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)

We argue that intelligible appeals to interlevel causes (top-down and bottom-up) can be understood, without remainder, as appeals to mechanistically mediated effects. Mechanistically mediated effects are hybrids of causal and constitutive relations, where the causal relations are exclusively intralevel. The idea of causation would have to stretch to the breaking point to accommodate interlevel causes. The notion of a mechanistically mediated effect is preferable because it can do all of the required work without appealing to mysterious interlevel causes. When interlevel (...) causes can be translated into mechanistically mediated effects, the posited relationship is intelligible and should raise no special philosophical objections. When they cannot, they are suspect. (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)

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)

This article deals with mechanisms conceived as composed of entities and activities. In response to many perplexities about the nature of activities, a number of arguments are developed concerning their epistemic and ontological status. Some questions concerning the relations between cause and causal explanation and mechanisms are also addressed.

Robustness is a common platitude: hypotheses are better supported with evidence generated by multiple techniques that rely on different background assumptions. Robustness has been put to numerous epistemic tasks, including the demarcation of artifacts from real entities, countering the “experimenter’s regress,” and resolving evidential discordance. Despite the frequency of appeals to robustness, the notion itself has received scant critique. Arguments based on robustness can give incorrect conclusions. More worrying is that although robustness may be valuable in ideal evidential circumstances (i.e., (...) when evidence is concordant), often when a variety of evidence is available from multiple techniques, the evidence is discordant. †To contact the author, please write to: Jacob Stegenga, Department of Philosophy, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093; e‐mail: [email protected]. (shrink)

This paper defends an interventionist treatment of mechanisms and contrasts this with Waskan (forthcoming). Interventionism embodies a difference-making conception of causation. I contrast such conceptions with geometrical/mechanical or “actualist” conceptions, associating Waskan’s proposals with the latter. It is argued that geometrical/mechanical conceptions of causation cannot replace difference-making conceptions in characterizing the behavior of mechanisms, but that some of the intuitions behind the geometrical/mechanical approach can be captured by thinking in terms of spatio-temporally organized difference-making information.

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)

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.

My aim in this paper is to make a case for the singularist view from the perspective of a mechanical theory of causation, and to explain what, from this perspective, causal generalizations mean, and what role they play within the mechanical theory.

Although there has been much recent discussion on mechanisms in philosophy of science and social theory, no shared understanding of the crucial concept itself has emerged. In this paper, a distinction between two core concepts of mechanism is made on the basis that the concepts correspond to two different research strategies: the concept of mechanism as a componential causal system is associated with the heuristic of functional decomposition and spatial localization and the concept of mechanism as an abstract form of (...) interaction is associated with the strategy of abstraction and simple models. The causal facts assumed and the theoretical consequences entailed by an explanation with a given mechanism differ according to which concept of mechanism is in use. Research strategies associated with mechanism concepts also involve characteristic biases that should be taken into account when using them, especially in new areas of application. (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)

I present an alternative account of causation in the biomedical and social sciences according to which the meaning of causal claims is given by their inferential relations to other claims. Specifically, I will argue that causal claims are inferentially related to certain evidential claims as well as claims about explanation, prediction, intervention and responsibility. I explain in some detail what it means for a claim to be inferentially related to another and finally derive some implication of the proposed account for (...) the epistemology, semantics and metaphysics of causation. (shrink)

The aim of this paper is to explicate causal generalizations such as.

Discontented people might talk of corruption in the Commons, closeness in the Commons and the necessity of reforming the Commons, said Mr. Spenlow solemnly, in conclusion; but when the price of wheat per bushel had been the highest, the Commons had been the busiest; and a man might lay his hand upon his heart, and say this to the whole world, – ‘Touch the Commons, and down comes the country!’.

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)