Douglas proposes a new ideal in which values serve an essential function throughout scientific inquiry, but where the role values play is constrained at key points, protecting the integrity and objectivity of science.

The Description for this book, Theory and Evidence, will be forthcoming.

This fascinating study in the sociology of science explores the way scientists conduct, and draw conclusions from, their experiments. The book is organized around three case studies: replication of the TEA-laser, detecting gravitational rotation, and some experiments in the paranormal. "In his superb book, Collins shows why the quest for certainty is disappointed. He shows that standards of replication are, of course, social, and that there is consequently no outside standard, no Archimedean point beyond society from which we can lever (...) the intellects of our fellows. "- -Donald M. McCloskey, Journal of Economic Psychology "Collins is one of the genuine innovators of the sociology of scientific knowledge.... Changing Order is a rich and entertaining book. "- - Isis "The book gives a vivid sense of the contingent nature of research and is generally a good read. "- -Augustine Brannigan, Nature "This provocative book is a review of [Collins's] work, and an attempt to explain how scientists fit experimental results into pictures of the world.... A promising start for new explorations of our image of science, too often presented as infallibly authoritative. "- -Jon Turney, New Scientist. (shrink)

This book presents the concept of “complementary science” which contributes to scientific knowledge through historical and philosophical investigations. It emphasizes the fact that many simple items of knowledge that we take for granted were actually spectacular achievements obtained only after a great deal of innovative thinking, painstaking experiments, bold conjectures, and serious controversies. Each chapter in the book consists of two parts: a narrative part that states the philosophical puzzle and gives a problem-centred narrative on the historical attempts to solve (...) the puzzle; and the analysis part which provides in-depth analyses of certain scientific, historical, and philosophical aspects of the story. (shrink)

Here the distinguished philosopher Ian Hacking uses the MPD epidemic and its links with the contemporary concept of child abuse to scrutinize today's moral...

This book introduces a new approach to the issue of radical scientific revolutions, or "paradigm-shifts," given prominence in the work of Thomas Kuhn. The book articulates a dynamical and historicized version of the conception of scientific a priori principles first developed by the philosopher Immanuel Kant. This approach defends the Enlightenment ideal of scientific objectivity and universality while simultaneously doing justice to the revolutionary changes within the sciences that have since undermined Kant's original defense of this ideal. Through a modified (...) Kantian approach to epistemology and philosophy of science, this book opposes both Quinean naturalistic holism and the post-Kuhnian conceptual relativism that has dominated recent literature in science studies. Focussing on the development of "scientific philosophy" from Kant to Rudolf Carnap, along with the parallel developments taking place in the sciences during the same period, the author articulates a new dynamical conception of relativized a priori principles. This idea applied within the physical sciences aims to show that rational intersubjective consensus is intricately preserved across radical scientific revolutions or "paradigm-shifts and how this is achieved. (shrink)

True to his longstanding bias against grand unifying theories, Hacking chooses to pursue these questions by focusing on a specific case of memory-thinking: the history of multiple personality. His excavation of the contemporary terrain leads him, however, to the surprisingly grand conclusion that the various sciences of memory—including neurological studies of localization, experimental studies of recall, and studies in the psychodynamics of memory—all emerged in connection with attempts to “scientize the soul,” as a result of which spiritual battles have been (...) recast as scientific controversies “where we suppose there is such a thing as knowledge to be had”. (shrink)

Surprisingly, modified versions of the confirmation theory (Carnap and Hempel) and truth approximation theory (Popper) turn out to be smoothly sythesizable. The glue between the two appears to be the instrumentalist methodology, rather than that of the falsificationalist. The instrumentalist methodology, used in the separate, comparative evaluation of theories in terms of their successes and problems (hence, even if already falsified), provides in theory and practice the straight road to short-term empirical progress in science ( à la Laudan). It is (...) also argued that such progress is also functional for all kinds of truth approximation: observational, referential, and theoretical. This sheds new light on the long-term dynamics of science and hence on the relation between the main epistemological positions, viz., instrumentalism (Toulmin, Laudan), constructive empiricism (Van Fraassen), referential realism (Hacking, Cartwright), and theory realism of a non-essentialist nature (constructive realism à la Popper). Readership: Open minded philosophers and scientists. The book explains and justifies the scientist's intuition that the debate among philosophers about instrumentalism and realism has almost no practical consequences. (shrink)

