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)

Evidence-based medicine (EBM) makes use of explicit procedures for grading evidence for causal claims. Normally, these procedures categorise evidence of correlation produced by statistical trials as better evidence for a causal claim than evidence of mechanisms produced by other methods. We argue, in contrast, that evidence of mechanisms needs to be viewed as complementary to, rather than inferior to, evidence of correlation. In this paper we first set out the case for treating evidence of mechanisms alongside evidence of correlation in (...) explicit protocols for evaluating evidence. Next we provide case studies which exemplify the ways in which evidence of mechanisms complements evidence of correlation in practice. Finally, we put forward some general considerations as to how the two sorts of evidence can be more closely integrated by EBM. (shrink)

According to Russo and Williamson (Int Stud Philos Sci 21(2):157–170, 2007, Hist Philos Life Sci 33:389–396, 2011a, Philos Sci 1(1):47–69, 2011b ), in order to establish a causal claim of the form, ‘_C_ is a cause of _E_’, one typically needs evidence that there is an underlying mechanism between _C_ and _E_ as well as evidence that _C_ makes a difference to _E_. This thesis has been used to argue that hierarchies of evidence, as championed by evidence-based movements, tend to (...) give primacy to evidence of difference making over evidence of mechanisms and are flawed because the two sorts of evidence are required and they should be treated on a par. An alternative approach gives primacy to evidence of mechanism over evidence of difference making. In this paper, we argue that this alternative approach is equally flawed, again because both sorts of evidence need to be treated on a par. As an illustration of this parity, we explain how scientists working in the ‘EnviroGenomarkers’ project constantly make use of the two evidential components in a dynamic and intertwined way. We argue that such an interplay is needed not only for causal assessment but also for policy purposes. (shrink)

In this article, I begin by giving a brief history of melanoma causation. I then discuss the current manner in which malignant melanoma is classified. In general, these systems of classification do not take account of the manner of tumour causation. Instead, they are based on phenomenological features of the tumour, such as size, spread, and morphology. I go on to suggest that misclassification of melanoma is a major problem in clinical practice. I therefore outline an alternative means of classifying (...) these tumours based on causal factors. By analogy with similar systems that have recently emerged for other cancers, I suggest that this causal classification is likely to be both workable and helpful, even in the absence of a full causal-mechanistic understanding of the aetiology of the tumour. (shrink)

The Darwinian theory of evolution is itself evolving and this book presents the details of the core of modern Darwinism and its latest developmental directions. The authors present current scientific work addressing theoretical problems and challenges in four sections, beginning with the concepts of evolution theory, its processes of variation, heredity, selection, adaptation and function, and its patterns of character, species, descent and life. The second part of this book scrutinizes Darwinism in the philosophy of science and its usefulness in (...) understanding ecosystems, whilst the third section deals with its application in disciplines beyond the biological sciences, including evolutionary psychology and evolutionary economics, Darwinian morality and phylolinguistics. The final section addresses anti-Darwinism, the creationist view and issues around teaching evolution in secondary schools. The reader learns how current experimental biology is opening important perspectives on the sources of variation, and thus of the very power of natural selection. This work examines numerous examples of the extension of the principle of natural selection and provides the opportunity to critically reflect on a rich theory, on the methodological rigour that presides in its extensions and exportations, and on the necessity to measure its advantages and also its limits. Scholars interested in modern Darwinism and scientific research, its concepts, research programs and controversies will find this book an excellent read, and those considering how Darwinism might evolve, how it can apply to the human sciences and other disciplines beyond its origins will find it particularly valuable. Originally produced in French (Les Mondes Darwiniens), the scope and usefulness of the book have led to the production of this English text, to reach a wider audience. This book is a milestone in the impressive penetration by Francophone scholars into the world of Darwinian science, its historiography and philosophy over the last two decades. Alex Rosenberg, R. Taylor Cole Professor of Philosophy, Duke University Until now this useful and comprehensive handbook has only been available to francophones. Thanks to this invaluable new translation, this collection of insightful and original essays can reach the global audience it deserves. Tim Lewens, University of Cambridge. (shrink)

