Philosophers of science typically associate the causal‐mechanical view of scientific explanation with the work of Railton and Salmon. In this paper I shall argue that the defects of this view arise from an inadequate analysis of the concept of mechanism. I contrast Salmon’s account of mechanisms in terms of the causal nexus with my own account of mechanisms, in which mechanisms are viewed as complex systems. After describing these two concepts of mechanism, I show how the complex‐systems approach avoids certain (...) objections to Salmon’s account of causal‐mechanical explanation. I conclude by discussing how mechanistic explanations can provide understanding by unification. (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)

Explanations in the life sciences frequently involve presenting a model of the mechanism taken to be responsible for a given phenomenon. Such explanations depart in numerous ways from nomological explanations commonly presented in philosophy of science. This paper focuses on three sorts of differences. First, scientists who develop mechanistic explanations are not limited to linguistic representations and logical inference; they frequently employ diagrams to characterize mechanisms and simulations to reason about them. Thus, the epistemic resources for presenting mechanistic explanations are (...) considerably richer than those suggested by a nomological framework. Second, the fact that mechanisms involve organized systems of component parts and operations provides direction to both the discovery and testing of mechanistic explanations. Finally, models of mechanisms are developed for specific exemplars and are not represented in terms of universally quantified statements. Generalization involves investigating both the similarity of new exemplars to those already studied and the variations between them. (shrink)

How do we know what we "know"? How did we –as individuals and as a society – come to accept certain knowledge as fact? In _Human Knowledge,_ Bertrand Russell questions the reliability of our assumptions on knowledge. This brilliant and controversial work investigates the relationship between ‘individual’ and ‘scientific’ knowledge. First published in 1948, this provocative work contributed significantly to an explosive intellectual discourse that continues to this day.

Part I of this paper introduces a range of mechanistic theories of causality, including process theories and the complex-systems theories, and some of the problems they face. Part II argues that while there is a decisive case against a purely mechanistic analysis, a viable theory of causality must incorporate mechanisms as an ingredient, and describes one way of providing an analysis of causality which reaps the rewards of the mechanistic approach without succumbing to its pitfalls.

The Recursive Bayesian Net (RBN) 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)

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)

This paper addresses questions about how the levels of causality (generic and single-case causality) are related. One question is epistemological: can relationships at one level be evidence for relationships at the other level? We present three kinds of answer to this question, categorised according to whether inference is top-down, bottom-up, or the levels are independent. A second question is metaphysical: can relationships at one level be reduced to relationships at the other level? We present three kinds of answer to this (...) second question, categorised according to whether single-case relations are reduced to generic, generic relations are reduced to single-case, or the levels are independent. We then explore causal inference in autopsy. This is an interesting case study, we argue, because it refutes all three epistemologies and all three metaphysics. We close by sketching an account of causality that survives autopsy—the epistemic theory. (shrink)

In a recent article in this journal, Federica Russo and Jon Williamson argue that an analysis of causality in terms of probabilistic relationships does not do justice to the use of mechanistic evidence to support causal claims. I will present Ronald Giere's theory of probabilistic causation, and show that it can account for the use of mechanistic evidence (both in the health sciences—on which Russo and Williamson focus—and elsewhere). I also review some other probabilistic theories of causation (of Suppes, Eells, (...) and Humphreys) and show that they cannot account for the use of mechanistic evidence. I argue that these theories are also inferior to Giere's theory in other respects. (shrink)

The philosophical theory of scientific explanation proposed here involves a radically new treatment of causality that accords with the pervasively statistical character of contemporary science. Wesley C. Salmon describes three fundamental conceptions of scientific explanation--the epistemic, modal, and ontic. He argues that the prevailing view is untenable and that the modal conception is scientifically out-dated. Significantly revising aspects of his earlier work, he defends a causal/mechanical theory that is a version of the ontic conception. Professor Salmon's theory furnishes a robust (...) argument for scientific realism akin to the argument that convinced twentieth-century physical scientists of the existence of atoms and molecules. To do justice to such notions as irreducibly statistical laws and statistical explanation, he offers a novel account of physical randomness. The transition from the "reviewed view" of scientific explanation to the causal/mechanical model requires fundamental rethinking of basic explanatory concepts. (shrink)

