolutionary detail. An evolutionary view of the origins of the body and its vulnerabilities that result in disease provides an objective foundation for recognizing pathology. Our social definition of disease will remain contentious, however, because values vary, and because the label “disease” changes judgments about the moral status of people with various conditions, and their rights to medical and social resources. (shrink)

Schizophrenia is a worldwide, prevalent disorder with a multifactorial but highly genetic aetiology. A constant prevalence rate in the face of reduced fecundity has caused some to argue that an evolutionary advantage exists in unaffected relatives. Here, I critique this adaptationist approach, and review – and find wanting – Crow's “speciation” hypothesis. In keeping with available biological and psychological evidence, I propose an alternative theory of the origins of this disorder. Schizophrenia is a disorder of the social brain, and it (...) exists as a costly trade-off in the evolution of complex social cognition. Paleoanthropological and comparative primate research suggests that hominids evolved complex cortical interconnectivity (in particular, frontotemporal and frontoparietal circuits) to regulate social cognition and the intellectual demands of group living. I suggest that the ontogenetic mechanism underlying this cerebral adaptation was sequential hypermorphosis and that it rendered the hominid brain vulnerable to genetic and environmental insults. I argue that changes in genes regulating the timing of neurodevelopment occurred prior to the migration of Homo sapiens out of Africa 100,000–150,000 years ago, giving rise to the schizotypal spectrum. While some individuals within this spectrum may have exhibited unusual creativity and iconoclasm, this phenotype was not necessarily adaptive in reproductive terms. However, because the disorder shared a common genetic basis with the evolving circuitry of the social brain, it persisted. Thus schizophrenia emerged as a costly trade-off in the evolution of complex social cognition. Key Words: cortical connectivity; evolution; heterochrony; metarepresentation; primates; psychiatry; schizophrenia; social brain; social cognition. (shrink)

Suppose that the human tendency to think of certain actions andomissions as morally required – a notion that surely lies at the heart of moral discourse – is a trait that has been naturallyselected for. Many have thought that from this premise we canjustify or vindicate moral concepts. I argue that this is mistaken, and defend Michael Ruse's view that the moreplausible implication is an error theory – the idea thatmorality is an illusion foisted upon us by evolution. Thenaturalistic fallacy (...) is a red herring in this debate,since there is really nothing that counts as a ‘fallacy’ at all. If morality is an illusion, it appears to followthat we should, upon discovering this, abolish moraldiscourse on pain of irrationality. I argue that thisconclusion is too hasty, and that we may be able usefullyto employ a moral discourse, warts and all, withoutbelieving in it. (shrink)

This “open letter” to Christopher Boorse is a response to his influential naturalist analysis of disease from the perspective of linguistic-analytic value theory. The key linguistic-analytic point against Boorse is that, although defining disease value free, he continue to use the term with clear evaluative connotations. A descriptivist analysis of disease would allow value-free definition consistently with value-laden use: but descriptivism fails when applied to mental disorder because it depends on shared values whereas the values relevant to mental disorders are (...) highly diverse. A part-function analysis, similarly, although initially persuasive for physical disorders, fails with the psychotic mental disorders because these, characteristically, involve disturbances of the rationality of the person as a whole. The difficulties encountered in applying naturalism to mental disorders point, linguistic-analytically, to the possibility that there is, after all, an evaluative element of meaning, deeply hidden but still logically operative, in the concept of disease. (shrink)

This paper reviews the debate on the notion of biological function and on functional explanation as this takes place in philosophy. It describes the different perspectives, issues, intuitions, theories and arguments that have emerged. The author shows that the debate has been too heavily influenced by the concerns of a naturalistic philosophy of mind and argues that in order to improve our understanding of biology the attention should be shifted from the study of intuitions to the study of the actual (...) practice of biological inquiry. (shrink)

In this paper I defend an etiological theory of biological functions (according to which the proper function of a trait is the effect for which it was selected by natural selection) against three objections which have been influential. I argue, contrary to Millikan, that it is wrong to base our defense of the theory on a rejection of conceptual analysis, for conceptual analysis does have an important role in philosophy of science. I also argue that biology requires a normative notion (...) of a "proper function", and that a normative notion is not ahistorical. (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.

Species are thought by many to be important units of evolution. In this paper, I argue against that view. My argument is based on an examination of the role of species in the synthetic theory of evolution. I argue that if one adopts a gradualist view of evolution, one cannot make sense of the claim that species are units in the minimal sense needed to claim that they are units of evolution, namely, that they exist as discrete entities over time. (...) My second argument is directed against an appeal to Eldredge and Gould's theory of punctuated equilibria to support the claim that species are units of evolution. If one adopts their view, it may be possible to identify discrete temporal entities that can plausibly be termed species, but there is no reason to claim that those entities are units of evolution. Thus, on two plausible interpretations of the role of natural selection in the process of evolution, species are of no special importance. I then consider some of the reasons why species have been thought to be important evolutionary units by many contemporary evolutionary biologists. Finally, I discuss briefly the implications of this conclusion for evolutionary biology. (shrink)

The thesis that natural selection explains the frequencies of traits in populations, but not why individual organisms have the traits tehy do, is here defended and elaborated. A general concept of ‘distributive explanation’ is discussed.