The definition of metabolic syndrome has been, and still is, extremely controversial. My purpose is not to give a solution to the associated debate but to argue that the controversy is at least partially due to the different ‘causal content’ of the various definitions: their theoretical validity and practical utility can be evaluated by reconstructing or making explicit the underlying causal structure. I will therefore propose to distinguish the alternative definitions according to the kinds of causal content they carry: definitions (...) grounded on associations, definitions presupposing a causal model built upon statistical associations, and definitions grounded on underlying mechanisms. I suggest that analysing definitions according to their causal content can be helpful in evaluating alternative definitions of some diseases. I want to show how the controversy over MetS suggests a distinction among three kinds of definitions based on how explicitly they characterise the syndrome in causal terms, and on the type of causality involved. I will call ‘type 1 definitions’ those definitions that are purely associative; ‘type 2 definitions’ the definitions based on statistical associations, plus generic medical and causal knowledge; and ‘type 3 definitions’ the definitions based on mechanisms. These kinds of definitions, although different, can be related to each other. A definition with more specific causal content may be useful in the evaluation of definitions characterised by a lower degree of causal specificity. Moreover, the identification of the type of causality involved is of help to constitute a good criterion for choosing among different definitions of a pathological entity. In section I introduce the controversy about MetS, in section I propose some remarks about medical definitions and their ‘causal import’, and in section I suggest that the different attitudes towards the definition of MetS are relevant to evaluate their explicative power. (shrink)

Many critics of medicalization express concern that the process privileges individualised, biologically grounded interpretations of medicalized phenomena, inhibiting understanding and communication of aspects of those phenomena that are less relevant to their biomedical modelling. I suggest that this line of critique views medicalization as a hermeneutical injustice—a form of epistemic injustice that prevents people having the hermeneutical resources available to interpret and communicate significant areas of their experience. Interpreting the critiques in this fashion shows they frequently fail because they: neglect (...) the ways in which medicalization may not obscure, but rather illuminate, individuals’ experiences; and neglect the testimony of those experiencing first-hand medicalized problems, thus may be guilty of perpetrating testimonial injustice. However, I suggest that such arguments are valuable insofar as they highlight the unwarranted epistemic privilege frequently afforded to medical institutions and medicalized models of phenomena, and a consequent need for greater epistemic humility on the part of health workers and researchers. (shrink)

Not only has the philosophical debate on causation been gaining ground in the last few decades, but it has also increasingly addressed the sciences. The biomedical sciences are among the most prominent fields that have been considered, with a number of works tackling the understanding of the notion of cause, the assessment of genuinely causal relations and the use of causal knowledge in applied contexts. Far from denying the merits of the debate on causation and the major theories it comprises, (...) this paper is meant as a stimulus for theorists of causation in the philosophy of biomedicine, with a focus on clinical matters. Without aiming at putting forward an original theory of causation and starting from the narration of two actual but paradigmatic cases at the joints between biomedical research and clinical practice, we want to point out that some pathological situations addressed by molecular medicine actually prove resistant to some of our major epistemological accounts of causal explanation. Given this scenario, which is very frequent in our hospitals, our analysis aims to provide a stimulus for the debate among theorists of causation in biomedicine interested in real cases in science in practice. We believe that this might in turn encourage some more general rethinking of the complex intertwinement of science, philosophy of science and ethics, as well as of the role of philosophy of science for clinical medicine itself. (shrink)

