This volume argues for a new image of science that understands both natural and social phenomena to be the product of mechanisms, casting the work of science as an effort to understand those mechanisms. Glennan offers an account of the nature of mechanisms and of the models used to represent them in physical, life, and social sciences.

After a decade of intense debate about mechanisms, there is still no consensus characterization. In this paper we argue for a characterization that applies widely to mechanisms across the sciences. We examine and defend our disagreements with the major current contenders for characterizations of mechanisms. Ultimately, we indicate that the major contenders can all sign up to our characterization.

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.

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)

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)

This article examines the central epistemological issues tied to the recognition of disagreement.

Evidential Pluralism maintains that in order to establish a causal claim one normally needs to establish the existence of an appropriate conditional correlation and the existence of an appropriate mechanism complex, so when assessing a causal claim one ought to consider both association studies and mechanistic studies. Hitherto, Evidential Pluralism has been applied to medicine, leading to the EBM+ programme, which recommends that evidence-based medicine should systematically evaluate mechanistic studies alongside clinical studies. This paper argues that Evidential Pluralism can also (...) be fruitfully applied to the social sciences. In particular, Evidential Pluralism provides (i) a new approach to evidence-based policy; (ii) an account of the evidential relationships in more theoretical research; and (iii) new philosophical motivation for mixed methods research. The application of Evidential Pluralism to the social sciences is also defended against two objections. (shrink)

Philosophers of science increasingly believe that much of science is concerned with understanding the mechanisms responsible for the production of natural phenomena. An adequate understanding of scientific research requires an account of how scientists develop and test models of mechanisms. This paper offers a general account of the nature of mechanical models, discussing the representational relationship that holds between mechanisms and their models as well as the techniques that can be used to test and refine such models. The analysis is (...) supported by study of two competing models of a mechanism of speech perception. (shrink)

One puzzle concerning highly idealized models is whether they explain. Some suggest they provide so-called ‘how-possibly explanations’. However, this raises an important question about the nature of how-possibly explanations, namely what distinguishes them from ‘normal’, or how-actually, explanations? I provide an account of how-possibly explanations that clarifies their nature in the context of solving the puzzle of model-based explanation. I argue that the modal notions of actuality and possibility provide the relevant dividing lines between how-possibly and how-actually explanations. Whereas how-possibly (...) explanations establish claims of possible explanations, how-actually explanations establish claims of actual ones. Models, in turn, simply provide evidence for these claims. (shrink)

We claim that the process of theoretical model refinement in economics is best characterised as robustness analysis: the systematic examination of the robustness of modelling results with respect to particular modelling assumptions. We argue that this practise has epistemic value by extending William Wimsatt's account of robustness analysis as triangulation via independent means of determination. For economists robustness analysis is a crucial methodological strategy because their models are often based on idealisations and abstractions, and it is usually difficult to tell (...) which idealisations are truly harmful. (shrink)

Philosophers of science have insisted that evidence of underlying mechanisms is required to support claims about the effects of medical interventions. Yet evidence about mechanisms does not feature on dominant evidence-based medicine “hierarchies.” After arguing that only inferences from mechanisms (“mechanistic reasoning”)—not mechanisms themselves—count as evidence, I argue for a middle ground. Mechanistic reasoning is not required to establish causation when we have high-quality controlled studies; moreover, mechanistic reasoning is more problematic than has been assumed. Yet where the problems can (...) be overcome, mechanistic reasoning can and should be used as evidence. (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)

The article argues for the epistemic rationale of triangulation, namely, the use of multiple and independent sources of evidence. It claims that triangulation is to be understood as causal reasoning from data to phenomenon, and it rationalizes its epistemic value in terms of controlling for likely errors and biases of particular data-generating procedures. This perspective is employed to address objections against triangulation concerning the fallibility and scope of the inference, as well as problems of independence, incomparability, and discordance of evidence. (...) The debate on the existence of social preferences is used as an illustrative case. (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)

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)

Approximately one in six top economic research papers draws an explicitly causal conclusion. But what do economists mean when they conclude that A 'causes' B? Does 'cause' say that we can influence B by intervening on A, or is it only a label for the correlation of variables? Do quantitative analyses of observational data followed by such causal inferences constitute sufficient grounds for guiding economic policymaking? The Philosophy of Causality in Economics addresses these questions by analyzing the meaning of causal (...) claims made by economists and the philosophical presuppositions underlying the research methods used. The book considers five key causal approaches: the regularity approach, probabilistic theories, counterfactual theories, mechanisms, and interventions and manipulability. Each chapter opens with a summary of literature on the relevant approach and discusses its reception amongst economists. The text details case studies, and goes on to examine papers which have adopted the approach in order to highlight the methods of causal inference used in contemporary economics. It analyses the meaning of the causal claim put forward, and finally reconstructs the philosophical presuppositions accepted implicitly by economists. The strengths and limitations of each method of causal inference are also considered in the context of using the results as evidence for policymaking. This book is essential reading to those interested in literature on the philosophy of economics, as well as the philosophy of causality and economic methodology in general. (shrink)

All univocal analyses of causation face counterexamples. An attractive response to this situation is to become a pluralist about causal relationships. "Causal pluralism" is itself, however, a pluralistic notion. In this article, I argue in favor of pluralism about concepts of cause in the social sciences. The article will show that evidence for, inference from, and the purpose of causal claims are very closely linked. Key Words: causation • pluralism • evidence • methodology.

This paper explores the scope and limits of rational consensus through mutual respect, with the primary focus on the best known formal model of consensus: the Lehrer–Wagner model. We consider various arguments against the rationality of the Lehrer–Wagner model as a model of consensus about factual matters. We conclude that models such as this face problems in achieving rational consensus on disagreements about unknown factual matters, but that they hold considerable promise as models of how to rationally resolve non-factual disagreements.

