After describing the disorder of psychopathy, I examine the theories and the evidence concerning the psychopaths’ deficient moral capacities. I first examine whether or not psychopaths can pass tests of moral knowledge. Most of the evidence suggests that they can. If there is a lack of moral understanding, then it has to be due to an incapacity that affects not their declarative knowledge of moral norms, but their deeper understanding of them. I then examine two suggestions: it is their deficient (...) practical reason or their stunted emotions that are at fault. The evidence supports both explanations. I conclude with an overview of the debate concerning whether they are morally or legally responsible for their actions. (shrink)

RésuméContrairement à ce que pourrait donner à penser la these de E. Mayr sur ľimportance actuelle des explications évolutives en biologie, par opposition aux explications fonctionnelles, ľauteur soutient que, pour ľépistémologie de la causalité, le second type ?on;explication reste plus significatif que le premier. II tente de le montrer en reprenant brièvement son analyse des travaux de P.E. Pilet sur les inhibiteurs de croissance , telle qu'elle a ete présentée dans quatre articles antérieurs.SummaryStarting from E. Mayr's distinction between functional and (...) evolutionary explanation, the author suggests that, as far as the epistemological analysis of causality is concerned, the former type of explanation remains of more interest than the latter. He illustrates this claim by briefly taking up his philosophical and logico‐linguistic study of P.E. Pilet's work on growth inhibitors in the field of plant growth regulation, which was presented in a series of four previous papers.ZusammenfassungVon E. Mayrs Unterscheidung zwischen funktionaler und evolutiver Erklärung ausgehend, weist der Autor nach, dass die erste Art der Erklärung in bezug auf die erkenntnistheoretische Analyse der Kansalität mehr Bedeutung hat. Er versucht aufgrund seiner früheren Analysen von P.E. Pilets Schriften über Wachstumsinhibitoren auf dem Gebiet der Wachstumsregulation von Pflanzen diese Auffassung zu erhärten. (shrink)

I raise a puzzle case for “cluster” accounts of natural kinds—the homeostatic property cluster and stable property cluster accounts, especially—on the basis of their expected treatment of the metaphysics of certain disease kinds. Some kinds, I argue, fail to exhibit the co-instantiated property clusters these cluster views take to be constitutive of natural kinds. Some genetic diseases, for example, have archetypical instances with few or none of the pathological processes or symptoms associated with the kind: their instances are typified by (...) a single dispositional property. I dub such kinds ‘amorphic’, owing to their limited morphology, and try out a number of ways in which these kinds might be treated in terms of property clusters, adapting responses cluster theorists have offered to the problem of polymorphic species. Finding these responses wanting, I conclude that cluster accounts are unlikely to be the best account of the metaphysics of amorphic kinds. (shrink)

It is argued that the common definition of diagnosis as the determination of the nature of a disease is misleading. Many diagnoses are not the names of disease entities. This finding reflects the integral relation of the diagnostic task to the rest of clinical reasoning. Diagnosis has no separate goal of its own, in particular it does not have the goal of determining the nature of a disease. Instead, diagnosis contributes to the general goals of clinical medicine. Any attempt to (...) model diagnostic reasoning abstracted from the rest of clinical reasoning will yield an inadequate representation of diagnosis. Such a distortion of medical reasoning will blind us to whatever implications an adequate epistemology of medicine may have for an understanding of the relation between theoretical and practical knowledge in other contexts. (shrink)

Identifying the necessary and sufficient conditions for individuating and classifying diseases is a matter of great importance in the fields of law, ethics, epidemiology, and of course, medicine. In this paper, I first propose a means of achieving this goal, ensuring that no two distinct disease-types could correctly be ascribed to the same disease-token. I then posit a metaphysical ontology of diseases—that is, I give an account of what a disease is. This is essential to providing the most effective means (...) of interfering with disease processes. Following existing work in the philosophy of medicine and epidemiology (primarily Christopher Boorse; Caroline Whitbeck; Alexander Broadbent), philosophy of biology (Joseph LaPorte; D.L. Hull), conditional analyses of causation (J.L. Mackie; David Lewis), and recent literature on dispositional essentialism (Stephen Mumford and Rani Anjum; Alexander Bird), I endorse a dispositional conception of disease. Following discussion of various conceptions of disease-identity, their relations to the clinical and pathological effects of the diseases in question, and how diseases are treated, I conclude (i) that diseases should be individuated by their causes, and (ii) that diseases are causal processes best seen as simultaneously acting sequences of mutually manifesting dispositions. (shrink)

The ontology of medicine—the question of whether disease entities are real or not—is an underdeveloped area of philosophical inquiry. This essay explains the primary question at issue in medical ontology, discusses why answering this question is important from both a philosophical and a practical perspective, and argues that the problem of medical ontology is unique, i.e., distinct, from the ontological problems raised by other sciences and therefore requires its own analysis.

