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)

Russo and Williamson put forward the following thesis: in order to establish a causal claim in medicine, one normally needs to establish both that the putative cause and putative effect are appropriately correlated and that there is some underlying mechanism that can account for this correlation. I argue that, although the Russo-Williamson thesis conflicts with the tenets of present-day evidence-based medicine, it offers a better causal epistemology than that provided by present-day EBM because it (...) better explains two key aspects of causal discovery. First, the thesis better explains the role of clinical studies in establishing causal claims. Second, it yields a better account of extrapolation. (shrink)

Russo and Williamson claim that establishing causal claims requires mechanistic and difference-making evidence. In this article, I will argue that Russo and Williamson's formulation of their thesis is multiply ambiguous. I will make three distinctions: mechanistic evidence as type vs object of evidence; what mechanism or mechanisms we want evidence of; and how much evidence of a mechanism we require. I will feed these more precise meanings back into the Russo–Williamson thesis and (...) argue that it is both true and false: two weaker versions of the thesis are worth supporting, while the stronger versions are not. Further, my distinctions are of wider concern because they allow us to make more precise claims about what kinds of evidence are required in particular cases. (shrink)

The teratogenicity of the Zika virus was considered established in 2016, and is an interesting case because three different sets of causal criteria were used to assess teratogenicity. This paper appeals to the thesis of Russo and Williamson (2007) to devise an epistemological framework that can be used to compare and evaluate sets of causal criteria. The framework can also be used to decide when enough criteria are satisfied to establish causality. Arguably, the three sets of causal (...) criteria considered here offer only a rudimentary assessment of mechanistic studies, and some suggestions are made as to alternative ways to establish causality. (shrink)

Russo and Williamson (Int Stud Philos Sci 21(2):157–170, 2007) put forward the thesis that, at least in the health sciences, to establish the claim that C is a cause of E, one normally needs evidence of an underlying mechanism linking C and E as well as evidence that C makes a difference to E. This epistemological thesis poses a problem for most current analyses of causality which, in virtue of analysing causality in terms of just one (...) of mechanisms or difference making, cannot account for the need for the other kind of evidence. Weber (Int Stud Philos Sci 23(2):277–295, 2009) has suggested to the contrary that Giere’s probabilistic analysis of causality survives this criticism. In this paper, we look in detail at the case of medical imaging technology, which, we argue, supports the thesis of Russo and Williamson, and we respond to Weber’s suggestion, arguing that Giere’s account does not survive the criticism. (shrink)

Establishing the effectiveness of medical treatments is one of the most important aspects of medical practice. Bradford Hill's viewpoints play an important role in inferring causality in medicine,...

The Russo Williamson thesis (RWT) states that a causal claim can be established only if it can be established that there is a difference-making relationship between the cause and the effect, and that there is a mechanism linking the cause and the effect that is responsible for such a difference-making relationship (Russo & Williamson, 2007). The applicability of Russo and Williamson’s idea was hugely debated in relation to biomedical research, and recently it has (...) been applied to the social sciences (Shan & Williamson, 2021). While many philosophers and social scientists have advocated the use of different kinds of evidence for causal discoveries, others have criticised this approach. With this paper, I aim to defend RWT from criticisms and to show its importance in the social sciences. The paper is structured as follows. After a brief introduction, in Sect. 2, I will summarise RWT, and in Sect. 3 I will describe how this approach can be applied to the social sciences. In Sect. 4, I will reconstruct two main criticisms of this thesis proposed in the philosophy of the social sciences literature: namely (i) RWT is not used in the social sciences, (ii) RWT does not work. For each criticism I will provide a defence of RWT. My defence will be based on two general considerations: (i) RWT appears perfectly in line with the research methods used in the social sciences and (ii) RWT can be applied successfully to establish causal claims. In Sect. 5, moreover, I will examine the causal accounts that have motivated such criticisms and I will argue that they should be rejected to endorse RWT and a causal account able to accommodate the current use of mechanistic and difference-making evidence in the social sciences. Section 6 will conclude with a note on the relevance of RWT in both its descriptive and normative form. (shrink)