The pivotal problem of comorbidity research lies in the psychometric foundation it rests on, that is, latent variable theory, in which a mental disorder is viewed as a latent variable that causes a constellation of symptoms. From this perspective, comorbidity is a (bi)directional relationship between multiple latent variables. We argue that such a latent variable perspective encounters serious problems in the study of comorbidity, and offer a radically different conceptualization in terms of a network approach, where comorbidity is hypothesized to (...) arise from direct relations between symptoms of multiple disorders. We propose a method to visualize comorbidity networks and, based on an empirical network for major depression and generalized anxiety, we argue that this approach generates realistic hypotheses about pathways to comorbidity, overlapping symptoms, and diagnostic boundaries, that are not naturally accommodated by latent variable models: Some pathways to comorbidity through the symptom space are more likely than others; those pathways generally have the same direction (i.e., from symptoms of one disorder to symptoms of the other); overlapping symptoms play an important role in comorbidity; and boundaries between diagnostic categories are necessarily fuzzy. (shrink)

Psychiatry has long struggled with the nature of its diagnoses. This book brings together established experts in the wide range of disciplines that have an interest in psychiatric nosology. The contributors include philosophers, psychologists, psychiatrists, historians and representatives of the efforts of DSM-III, DSM-IV and DSM-V.

In lieu of an abstract, here is a brief excerpt of the content:About and Beyond Comorbidity:Does the Crisis of the DSM Bring on a Radical Rethinking of Descriptive Psychopathology?Massimiliano Aragona (bio)Keywordscomorbidity, nosography, phenomenology, philosophy of scienceThe problem of psychiatric comorbidity is part of a series of difficulties of the current diagnostic system which at once were considered as a consequence of the way the system itself is organized (Aragona 2006). It was then believed that a Kuhnian reformulation of the contemporary (...) debate on the problems of the psychiatric diagnosis was very useful because it allowed clarification in a comprehensive picture of the many rivulets of conceptual research in that field.In their comments Zachar (2009) and Banzato (2009) seem to agree with my analysis of psychiatric comorbidity (Aragona 2009a) when it stresses that abnormally high frequencies of co-occurrence are to be explained, in important respects, as a consequence of the way mental disorders are operationalized in the Diagnostic and Statistical Manual of Mental Disorders (DSM; also showing the importance of conceptual clarification to deal with this sort of only apparently pure factual problems). On the contrary, they are both unconvinced of the appropriateness and/or fruitfulness of the use of the Kuhnian technical terms and theory in this context.It could be said that the major aim of the paper was to let clinicians understand the effect of conceptual decisions on what would otherwise seem as a simple empirical finding (in this case, high levels of comorbidity), and that this result seems to be achieved in any case, thus minimizing the importance of a disagreement about the philosophical terms as a pure terminological dispute. Nevertheless, in my work the Kuhnian model had a significant role in the clarification of this matter and it also suggests to the reader a range of possible consequences that are not trivial (Zachar, for example, says to be skeptical about the possibility of a crisis and also about the possibility that a new paradigm could eliminate what I call the [End Page 29] comorbidity anomaly). As a consequence, some of the Kuhnian concepts that seemed to be at odds in this context have to be considered in detail to justify my analysis and its consequences. For reasons of space, I avoid a point-by-point reply to all the comments and I concentrate my discussion on three main points. First, I discuss the background of Kuhn's definition of terms such as anomaly and paradigm, as well as my own reasons for using them. In doing so the details of the psychiatric items under study that I wanted to highlight through the use of these philosophical concepts should emerge more clearly. Second, I discuss the problem of having distinguished between artifactual and real comorbidity. Third, I reconsider some of these problems, looking for their implications for future psychopathological research.Anomalies and ParadigmsBanzato (2009) stresses that comorbidity cannot be a truly Kuhnian anomaly because it is an anticipated side effect of the initial setup of the DSM, and not some unexpected discovery that violates the paradigm-induced expectation. This is a basically correct account of the most known version of Kuhnian anomalies; that is, the tale of some evident nature's failure to conform to clear paradigm expectations, which immediately forces researchers to recognize its importance as a possible source of crisis. However, as is the case for many other Kuhnian terms, he discussed anomalies in several scripts and there are other possible versions of its meaning. In particular, Kuhn (1977, XVII) highlighted that only in very rare cases are anomalies completely unexpected and come out of blue to announce an imminent crisis that leads to a large revolution. More frequently, scientific revolutions are much more smaller, like the discovery of oxygen, and in these cases the process is so gradual that historians find it difficult to say exactly when a discovery was made and who did it. Even in these much smaller cases the usual prelude to changes of this sort is the awareness of anomaly, but here anomalies are not extraordinary events; rather, they are "countless discrepancies between theory and experiment [that] during the course of his career, every natural scientist again and again notices and passes by" (Kuhn... (shrink)

Cramer et al.'s critique of latent variables implicitly advocates a type of scientific anti-realism which can be extended to many dispositional constructs in scientific psychology. However, generalizing Cramer et al.'s network model in this way raises concerns about its applicability to psychopathology. The model could be improved by articulating why a given cluster of symptoms should be considered disordered.