Many philosophers and medical scientists assume thatdisease categories or entities used to classify concrete cases ofdisease, are often defined by disease mechanisms or causalprocesses. Others suggest that diseases should always be definedin this manner. This paper discusses these standpoints criticallyand concludes that they are untenable, not only when `diseasemechanism' refers to an objective mechanism, but also when`mechanism' refers to a pragmatically demarcated part of thetotal ``objective'' causal structure of diseases. As an alternativeto principles that use the concept of disease mechanism (...) oranalogous concepts, a pragmatic approach is suggested anddescribed. This approach has been suggested before, but inproblematic or inadequate versions. This paper proposes a versioncompiled of two ``pragmatic principles'' and shows that they aremuch more adequate than the principle of disease mechanism. Withreference to a case study of a still ongoing internationaldiscussion of various candidates for a classification system formalignant lymphomas, including REAL (Revised European–AmericanClassification of Lymphoid Neoplasms) in which the concept ofdisease mechanism or analogous concepts plays a very small part,it is shown just how pivotal these two pragmatic principles canbe in actual discussions of definitions of diseases. Finally, itis pointed out that with regard to modern philosophy of languageit may, at least in some cases, be problematic to distinguishbetween the two pragmatic principles as they stand. (shrink)

There is a conceptual crisis in the biomedical sciences that is particularly salient in psychopathology research. Underlying the crisis is a controversy that pertains to the current medical model of disease that largely draws from causal-mechanistic explanations. The bedrock of this model is the analysis of biological part-dysfunctions that aims at unequivocally defining a pathological condition and demarcating it from its neighboring entities. This endeavor has led to a quest for physiological, biochemical, and genetic signatures. Yet, so far there is (...) little evidence for reliable biomarkers for any mental disorder. The contemporary biomedical paradigm largely ignores historical, dynamic, and system-level aspects—a view that has contributed much to the conceptual disjunction of the patient as a person from his/her disease. Notwithstanding the impressive progress in the biomedical sciences, increasingly more critics question whether the constituting framework is sufficient to convey a comprehensive understanding of illnesses, especially mental illnesses. Thus, the medical model urgently requires an update. But rather than revamping it by methodological advancements, it will be necessary to critically review its philosophical roots. The most problematic issues that require reworking are: the preponderance of the biostatistical theory; the undue decoupling of physiological from evolutionary explanations of function; the clinging to the Modern Synthesis ; and the neglect of dynamic and system-level properties. The proposed overhaul requires the heeding of historical explanations that draw from the Extended Evolutionary Synthesis as well as systems biology approaches for tackling multilevel and dynamic phenomena of complex systems. (shrink)

There is a conceptual crisis in the biomedical sciences that is particularly salient in psychopathology research. Underlying the crisis is a controversy that pertains to the current medical model of disease that largely draws from causal-mechanistic explanations. The bedrock of this model is the analysis of biological part-dysfunctions that aims at unequivocally defining a pathological condition and demarcating it from its neighboring entities. This endeavor has led to a quest for physiological, biochemical, and genetic signatures. Yet, so far there is (...) little evidence for reliable biomarkers for any mental disorder. The contemporary biomedical paradigm largely ignores historical, dynamic, and system-level aspects—a view that has contributed much to the conceptual disjunction of the patient as a person from his/her disease. Notwithstanding the impressive progress in the biomedical sciences, increasingly more critics question whether the constituting framework is sufficient to convey a comprehensive understanding of illnesses, especially mental illnesses. Thus, the medical model urgently requires an update. But rather than revamping it by methodological advancements, it will be necessary to critically review its philosophical roots. The most problematic issues that require reworking are: the preponderance of the biostatistical theory; the undue decoupling of physiological from evolutionary explanations of function; the clinging to the Modern Synthesis ; and the neglect of dynamic and system-level properties. The proposed overhaul requires the heeding of historical explanations that draw from the Extended Evolutionary Synthesis as well as systems biology approaches for tackling multilevel and dynamic phenomena of complex systems. (shrink)