A recent movement in the social sciences and philosophy of the social sciences focuses on mechanisms as a central analytical unit. Starting from a pluralist perspective on the aims of the social sciences, I argue that there are a number of important aims to which knowledge about mechanisms—whatever their virtues relative to other aims—contributes very little at best and that investigating mechanisms is therefore a methodological strategy with fairly limited applicability. Key Words: social science • mechanisms • explanation • critical (...) realism • methodology. (shrink)

Proponents of evidence-based medicine (EBM) provide the “hierarchy of evidence” as a criterion for judging the reliability of therapeutic decisions. EBM's hierarchy places randomized interventional studies (and systematic reviews of such studies) higher in the hierarchy than observational studies, unsystematic clinical experience, and basic science. Recent philosophical work has questioned whether EBM's special emphasis on evidence from randomized interventional studies can be justified. Following the critical literature, and in particular the work of John Worrall, I agree that many of the (...) arguments put forward by advocates of EBM do not justify the ambitious claims that are often made on behalf of randomization. However, in contrast to the recent philosophical work, I argue that a justification for EBM's hierarchy of evidence can be provided. The hierarchy should be viewed as a hierarchy of comparative internal validity. Although this justification is defensible, the claims that EBM's hierarchy substantiates when viewed in this way are considerably more circumscribed than some claims found in the EBM literature. (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)

This article examines the issue of whether consideration of so-called minimal models can prompt learning about real-world targets. Using a widely cited example as a test case, it argues against the increasingly popular view that consideration of minimal models can prompt learning about such targets. The article criticizes influential defenses of this view for failing to explicate by virtue of what properties or features minimal models supposedly prompt learning. It then argues that consideration of minimal models cannot prompt learning about (...) real-world targets unless one supplements these models with additional information or presuppositions concerning such targets. (shrink)

Social research, from economics to demography and epidemiology, makes extensive use of statistical models in order to establish causal relations. The question arises as to what guarantees the causal interpretation of such models. In this paper we focus on econometrics and advance the view that causal models are ‘augmented’ statistical models that incorporate important causal information which contributes to their causal interpretation. The primary objective of this paper is to argue that causal claims are established on the basis of a (...) plurality of evidence. We discuss the consequences of ‘evidential pluralism’ in the context of econometric modelling. (shrink)

In his recent paper in the Journal of Economic Methodology, Tobias Henschen puts forth a manipulationist definition of macroeconomic causality that strives for adequacy. As the notion of ‘adequacy’...

Rational addiction theories illustrate how absurd choice theories in economics get taken seriously as possibly true explanations and tools for welfare analysis despite being poorly interpreted, empirically unfalsifiable, and based on wildly inaccurate assumptions selectively justified by ad-hoc stories. The lack of transparency introduced by poorly anchored mathematical models, the psychological persuasiveness of stories, and the way the profession neglects relevant issues are suggested as explanations for how what we perhaps should see as displays of technical skill and ingenuity are (...) allowed to blur the lines between science and games. (shrink)

Psychological constructs such as personality dimensions or cognitive traits are typically unobserved and are therefore measured by observing so-called indicators of the latent construct. The Common Factor Model models the relations between the observed indicators and the latent variable. In this article we argue in favor of interpreting the CFM as a causal model rather than merely a statistical model, in which common factors are only descriptions of the indicators. When there is sufficient reason to hypothesize that the underlying causal (...) structure of the data is a common cause structure, a causal interpretation of the CFM has several benefits over a merely statistical interpretation of the model. We argue that a causal interpretation conforms with most research questions in which the goal is to explain the correlations between indicators rather than merely summarizing them; a causal interpretation of the factor model legitimizes the focus on shared, rather than unique variance of the indicators; and a causal interpretation of the factor model legitimizes the assumption of local independence. (shrink)

One way social scientists explain phenomena is by building structural models. These models are explanatory insofar as they manage to perform a recursive decomposition on an initial multivariate probability distribution, which can be interpreted as a mechanism. Explanations in social sciences share important aspects that have been highlighted in the mechanisms literature. Notably, spelling out the functioning the mechanism gives it explanatory power. Thus social scientists should choose the variables to include in the model on the basis of their function (...) in the mechanism. This paper examines the notion of ‘function’ within structural modelling. We argue that ‘functions’ ought to be understood as the theoretical underpinnings of the causes, namely as the role that causes play in the functioning of the mechanism. (shrink)

Inconsistencies between scientific theories have been studied, by and large, from the perspective of paraconsistent logic. This approach considered the formal properties of theories and the structure of inferences one can legitimately draw from theories. However, inconsistencies can be also analysed from the perspective of modelling practices, in particular how modelling practices may lead scientists to form opinions and attitudes that are different, but not necessarily inconsistent. In such cases, it is preferable to talk about disagreement, rather than inconsistency. Disagreement (...) may originate in, or concern, a number of epistemic, socio-political or psychological factors. In this paper, we offer an account of the ‘loci and reasons’ for disagreement at different stages of the scientific process. We then present a controversial episode in the health sciences: the studies on hypercholesterolemia. The causes and effects of high levels of cholesterol in blood have been long and hotly debated, to the point of deserving the name of ‘cholesterol wars’; the debate, to be sure, isn’t settled yet. In this contribution, we focus on some selected loci and reasons for disagreement that occurred between 1920 and 1994 in the studies on hypercholesterolemia. We hope that our analysis of ‘loci and reasons’ for disagreement may shed light on the cholesterol wars, and possibly on other episodes of scientific disagreement. (shrink)