A particular tradition in medicine claims that a variety of evidence is helpful in determining whether an observed correlation is causal. In line with this tradition, it has been claimed that establishing a causal claim in medicine requires both probabilistic and mechanistic evidence. This claim has been put forward by Federica Russo and Jon Williamson. As a result, it is sometimes called the Russo–Williamson thesis. In support of this thesis, Russo and Williamson (...) appeal to the practice of the International Agency for Research on Cancer. However, this practice presents some problematic cases for the Russo–Williamson thesis. One response to such cases is to argue in favour of reforming these practices. In this paper, we propose an alternative response according to which such cases are in fact consistent with the Russo–Williamson thesis. This response requires maintaining that there is a role for mechanism-based extrapolation in the practice of the IARC. However, the response works only if this mechanism-based extrapolation is reliable, and some have argued against the reliability of mechanism-based extrapolation. Against this, we provide some reasons for believing that reliable mechanism-based extrapolation is going on in the practice of the IARC. The reasons are provided by appealing to the role of robustness analysis. (shrink)

According to the Russo-Williamson Thesis, causal claims in the health sciences need to be supported by both difference-making and mechanistic evidence. In this article, we attempt to determine whether Evidence-based Medicine can be improved through the consideration of mechanistic evidence. We discuss the practical composition and function of each RWT evidence type and propose that exposure-outcome evidence provides associations that can be explained through a hypothesis of causation, while mechanistic evidence provides finer-grained associations and knowledge of entities (...) that ultimately explains a causal hypothesis. We suggest that mechanistic evidence holds untapped potential to add value to the assessment of evidence quality in EBM and propose initial recommendations for the integration of mechanistic and exposure-outcome evidence to improve EBM by robustly leveraging available evidence in support of good medical decisions. (shrink)

This article examines two theses formulated by Russo and Williamson in their study of causal inference in the health sciences. The two theses are assessed against evidence from a specific case in the social sciences, i.e., research on the institutional determinants of the aggregate unemployment rate. The first Russo–Williamson Thesis is that a causal claim can only be established when it is jointly supported by difference-making and mechanistic evidence. This thesis is shown not to (...) hold. While researchers in my case study draw extensively on both types of evidence, one causal claim out of the three analyzed is established even though it is exclusively supported by mechanistic evidence. The second Russo–Williamson Thesis is that standard accounts of causality fail to handle the dualist epistemology highlighted in the first Thesis. I argue that a counterfactual-manipulationist account of causality—which is endorsed by many philosophers as well as many social scientists—can perfectly make sense of the typical strategy in my case study to draw on both difference-making and mechanistic evidence; it is just an instance of the common strategy of increasing evidential variety. (shrink)

We argue that the health sciences make causal claims on the basis of evidence both of physical mechanisms, and of probabilistic dependencies. Consequently, an analysis of causality solely in terms of physical mechanisms or solely in terms of probabilistic relationships, does not do justice to the causal claims of these sciences. Yet there seems to be a single relation of cause in these sciences - pluralism about causality will not do either. Instead, we maintain, the health sciences require a theory (...) of causality that unifies its mechanistic and probabilistic aspects. We argue that the epistemic theory of causality provides the required unification. (shrink)

Causal claims in biomedical contexts are ubiquitous albeit they are not always made explicit. This paper addresses the question of what causal claims mean in the context of disease. It is argued that in medical contexts causality ought to be interpreted according to the epistemic theory. The epistemic theory offers an alternative to traditional accounts that cash out causation either in terms of “difference-making” relations or in terms of mechanisms. According to the epistemic approach, causal claims tell us about which (...) inferences (e.g., diagnoses and prognoses) are appropriate, rather than about the presence of some physical causal relation analogous to distance or gravitational attraction. It is shown that the epistemic theory has important consequences for medical practice, in particular with regard to evidence-based causal assessment. (shrink)

Why do ideas of how mechanisms relate to causality and probability differ so much across the sciences? Can progress in understanding the tools of causal inference in some sciences lead to progress in others? This book tackles these questions and others concerning the use of causality in the sciences.

