Causation is in trouble—at least as it is pictured in current theories in philosophy and in economics as well, where causation is also once again in fashion. In both disciplines the accounts of causality on offer are either modelled too closely on one or another favoured method for hunting causes or on assumptions about the uses to which causal knowledge can be put—generally for predicting the results of our efforts to change the world. The first kind of account supplies no (...) reason to think that causal knowledge, as it is pictured, is of any use; the second supplies no reason to think our best methods will be reliable for establishing causal knowledge. So, if these accounts are all there is to be had, how do we get from method to use? Of what use is knowledge of causal laws that we work so hard to obtain? (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)

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)

There is a takeover movement fast gaining influence in development economics, a movement that demands that predictions about development outcomes be based on randomized controlled trials. The problem it takes up—of using evidence of efficacy from good studies to predict whether a policy will be effective if we implement it—is a general one, and affects us all. My discussion is the result of a long struggle to develop the right concepts to deal with the problem of warranting effectiveness predictions. Whether (...) I have it right or not, these are questions of vast social importance that philosophers of science can, and should, help answer. (shrink)

Causation is in trouble—at least as it is pictured in current theories in philosophy and in economics as well, where causation is also once again in fashion. In both disciplines the accounts of causality on offer are either modelled too closely on one or another favoured method for hunting causes or on assumptions about the uses to which causal knowledge can be put—generally for predicting the results of our efforts to change the world. The first kind of account supplies no (...) reason to think that causal knowledge, as it is pictured, is of any use; the second supplies no reason to think our best methods will be reliable for establishing causal knowledge. So, if these accounts are all there is to be had, how do we get from method to use? Of what use is knowledge of causal laws that we work so hard to obtain? (shrink)

This article focuses on the assessment of mechanistic relations with specific attention to medicine, where mechanistic models are widely employed. I first survey recent contributions in the philosophical literature on mechanistic causation, and then take issue with Federica Russo and Jon Williamson’s thesis that two types of evidence, probabilistic and mechanistic, are at stake in the health sciences. I argue instead that a distinction should be drawn between previously acquired knowledge of mechanisms and yet-to-be-discovered knowledge of mechanisms and that both (...) probabilistic evidence and manipulation are essential with respect to newly discovered mechanisms. (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)

In this field guide, I distinguish five separate senses with which the term ‘mechanism’ is used in contemporary philosophy of science. Many of these senses have overlapping areas of application but involve distinct philosophical claims and characterize the target mechanisms in relevantly different ways. This field guide will clarify the key features of each sense and introduce some main debates, distinguishing those that transpire within a given sense from those that are best understood as concerning distinct senses. The ‘new mechanisms’ (...) sense is at the center of most of these contemporary debates and will be treated at greater length; subsequent senses of mechanism will be primarily distinguished from this one. In part I of this paper, I distinguish two senses of the term ‘mechanism’, both of which are explicitly hierarchical and nested in character, such that any given mechanism is comprised of smaller sub-mechanisms, in turn comprised of yet smaller sub-sub-mechanisms and so on. While both of the senses discussed here are anti-reductive, they differ in their focus on scientific practice versus metaphysics, in the degree of regularity they attribute to mechanisms, and in terms of their relationships to the discussions of mechanisms in the history of philosophy and science. (shrink)

Evidence-Based Medicine is a relatively new movement that seeks to put clinical med- icine on a firmer scientific footing. I take it as uncontroversial that medical practice should be based on best evidence-the interesting questions concern the details. This paper tries to move towards a coherent and unified account of best evidence in medicine, by exploring in particular the EBM position on RCTs (randomized controlled trials).

Evidence-Based Medicine is a relatively new movement that seeks to put clinical medicine on a firmer scientific footing. I take it as uncontroversial that medical practice should be based on best evidence—the interesting questions concern the details. This paper tries to move towards a coherent and unified account of best evidence in medicine, by exploring in particular the EBM position on RCTs.

This paper presents a counterfactual account of what a mechanism is. Mechanisms consist of parts, the behavior of which conforms to generalizations that are invariant under interventions, and which are modular in the sense that it is possible in principle to change the behavior of one part independently of the others. Each of these features can be captured by the truth of certain counterfactuals.

This paper presents a counterfactual account of what a mechanism is. Mechanisms consist of parts, the behavior of which conforms to generalizations that are invariant under interventions, and which are modular in the sense that it is possible in principle to change the behavior of one part independently of the others. Each of these features can be captured by the truth of certain counterfactuals.

A number of writers, myself included, have recently argued that an “interventionist” treatment of causation of the sort defended in Woodward, 2003 can be used to cast light on so-called “causal exclusion” arguments. This interventionist treatment of causal exclusion has in turn been criticized by other philosophers. This paper responds to these criticisms. It describes an interventionist framework for thinking about causal relationships when supervenience relations are present. I contend that this framework helps us to see that standard arguments for (...) causal exclusion involve mistaken assumptions about what it is appropriate to control for or hold fixed in assessing causal claims. The framework also provides a natural way of capturing the idea that properties that supervene on but that are not identical with realizing properties can be causally efficacious. (shrink)

Evidence hierarchies are widely used to assess evidence in systematic reviews of medical studies. I give several arguments against the use of evidence hierarchies. The problems with evidence hierarchies are numerous, and include methodological shortcomings, philosophical problems, and formal constraints. I argue that medical science should not employ evidence hierarchies, including even the latest and most-sophisticated of such hierarchies.