This contribution claims that the two fundamental notions of causation at work in the health sciences are manipulative and mechanistic, and investigates what kinds of evidence matter for the assessment of causal relations. This article is a development of our 2007 article, ‘Plurality of Causality’, where we argue for a pluralistic account of causation with an eye to econometrics and a single medical example. The present contribution has a wider focus, and considers the notion of evidence within a whole range (...) of disciplines belonging to the health sciences. Section 1 addresses the relations between kinds of evidence and causal accounts, and it is shown how different notions of causation can be employed in various medical cases. Section 2 calls attention to issues crucial for any adequate epistemological theory of causation, such as the distinctions between types and tokens, observational and experimental regimes, explanation and prediction. Lastly, the notion of context is articulated, highlighted in its role in the assessment of causal links. All these issues are tackled in the framework of what we label a ‘bottom–up’ epistemology. (shrink)

This thesis analyses the use of 'Evidence-Based' methodologies of evidence assessment and intervention and policy design from medicine, and their use in sport and exercise science. It argues that problems exist with the application of Evidence-Based methodologies in sports science, meaning that the quality of evidence used to inform decision-making is lower than is often assumed. This thesis also offers realistic solutions to these problems, broadly arguing for the importance of taking evidence from mechanistic studies seriously, in addition to evidence (...) from RCTs. (shrink)

It has recently been argued that successful evidence-based policy should rely on two kinds of evidence: statistical and mechanistic. The former is held to be evidence that a policy brings about the desired outcome, and the latter concerns how it does so. Although agreeing with the spirit of this proposal, we argue that the underlying conception of mechanistic evidence as evidence that is different in kind from correlational, difference-making or statistical evidence, does not correctly capture the role that information about (...) mechanisms should play in evidence-based policy. We offer an alternative account of mechanistic evidence as information concerning the causal pathway connecting the policy intervention to its outcome. Not only can this be analyzed as evidence of difference-making, it is also to be found at any level and is obtainable by a broad range of methods, both experimental and observational. Using behavioral policy as an illustration, we draw the implications of this revised understanding of mechanistic evidence for debates concerning policy extrapolation, evidence hierarchies, and evidence integration. (shrink)

The notion of causal evidence in medicine has been the subject of wide philosophical debate in recent years. The notion of evidence has been discussed mostly in connection with Evidence Based Medicine and, more in general, with the assessment of causal nexus in medical, and especially research contexts. “Manipulative evidence” is one of the notions of causal evidence that has stimulated much debate. It has been defined in slightly different ways, attributed different relevance, and recently placed at the core of (...) Gillies’ “action-related theory of causality”, a view specifically meant to address causation in medicine. While in general sympathetic to Gillies’ account, and totally convinced of the relevance of manipulative evidence and different sorts of interventions in the biomedical sciences, we believe that some further qualifications are needed to allow the notion of manipulative evidence to better express features of medical practice. In particular, we provide some qualification of the role of “interventional evidence” proposed by Gillies, suggesting a distinction between “interventional evidence” and “evidence for interventions”. A case study from research on rare diseases is analyzed in depth and a multifaceted notion of manipulative evidence put forward that allows better understanding of what manipulations in medical contexts amount to and what their targets are. (shrink)

In this article, I argue that distinguishing ‘evolutionary’ from ‘Darwinian’ medicine will help us assess the variety of roles that evolutionary explanations can play in a number of medical contexts. Because the boundaries of evolutionary and Darwinian medicine overlap to some extent, however, they are best described as distinct ‘research traditions’ rather than as competing paradigms. But while evolu- tionary medicine does not stand out as a new scientific field of its own, Darwinian medicine is united by a number of (...) distinctive theoretical and methodological claims. For example, evolutionary medicine and Darwinian medicine can be distinguished with respect to the styles of evolutionary explanations they employ. While the former primarily involves ‘forward looking’ explanations, the latter depends mostly on ‘backward looking’ explanations. A forward looking explanation tries to predict the effects of ongoing evolutionary processes on human health and disease in contem- porary environments (e.g., hospitals). In contrast, a backward looking explanation typically applies evolutionary principles from the vantage point of humans’ distant biological past in order to assess present states of health and disease. Both approaches, however, are concerned with the prevention and control of human diseases. In con- clusion, I raise some concerns about the claim that ‘nothing in medicine makes sense except in the light of evolution’. (shrink)