Causal inference is perhaps the most important form of reasoning in the sciences. A panoply of disciplines, ranging from epidemiology to biology, from econometrics to physics, make use of probability and statistics to infer causal relationships. The social and health sciences analyse population-level data using statistical methods to infer average causal relations. In diagnosis of disease, probabilistic statements are based on population-level causal knowledge combined with knowledge of a particular person’s symptoms. For the physical sciences, the Salmon-Dowe account develops an (...) analysis of causation based on the notion of process and interaction. In artificial intelligence, the development of graphical methods has leant impetus to a probabilistic analysis of causality. The biological sciences use probabilistic methods to look for evolutionary causes of the state of a current species and to look for genetic causal factors. This variegated situation raises at least two fundamental philosophical issues: about the relation between causality and probability, and about the interpretation of probability in causal analysis. In this book we bring philosophers and scientists together to discuss the relation between causality and probability, and the applications of these concepts within the sciences. (shrink)

How should probabilities be interpreted in causal models in the social and health sciences? In this paper we take a step towards answering this question by investigating the case of cancer in epidemiology and arguing that the objective Bayesian interpretation is most appropriate in this domain.

Key Terms in Logic offers the ideal introduction to this core area in the study of philosophy, providing detailed summaries of the important concepts in the study of logic and the application of logic to the rest of philosophy. A brief introduction provides context and background, while the following chapters offer detailed definitions of key terms and concepts, introductions to the work of key thinkers and lists of key texts. Designed specifically to meet the needs of students and assuming no (...) prior knowledge of the subject, this is the ideal reference tool for those coming to Logic for the first time. (shrink)

The book tackles these questions as well as others concerning the use of causality in the sciences.

Key Terms in Logic offers the ideal introduction to this core area in the study of philosophy, providing detailed summaries of the important concepts in the study of logic and the application of logic to the rest of philosophy. A brief introduction provides context and background, while the following chapters offer detailed definitions of key terms and concepts, introductions to the work of key thinkers and lists of key texts. Designed specifically to meet the needs of students and assuming no (...) prior knowledge of the subject, this is the ideal reference tool for those coming to Logic for the first time. (shrink)

Key Terms in Logic offers the ideal introduction to this core area in the study of philosophy, providing detailed summaries of the important concepts in the study of logic and the application of logic to the rest of philosophy. A brief introduction provides context and background, while the following chapters offer detailed definitions of key terms and concepts, introductions to the work of key thinkers and lists of key texts. Designed specifically to meet the needs of students and assuming no (...) prior knowledge of the subject, this is the ideal reference tool for those coming to Logic for the first time. (shrink)

An accessible guide for those facing the study of Logic For The first time, this book covers key thinkers, terms and texts.

Key Terms in Logic offers the ideal introduction to this core area in the study of philosophy, providing detailed summaries of the important concepts in the study of logic and the application of logic to the rest of philosophy. A brief introduction provides context and background, while the following chapters offer detailed definitions of key terms and concepts, introductions to the work of key thinkers and lists of key texts. Designed specifically to meet the needs of students and assuming no (...) prior knowledge of the subject, this is the ideal reference tool for those coming to Logic for the first time. (shrink)

Key Terms in Logic offers the ideal introduction to this core area in the study of philosophy, providing detailed summaries of the important concepts in the study of logic and the application of logic to the rest of philosophy. A brief introduction provides context and background, while the following chapters offer detailed definitions of key terms and concepts, introductions to the work of key thinkers and lists of key texts. Designed specifically to meet the needs of students and assuming no (...) prior knowledge of the subject, this is the ideal reference tool for those coming to Logic for the first time. (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)

The use of evidence in medicine is something we should continuously seek to improve. This book seeks to develop our understanding of evidence of mechanism in evaluating evidence in medicine, public health, and social care; and also offers tools to help implement improved assessment of evidence of mechanism in practice. In this way, the book offers a bridge between more theoretical and conceptual insights and worries about evidence of mechanism and practical means to fit the results into evidence assessment procedures.

According to current hierarchies of evidence for EBM, evidence of correlation is always more important than evidence of mechanisms when evaluating and establishing causal claims. We argue that evidence of mechanisms needs to be treated alongside evidence of correlation. This is for three reasons. First, correlation is always a fallible indicator of causation, subject in particular to the problem of confounding; evidence of mechanisms can in some cases be more important than evidence of correlation when assessing a causal claim. Second, (...) evidence of mechanisms is often required in order to obtain evidence of correlation. Third, evidence of mechanisms is often required in order to generalise and apply causal claims. While the EBM movement has been enormously successful in making explicit and critically examining one aspect of our evidential practice, i.e., evidence of correlation, we wish to extend this line of work to make explicit and critically examine a second aspect of our evidential practices: evidence of mechanisms. (shrink)