The goal of this paper is two-fold: first, to emphasize causality in disease ontology and knowledge representation, presenting a general and cursory discussion of causality and causal chains; and second, to clarify and develop the River Flow Model of Diseases (RFM). The RFM is an ontological account of disease, representing the causal structure of pathology. It applies general knowledge of causality using the concept of causal chains. The river analogy of disease is explained, formal descriptions are offered, and the RFM (...) disease definition is refined by describing causal chains in terms of causal relations. The definition is updated to coincide with the actual RFM classes found in its upper-level ontology, YAMATO, which brings to light some challenges in developing both YAMATO and the RFM. The RFM is also discussed in relation to another ontological account of disease. Strategies are offered toward interoperability between these theories. (shrink)

The paper discusses the evolving concept of causationin epidemiology and its potential interaction with logic and scientific philosophy. Causes arecontingent but the necessity which binds them totheir effects relies on contrary-to-fact conditionals,i.e. conditional statements whose antecedent is false.Chance instead of determinism plays a growing role inscience and, although rarely acknowledged yet, inepidemiology: causes are multiple and chancy; a priorevent causes a subsequent event if the probabilitydistribution of the subsequent event changesconditionally upon the probability of the prior event.There are no known (...) sufficient causes in epidemiology.We merely observe tendencies toward sufficiency ortendencies toward necessity: cohort studies evaluatethe first tendencies, and case-control studies thelatter.In applied sciences, such as medicine andepidemiology, causes are intrinsically connected withgoals and effective strategies: they are recipewhich have a potential harmful or sucessful use; theyare contrastive since they make a differencebetween circumstances in which they are present andthose in which they are absent: causes do notexplain Event E but event E rather thaneven F. Causation is intrinsically linked with thenotion of ``what is pathological''.Any definition of causation will inevitably collapseinto the use made of epidemiologic methods. Theprogressive methodological sophistication of the lastforty years is in perfect alignment with a gradualimplicit overhaul of our concept of causation. (shrink)

There is a profound paradox in modern medical knowledge production: The more we know, the more we know that we (still) do not know. Nowhere is this more visible than in diagnostics and early detection of disease. As we identify ever more markers, predictors, precursors, and risk factors of disease ever earlier, we realize that we need knowledge about whether they develop into something experienced by the person and threatening to the person’s health. This study investigates how advancements in science (...) and technology alter one type of uncertainty, i.e., temporal uncertainty of disease diagnosis. As diagnosis is related to anamnesis and prognosis it identifies how uncertainties in all these fields are interconnected. In particular, the study finds that uncertainty in disease diagnosis has become more subject to prognostic uncertainty because diagnosis is more connected to technologically detected indicators and less closely connected to manifest and experienced disease. These temporal uncertainties pose basic epistemological and ethical challenges as they can result in overdiagnosis, overtreatment, unnecessary anxiety and fear, useless and even harmful diagnostic odysseys, as well as vast opportunity costs. The point is not to stop our quest for knowledge about disease but to encourage real diagnostic improvements that help more people in ever better manner as early as possible. To do so, we need to pay careful attention to specific types of temporal uncertainty in modern diagnostics. (shrink)

What kind of a thing are chronic diseases? Are they objects, bundles of signs and symptoms, properties, processes, or fictions? Rather than using concept analysis—the standard approach to disease in the philosophy of medicine—to answer this metaphysical question, I use a bottom-up, inductive approach. I argue that chronic diseases are bodily states or properties—often dispositional, but sometimes categorical. I also investigate the nature of related pathological entities: pathogenesis, etiology, and signs and symptoms. Finally, I defend my view against alternate accounts (...) of the nature of disease. (shrink)

I raise a puzzle case for “cluster” accounts of natural kinds—the homeostatic property cluster and stable property cluster accounts, especially—on the basis of their expected treatment of the metaphysics of certain disease kinds. Some kinds, I argue, fail to exhibit the co-instantiated property clusters these cluster views take to be constitutive of natural kinds. Some genetic diseases, for example, have archetypical instances with few or none of the pathological processes or symptoms associated with the kind: their instances are typified by (...) a single dispositional property. I dub such kinds ‘amorphic’, owing to their limited morphology, and try out a number of ways in which these kinds might be treated in terms of property clusters, adapting responses cluster theorists have offered to the problem of polymorphic species. Finding these responses wanting, I conclude that cluster accounts are unlikely to be the best account of the metaphysics of amorphic kinds. (shrink)