This paper discusses several distinct process theories of causality offered in recent years by Phil Dowe and me. It addresses problems concerning the explication of causal process, causal interaction, and causal transmission, whether given in terms of transmission of marks, transmission of invariant or conserved quantities, or mere possession of conserved quantities. Renouncing the mark-transmission and invariant quantity criteria, I accept a conserved quantity theory similar to Dowe's--differing basically with respect to causal transmission. This paper also responds to several fundamental (...) constructive criticisms contained in Christopher Hitchcock's discussion of both the mark-transmission and the conserved quantity theories. (shrink)

The paper addresses the question of how different types of evidence ought to inform public health policy. By analysing case studies on obesity, the paper draws lessons about the different roles that different types of evidence play in setting up public health policies. More specifically, it is argued that evidence of difference-making supports considerations about ‘what works for whom in what circumstances’, and that evidence of mechanisms provides information about the ‘causal pathways’ to intervene upon.

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)

The concept of mechanism is analyzed in terms of entities and activities, organized such that they are productive of regular changes. Examples show how mechanisms work in neurobiology and molecular biology. Thinking in terms of mechanisms provides a new framework for addressing many traditional philosophical issues: causality, laws, explanation, reduction, and scientific change.

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.

In this paper, I examine the comparatively neglected intuition of production regarding causality. I begin by examining the weaknesses of current production accounts of causality. I then distinguish between giving a good production account of causality and a good account of production. I argue that an account of production is needed to make sense of vital practices in causal inference. Finally, I offer an information transmission account of production based on John Collier’s work that solves the primary weaknesses of current (...) production accounts: applicability and absences. (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)

Philosophers of science typically associate the causal-mechanical view of scientific explanation with the work of Railton and Salmon. In this paper I shall argue that the defects of this view arise from an inadequate analysis of the concept of mechanism. I contrast Salmon's account of mechanisms in terms of the causal nexus with my own account of mechanisms, in which mechanisms are viewed as complex systems. After describing these two concepts of mechanism, I show how the complex-systems approach avoids certain (...) objections to Salmon's account of causal-mechanical explanation. I conclude by discussing how mechanistic explanations can provide understanding by unification. (shrink)

Philosophers of science typically associate the causal-mechanical view of scientific explanation with the work of Railton and Salmon. In this paper I shall argue that the defects of this view arise from an inadequate analysis of the concept of mechanism. I contrast Salmon's account of mechanisms in terms of the causal nexus with my own account of mechanisms, in which mechanisms are viewed as complex systems. After describing these two concepts of mechanism, I show how the complex-systems approach avoids certain (...) objections to Salmon's account of causal-mechanical explanation. I conclude by discussing how mechanistic explanations can provide understanding by unification. (shrink)

This paper examines Wesley Salmon's "process" theory of causality, arguing in particular that there are four areas of inadequacy. These are that the theory is circular, that it is too vague at a crucial point, that statistical forks do not serve their intended purpose, and that Salmon has not adequately demonstrated that the theory avoids Hume's strictures about "hidden powers". A new theory is suggested, based on "conserved quantities", which fulfills Salmon's broad objectives, and which avoids the problems discussed.

Bayesian nets are widely used in artificial intelligence as a calculus for causal reasoning, enabling machines to make predictions, perform diagnoses, take decisions and even to discover causal relationships. This book, aimed at researchers and graduate students in computer science, mathematics and philosophy, brings together two important research topics: how to automate reasoning in artificial intelligence, and the nature of causality and probability in philosophy.

Thirty years after Lewis's paper, this book brings together some of the most important recent work connecting—or, in some cases, disputing the connection ...

Inferences like these are known as extrapolations.