The Recursive Bayesian Net formalism was originally developed for modelling nested causal relationships. In this paper we argue that the formalism can also be applied to modelling the hierarchical structure of mechanisms. The resulting network contains quantitative information about probabilities, as well as qualitative information about mechanistic structure and causal relations. Since information about probabilities, mechanisms and causal relations is vital for prediction, explanation and control respectively, an RBN can be applied to all these tasks. We show in particular how (...) a simple two-level RBN can be used to model a mechanism in cancer science. The higher level of our model contains variables at the clinical level, while the lower level maps the structure of the cell's mechanism for apoptosis. (shrink)

The paper studies the relation between systems of modal logic and systems of consequential implication, a non-material form of implication satisfying "Aristotle's Thesis" (p does not imply not p) and "Weak Boethius' Thesis" (if p implies q, then p does not imply not q). Definitions are given of consequential implication in terms of modal operators and of modal operators in terms of consequential implication. The modal equivalent of "Strong Boethius' Thesis" (that p implies q implies that p (...) does not imply not q) is identified. (shrink)

Current research in molecular epidemiology uses biomarkers to model the different disease phases from environmental exposure, to early clinical changes, to development of disease. The hope is to get a better understanding of the causal impact of a number of pollutants and chemicals on several diseases, including cancer and allergies. In a recent paper Russo and Williamson address the question of what evidential elements enter the conceptualisation and modelling stages of this type of biomarkers research. Recent research in (...) causality has examined Ned Hall’s distinction between two concepts of causality: production and dependence. In another recent paper, Illari examined the relatively under-explored production approach to causality, arguing that at least one job of an account of causal production is to illuminate our inferential practices concerning causal linking. Illari argued that an informational account solves existing problems with traditional accounts. This paper follows up this previous work by investigating the nature of the causal links established in biomarkers research. We argue that traditional accounts of productive causality are unable to provide a sensible account of the nature of the causal link in biomarkers research, while an informational account is very promising. (shrink)

Let DDQ be the thesis that definite descriptions are quantifiers. Philosophers often deny DDQ because they believe that quantifiers do not depend on context in certain ways, ways in which definite descriptions do depend on context. In this paper, we examine one such argument, which, if sound, would entail the negation of DDQ.We show that this argument fails, and draw some consequences from its failure.

Let DDQ be the thesis that definite descriptions are quantifiers. Philosophers often deny DDQ because they believe that quantifiers do not depend on context in certain ways, ways in which definite descriptions do depend on context. In this paper, we examine one such argument, which, if sound, would entail the negation of DDQ.We show that this argument fails, and draw some consequences from its failure.

It is natural to ask under what conditions negating a conditional is equivalent to negating its consequent. Given a bivalent background logic, this is equivalent to asking about the conjunction of Conditional Excluded Middle (CEM, opposite conditionals are not both false) and Weak Boethius' Thesis (WBT, opposite conditionals are not both true). In the system CI.0 of consequential implication, which is intertranslatable with the modal logic KT, WBT is a theorem, so it is natural to ask which instances of (...) CEM are derivable. We also investigate the systems CIw and CI of consequential implication, corresponding to the modal logics K and KD respectively, with occasional remarks about stronger systems. While unrestricted CEM produces modal collapse in all these systems, CEM restricted to contingent formulas yields the Alt2 axiom (semantically, each world can see at most two worlds), which corresponds to the symmetry of consequential implication. It is proved that in all the main systems considered, a given instance of CEM is derivable if and only if the result of replacing consequential implication by the material biconditional in one or other of its disjuncts is provable. Several related results are also proved. The methods of the paper are those of propositional modal logic as applied to a special sort of conditional. (shrink)

OElig;he thesis is sustained that the definitions of fundamental geometric entities which open Euclids Elements actually are excerpts from the Definitions by Heron of Alexandria, interpolated in late antiquity into Euclids treatise. As a consequence, one of the main bases of the traditional Platonist interpretation of Euclid is refuted. Arguments about the constructivist nature of Euclids mathematical philosophy are given.