In this paper I offer an anti-Humean critique to Williamson and Russo’s approach to medical mechanisms. I focus on one of the specific claims made by Williamson and Russo, namely the claim that micro-structural ‘mechanisms’ provide evidence for the stability across populations of causal relationships ascertained at the (macro-) level of (test) populations. This claim is grounded in the epistemic account of causality developed by Williamson, an account which—while not relying exclusively on mechanistic evidence for justifying causal judgements—appeals nevertheless to (...) mechanisms, and rejects their anti-Humean interpretation in terms of capacities, powers, potencies, etc. By using (and expanding on) Cartwright’s basic critique against Humean mechanisms, I suggest that, in order to move beyond the level of plausibility, Williamson and Russo’s position is in need of a clarification as to the occurent reading of the components, functioning and interferences of mechanisms. Relatedly, as concerns Williamson’s epistemic account of causation, I argue that this account is in need of a more straightforward answer as to what truth-makers its causal claims should have. (shrink)

Abstract In this paper I offer an anti-Humean interpretation of the causal interactions in somatic medicine. I focus on life-threatening pathological states and show how Nancy Cartwright’s capacities can offer a plausible epistemology for medical processes and the singular causal claims advanced in medical diagnoses. I argue that the capacities manifested in the emergence of symptoms and signs could be tracked down if healthy organisms are construed as nomological machines and suggest that the causal reasoning from current medical practice bears (...) a tacit adherence to anti-Humean assumptions. Content Type Journal Article Pages 1-28 DOI 10.1007/s12136-011-0141-1 Authors Stefan Dragulinescu, Drumul Taberei 20, Bucharest, Romania Journal Acta Analytica Online ISSN 1874-6349 Print ISSN 0353-5150. (shrink)

The term, idiopathic, emerged as a key concept in the classification of disease in the 18th century and has become ingrained in our terminology in defining diseases and their aetiologies throughout all fields of medicine. Despite, or perhaps because of this, little has been written about the meaning or meanings of the word itself. Although most medical professionals will be able to offer a definition of idiopathic, different definitions of the word are in use and are often confused or used (...) without an appreciation of the range of meanings. This article aims to clarify these different meanings with reference to historic and current uses. The change from the earlier nosological definition of ‘primary’ to the most widely accepted current definition, ‘of unknown cause’, occurred in the late 19th century, reflecting changing perspectives of disease causation. Far from being an innocent translation of ‘unknown’, idiopathic creates problems for future terminology and adds little to medical understanding. In masking the unknown, the term idiopathic maintains a paternalistic patient–practitioner relationship, and so should be avoided in modern medical terminology. (shrink)

Although cases are central to the epistemic practices utilized within clinical medicine, they appear to be limited in their ability to provide evidence about causal relations because they provide detailed accounts of particular patients without explicit filtering of those attributes most likely to be relevant for explaining the phenomena observed. This paper uses a series of recent case reports to explore the role of cases in casual attribution in medical diagnosis. It is argued that cases are brought together by practitioners (...) to generate causal attributions and testable predictions using a manipulability view of causation. (shrink)

According to one large family of views, scientific explanations explain a phenomenon (such as an event or a regularity) by subsuming it under a general representation, model, prototype, or schema (see Bechtel, W., & Abrahamsen, A. (2005). Explanation: A mechanist alternative. Studies in History and Philosophy of Biological and Biomedical Sciences, 36(2), 421–441; Churchland, P. M. (1989). A neurocomputational perspective: The nature of mind and the structure of science. Cambridge: MIT Press; Darden (2006); Hempel, C. G. (1965). Aspects of scientific (...) explanation. In C. G. Hempel (Ed.), Aspects of scientific explanation (pp. 331–496). New York: Free Press; Kitcher (1989); Machamer, P., Darden, L., & Craver, C. F. (2000). Thinking about mechanisms. Philosophy of Science, 67(1), 1–25). My concern is with the minimal suggestion that an adequate philosophical theory of scientific explanation can limit its attention to the format or structure with which theories are represented. The representational subsumption view is a plausible hypothesis about the psychology of understanding. It is also a plausible claim about how scientists present their knowledge to the world. However, one cannot address the central questions for a philosophical theory of scientific explanation without turning one’s attention from the structure of representations to the basic commitments about the worldly structures that plausibly count as explanatory. A philosophical theory of scientific explanation should achieve two goals. The first is explanatory demarcation. It should show how explanation relates with other scientific achievements, such as control, description, measurement, prediction, and taxonomy. The second is explanatory normativity. It should say when putative explanations succeed and fail. One cannot achieve these goals without undertaking commitments about the kinds of ontic structures that plausibly count as explanatory. Representations convey explanatory information about a phenomenon when and only when they describe the ontic explanations for those phenomena. (shrink)