The anti-causal prophecies of last century have been disproved. Causality is neither a ‘relic of a bygone’ nor ‘another fetish of modern science’; it still occupies a large part of the current debate in philosophy and the sciences. This investigation into causal modelling presents the rationale of causality, i.e. the notion that guides causal reasoning in causal modelling. It is argued that causal models are regimented by a rationale of variation, nor of regularity neither invariance, thus breaking down the dominant (...) Human paradigm. The notion of variation is shown to be embedded in the scheme of reasoning behind various causal models: e.g. Rubin’s model, contingency tables, and multilevel analysis. It is also shown to be latent – yet fundamental – in many philosophical accounts. Moreover, it has significant consequences for methodological issues: the warranty of the causal interpretation of causal models, the levels of causation, the characterisation of mechanisms, and the interpretation of probability. This book offers a novel philosophical and methodological approach to causal reasoning in causal modelling and provides the reader with the tools to be up to date about various issues causality rises in social science. (shrink)

This chapter explores the idea that causal inference is warranted if and only if the mechanism underlying the inferred causal association is identified. This mechanistic stance is discernible in the epidemiological literature, and in the strategies adopted by epidemiologists seeking to establish causal hypotheses. But the exact opposite methodology is also discernible, the black box stance, which asserts that epidemiologists can and should make causal inferences on the basis of their evidence, without worrying about the mechanisms that might underlie their (...) hypotheses. I argue that the mechanistic stance is indeed a bad methodology for causal inference. However, I detach and defend a mechanistic interpretation of causal generalisations in epidemiology as existence claims about underlying mechanisms. (shrink)

After introducing a range of mechanistic theories of causality and some of the problems they face, I argue that while there is a decisive case against a purely mechanistic analysis, a viable theory of causality must incorporate mechanisms as an ingredient. I describe one way of providing an analysis of causality which reaps the rewards of the mechanistic approach without succumbing to its pitfalls.

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)

The notion of ‘causal web’ emerged in the epidemiological literature in the early Sixties and had to wait until the Nineties for a thorough critical appraisal. Famously, Nancy Krieger argued that such a notion isn’t helpful unless we specify what kind of spiders create the webs. This means, according to Krieger, (i) that the role of the spiders is to provide an explanation of the yarns of the web and (ii) that the sought spiders have to be biological and social. (...) This paper contributes to the development of the notion of causal web, elaborating on the two following points: (i) to catch the spiders we need multi-fold evidence—specifically, mechanistic and difference-making—and (ii) for the eco-social to be explanatory, the web has to be mechanistic in a sense to be specified. (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)

This chapter provides an overview of a range of probabilistic theories of causality, including those of Reichenbach, Good and Suppes, and the contemporary causal net approach. It discusses two key problems for probabilistic accounts: counterexamples to these theories and their failure to account for the relationship between causality and mechanisms. It is argued that to overcome the problems, an epistemic theory of causality is required.

& Carnegie Mellon University Abstract The rationality of human causal judgments has been the focus of a great deal of recent research. We argue against two major trends in this research, and for a quite different way of thinking about causal mechanisms and probabilistic data. Our position rejects a false dichotomy between "mechanistic" and "probabilistic" analyses of causal inference -- a dichotomy that both overlooks the nature of the evidence that supports the induction of mechanisms and misses some important probabilistic (...) implications of mechanisms. This dichotomy has obscured an alternative conception of causal learning: for discrete events, a central adaptive task is to induce causal mechanisms in the environment from probabilistic data and prior knowledge. Viewed from this perspective, it is apparent that the probabilistic norms assumed in the human causal judgment literature often do not map onto the mechanisms generating the probabilities. Our alternative conception of causal judgment is more congruent with both scientific uses of the notion of causation and observed causal judgments of untutored reasoners. We illustrate some of the relevant variables under this conception, using a framework for causal representation now widely adopted in computer science and, increasingly, in statistics. We also review the formulation and evidence for a theory of human causal induction (Cheng, 1997) that adopts this alternative conception. (shrink)