In 1964, the young Walter Kasper (born in 1933) was granted by the Faculty of Catholic Theology at Tübingen the licence to teach dogmatic theology on the basis of a thesis on Philosophie und Theologie der Geschichte in der Spätphilosophie Schellings (Philosophy and Theology of History in Schelling’s Late Philosophy). Kasper’s interest in Schelling, himself a student at the Evangelisches Stift at Tübingen, thus originated in the context of his university studies in the school of J.R. Geiselmann and developed (...) in parallel with his theological education. For this reason, it is impossible to form a correct idea of Kasper and his whole theology unless one is willing to take into account this background, not least because he himself has always consciously and forcefully recognised this fact and seen in it his own centre of gravity. Kasper’s work and thought were shaped in a lasting manner during his university years. In fact, his entire academic oeuvre has been nurtured from this fecund origin so much so that he became one of the most well known names associated with the Catholic school at Tübingen to which he gave a new, creative impulse having himself been profoundly inspired by it. ‘He always emphasised his own roots not only as a teacher of theology and a member of the teaching faculty of this institution, but also as bishop’ and cardinal. The principal intention of the present article is precisely this: to return to this beginning and elucidate these decisive years for Kasper in broad outline by way of a relecture and interpretation of his book on The Absolute in History and the particular manner in which he interpreted the so-called second Schelling, an author whom he approached in the wake of Walter Schulz and at practically the same time as Xavier Tilliette. The analysis will subsequently move on into the more properly theological field. (shrink)

The paper explains how to integrate the knowledge-first approach to epistemology with the intellectualist thesis that knowing-how is a kind of knowing-that, with emphasis on their role in practical reasoning. One component of this integration is a belief-based account of desire.

Bioethicists have recently expressed concern over a lack of quality control within the field. This apprehension focuses on bioethics expanding in ways that obscure its distinctive ethical remit and the specialist reasoning skills it requires. This thesis about the quality and conduct of bioethics may have particular relevance for clinical ethics. As one of the youngest offshoots of bioethics, the field focuses on the ethical issues that arise specifically in a clinical context. However, non-ethics specialists are increasingly involved in (...) this field. This means that clinical ethics could be especially vulnerable to the quality control concerns articulated within bioethics. The growing public profile of clinical ethics means that concerns over quality in this area warrant specific attention by those concerned with declining standards in bioethics and those working in clinical ethics. (shrink)

Mental causation is a problem and not just a problem for the nonphysicalist. One of the many lessons learned from Jaegwon Kim’s writings in the philosophy of mind is that mental causation is a problem for the nonreductive physicalist as well. A central component of the common sense picture we have of ourselves as persons is that our beliefs and desires causally explain our actions. But the completeness of the “brain sciences” threatens this picture. If all of our actions are (...) causally explained by neurophysiological events occurring in our brains, what causal role is left for our reasons and motives? It would seem that these brain events do all the causal work there is to do, thus robbing the mental of its efficacy altogether or else making it a merely superfluous or redundant causal factor. This essay presents a systematic treatment of this exclusion dilemma from the perspective of a nonreductive physicalist. I argue that both horns of this dilemma can be avoided if we ground mental causation in counterfactual dependence between distinct events and understand the mind-body relation as event realization. Although in the final analysis our actions are overdetermined by their mental and neurophysiological antecedents, this overdetermination is entirely unproblematic. (shrink)

The central thesis of the book is that the proposition a vague sentence expresses in a borderline case is true or false, and we cannot know which. We are ignorant of its truth-value. This is the epistemic view of vagueness. It allows us to preserve both classical logic and disquotational principles about truth and falsity, with all their advantages: simplicity, clarity, power, past success, integration with well-confirmed theories in other domains. Consequently, the epistemic view has a head start over (...) its rivals. The gap is widened by each rival theory's specific disadvantages, many of them related to higher-order vagueness. The epistemic view is then strengthened by an explanation of our ignorance in borderline cases. The explanation predicts higher order vagueness. (shrink)

The central thesis of the book is that the proposition a vague sentence expresses in a borderline case is true or false, and we cannot know which. We are ignorant of its truth-value. This is the epistemic view of vagueness. It allows us to preserve both classical logic and disquotational principles about truth and falsity, with all their advantages: simplicity, clarity, power, past success, integration with well-confirmed theories in other domains. Consequently, the epistemic view has a head start over (...) its rivals. The gap is widened by each rival theory's specific disadvantages, many of them related to higher-order vagueness. The epistemic view is then strengthened by an explanation of our ignorance in borderline cases. The explanation predicts higher order vagueness. (shrink)