Amalgamating evidence of different kinds for the same hypothesis into an overall confirmation is analogous, I argue, to amalgamating individuals’ preferences into a group preference. The latter faces well-known impossibility theorems, most famously “Arrow’s Theorem”. Once the analogy between amalgamating evidence and amalgamating preferences is tight, it is obvious that amalgamating evidence might face a theorem similar to Arrow’s. I prove that this is so, and end by discussing the plausibility of the axioms required for the theorem.

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)

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)

Proponents of Evidence-based medicine (EBM) do not provide a clear role for basic science in therapeutic decision making. Of what they do say about basic science, most of it is negative. Basic science resides on the lower tiers of EBM's hierarchy of evidence. Therapeutic decisions, according to proponents of EBM, should be informed by evidence from randomised studies (and systematic reviews of randomised studies) rather than basic science. A framework of models explicates the links between the mechanisms of basic science, (...) experimental inquiry, and observed data. Relying on the framework of models I show that basic science often plays a role not only in specifying experiments, but also analysing and interpreting the data that is provided. Further, and contradicting what is implied in EBM's hierarchy of evidence, appeals to basic science are often required to apply clinical research to therapeutic questions. © 2010 Springer Science+Business Media B.V. (shrink)

Research on bounded rationality has two cultures, which I call ‘idealistic’ and ‘pragmatic’. Technically, the cultures differ on whether they build models based on normative axioms or empirical facts, assume that people's goal is to optimize or to satisfice, do not or do model psychological processes, let parameters vary freely or fix them, aim at explanation or prediction and test models from one or both cultures. Each culture tells a story about people's rationality. The story of the idealistic culture is (...) frustrating, with people in principle being able to know what they should do, but in practice systematically failing to do it. This story makes one hide in books for intellectual solace or surrender to the designs of someone smarter. The story of the pragmatic culture is empowering: If people are educated to use the right tool in the right situation, they do well. (shrink)

This paper sets out to analyze how causation works by focusing on biology, as represented by epidemiology and by scientific information on how the body works (“physiology”). It starts by exploring the specificity of evolved physiological systems, in which evolutionary, developmental and proximal causes all fit together, and the concept of function is meaningful; in contrast, this structure does not apply in epidemiology (or outside biology). Using these two contrasting branches of biology, I examine the role both of mechanism and (...) of difference making in causation. I find that causation necessarily involves both mechanism and difference making, and that they play complementary roles. Both are seen as ontologically necessary, even if the evidence is not always available for both. Influential monist accounts that focus on one of these, at the expense of ignoring the other, are found to be inadequate on these and on other grounds. Recent attempts to combine them are reviewed, notably that of Russo and Williamson (Int Stud Philos Sci 21:157–170, 2007), and it is argued that their epistemic view requires there to be a source of the different types of evidence that a rational agent would consider, and that this source must be ontic. I then analyze how causal relationships work in evolved physiological systems and in those studied by epidemiology, with a particular focus on how mechanism interacts with input. Finally, I consider this concept of causation from the perspective of everyday language, and of its possible generalisability outside biology. (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)

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)

:Proponents of behavioural policies seek to justify them as ‘evidence-based’. Yet they typically fail to show through which mechanisms these policies operate. This paper shows – at the hand of examples from economics and psychology – that without sufficient mechanistic evidence, one often cannot determine whether a given policy in its target environment will be effective, robust, persistent or welfare-improving. Because these properties are important for justification, policies that lack sufficient support from mechanistic evidence should not be called ‘evidence-based’.

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)

Inferences like these are known as extrapolations.

This 1996 book defends the prospects for a science of society. It argues that behind the diverse methods of the natural sciences lies a common core of scientific rationality that the social sciences can and sometimes do achieve. It also argues that good social science must be in part about large-scale social structures and processes and thus that methodological individualism is misguided. These theses are supported by a detailed discussion of actual social research, including theories of agrarian revolution, organizational ecology, (...) social theories of depression, and supply-demand explanations in economics. Professor Kincaid provides a general picture of explanation and confirmation in the social sciences and discusses the nature of scientific rationality, functional explanation, optimality arguments, meaning and interpretation, the place of microfoundations in social explanation, the status of neo-classical economics, the role of idealizations and non-experimental evidence, and other specific controversies. (shrink)

During the past decade, social mechanisms and mechanism-based ex- planations have received considerable attention in the social sciences as well as in the philosophy of science. This article critically reviews the most important philosophical and social science contributions to the mechanism approach. The first part discusses the idea of mechanism- based explanation from the point of view of philosophy of science and relates it to causation and to the covering-law account of explanation. The second part focuses on how the idea (...) of mechanisms has been used in the social sciences. The final part discusses recent developments in analytical sociology, covering the nature of sociological explananda, the role of theory of action in mechanism-based explanations, Merton’s idea of middle-range theory, and the role of agent-based simulations in the development of mechanism-based explanations. (shrink)

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)