In lieu of an abstract, here is a brief excerpt of the content:Psychiatric Comorbidity:More Than a Kuhnian AnomalyPeter Zachar (bio)Keywordscomorbidity, classification, epidemiology, differential diagnosis, personality disorderDr. Aragona's article in this issue of Philosophy, Psychiatry, & Psychology makes some important points regarding the relationship between comorbidity rates and the classification system currently used in psychiatry. Particularly persuasive is his claim that observed patterns of comorbidity are, in important respects, consequences of the structure of the classification system. I am not convinced, however, (...) that comorbidity is best conceptualized as an artifact of the taxonic structure of the Diagnostic and Statistical Manual of Mental Disorders (DSM) and the International Classification of Diseases (ICD). Instead, I suggest that the use of dichotomies such as true versus artifactual should be used with caution when psychiatric classification is being discussed.In contrast with the artifact hypothesis, I argue that the phenomena covered by the term "comorbidity" are real, expectable features of the psychiatric domain. They are not the phlogiston and luminiferous ether of psychiatry. I am skeptical of the notion that high comorbidity rates as a whole can be understood as Kuhnian anomalies, or that there is a crisis, or that after a period of revolutionary science a new paradigm would eliminate these 'anomalies.' In short, high rates of comorbidity in psychiatry will not simply disappear once scientists develop a better nosological paradigm. High levels of comorbidity can, however, be both lowered and provided a better, evidence-based conceptual framework.Many Conditions, One OrganIn general medicine, comorbidity conventionally refers to the simultaneous occurrence of two independent disease processes or distinct clinical entities, such as heart disease and liver cancer (Feinstein, 1970; Jablensky 2004). The presence of one disease is supposed to affect the other in such a way that the co-occurrence of the two has implications for prognosis and treatment.Comorbidity in psychiatry is a broader concept, referring to a variety of conditions that overlap in multiple ways. The different kinds of overlap are amenable to detailed empirical analysis (e. g., Klein and Riso 1993; Neale and Kendler 1995). Depressive reactions to primary disorders, attention deficit symptoms associated with mania, panic attacks in the context of severe borderline personality disorder, substance abuse disorders among psychopaths, histrionic dynamics combined [End Page 13] with narcissistic personality traits, and emergent conditions such as schizoaffective disorder are all distinct types of comorbidity. The kinds of overlapping conditions just listed are sometimes termed psychiatric comorbidity. Also important is comorbidity between psychiatric disorders and general medical conditions as is studied in behavioral medicine and health psychology. The crisis, if there is one, is a crisis of comorbidities.The heart disease and liver cancer type of comorbidity as independent organ systems being affected is ruled out a priori in psychiatric comorbidity proper. In psychiatry, "psychopathological disease processes" can all be expected to affect a single organ, namely the brain or, more likely, affect the different systems that are tightly integrated in the brain. The tight integration can make putative comorbid psychiatric disorders difficult to disentangle.It is a widely held consensus that causes, not organ systems, are what matter in comorbidity. In this tradition, Dr. Aragona claims that in general medicine shared symptoms between two diseases (such as fever and fatigue) are not a problem because the diseases are differentiated with respect to etiology; in psychiatry, however, where syndromes are differentiated by a description of symptoms only, symptomatic overlap is a problem.Is descriptive psychopathology, therefore, a root cause of the "crisis of comorbidity" and should it be abandoned in favor of etiological classification? Unfortunately, forcing psychiatric nosology to conform to an etiological paradigm is unlikely to resolve the problem of psychiatric comorbidity. As noted, the problem is one of distinguishing between the different etiological disease processes that are affecting tightly integrated systems in the brain. The brain as a whole is a multilevel, dynamic, and open system, which has an ecology (Zachar 2000). As argued by Kendler (2005) and Schaffner (2002, 2008), it has not thus far, and may never be fully possible to segregate causes and their associated psychiatric disorders into parsimonious etiological packages. In the ecology of neuroscience, causes and effects tend to merge in a continuous series of common pathways.It would be foolish... (shrink)