In this thesis, I give a metascientific account of causality in medicine. I begin with two historical cases of causal discovery. These are the discovery of the causation of Burkitt’s lymphoma by the Epstein-Barr virus, and of the various viral causes suggested for cervical cancer. These historical cases then support a philosophical discussion of causality in medicine. This begins with an introduction to the Russo- Williamson thesis (RWT), and discussion of a range of counter-arguments against it. (...) Despite these, I argue that the RWT is historically workable, given a small number of modifications. I then expand Russo and Williamson’s account. I first develop their suggestion that causal relationships in medicine require some kind of evidence of mechanism. I begin with a number of accounts of mechanisms and produce a range of consensus features of them. I then develop this consensus position by reference to the two historical case studies with an eye to their operational competence. In particular, I suggest that it is mechanistic models and their representations which we are concerned with in medicine, rather than the mechanism as it exists in the world. -/- I then employ these mechanistic models to give an account of the sorts of evidence used in formulating and evaluating causal claims. Again, I use the two human viral oncogenesis cases to give this account. I characterise and distinguish evidence of mechanism from evidence of difference-making, and relate this to mechanistic models. I then suggest the relationship between types of evidence presents us with a means of tackling the reference-class problem. This sets the scene for the final chapter. Here, I suggest the manner in which these two different classes of evidence become integrated is also reflected in the way that developing research programmes change as their associated causal claims develop. (shrink)

The results of econometric modeling are fragile in the sense that minor changes in estimation techniques or sample can lead to statistical models that support inconsistent causal hypotheses. The fragility of econometric results undermines making conclusive inferences from the empirical literature. I argue that the program of evidential pluralism, which originated in the context of medicine and encapsulates to the normative reading of the Russo-Williamson Thesis that causal claims need the support of both difference-making and mechanistic evidence, (...) offers a ground for resolving empirical disagreements. I analyze a recent econometric controversy regarding the tax elasticity of cigarette consumption and smoking intensity. Both studies apply plausible estimation techniques but report inconsistent results. I show that mechanistic evidence allows for discriminating econometric models representing genuine causal relations from accidental dependencies in data. Furthermore, I discuss the differences between biological and social mechanisms and mechanistic evidence across the disciplines. I show that economists mainly rely on mathematical models to represent possible mechanisms. Still, claiming the actuality of the represented mechanisms requires establishing that crucial assumptions of these models are descriptively adequate. I exemplify my approach to assessing the quality of mechanistic evidence in economics with an analysis of two models of rational addiction. (shrink)

In current philosophical discussions on evidence in the medical sciences, epidemiology has been used to exemplify a specific version of evidential pluralism. According to this view, known as the Russo–Williamson Thesis, evidence of both difference-making and mechanisms is produced to make causal claims in the health sciences. In this paper, I present an analysis of data and evidence in epidemiological practice, with a special focus on research on the exposome, and I cast doubt on the extent to (...) which evidential pluralism holds in this case. I start by focusing on the claim that molecular data allows for the production of mechanistic evidence. On the basis of a close look at the ways in which molecular data is used in exposome research, I caution against interpretations in terms of mechanistic evidence. Secondly, I expand my critical remarks on the thesis by addressing the conditions under which data is categorised as evidence in exposome research. I argue that these show that the classification of a dataset as a type of evidence is dependent on the ways in which the data is used. This is in contrast with the approach of evidential pluralism, where evidence is classified in different types on the basis of its intrinsic properties. Finally, I come back to what I consider the core of the thesis and suggest that the epidemiological research analysed in the paper indicates different interpretations of evidential pluralism and its applicability in the health sciences. (shrink)

I argue that difference-making should be a crucial element for evaluating the quality of evidence for mechanisms, especially with respect to the robustness of mechanisms, and that it should take central stage when it comes to the general role played by mechanisms in establishing causal claims in medicine. The difference- making of mechanisms should provide additional compelling reasons to accept the gist of Russo-Williamson thesis and include mechanisms in the protocols for Evidence- Based Medicine, as the EBM+ (...) research group has been advocating. (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)