Online research in philosophy

It is argued in this paper that although much attention has been paid to causal chains and common causes within the literature on probabilistic causality, a primary virtue of that approach is its ability to deal with cases of multiple causation. In doing so some ways are indicated in which contemporary sine qua non analyses of causation are too narrow (and ways in which probabilistic causality is not) and an argument by Reichenbach designed to provide a basis for the asymmetry of causation is refined. The importance of referring causal claims to an abstract model is also emphasized.

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.

During the past decades several philosophers of science and social scientists have been interested in the problems of causation. Recently attention has been given to probabilistic causation in dichotomous causal systems. The paper uses the basic features of probabilistic causation to argue that the causal modeling approaches developed by such researchers as Blalock (1964) and Duncan (1975) can provide, when an additional assumption is added, adequate qualitative measures of one variableś causal influence upon another. Finally, some of the difficulties and issues involved in developing adequate quantitative measures are discussed, and it is concluded that the causal modeling measures cannot provide adequate quantitative measures.

During the past decades several philosophers of science and social scientists have been interested in the problems of causation. Recently attention has been given to probabilistic causation in dichotomous causal systems. The paper uses the basic features of probabilistic causation to argue that the causal modeling approaches developed by such researchers as Blalock (1964) and Duncan (1975) can provide, when an additional assumption is added, adequate qualitative measures of one variable causal influence upon another. Finally, some of the difficulties and issues involved in developing adequate quantitative measures are discussed, and it is concluded that the causal modeling measures cannot provide adequate quantitative measures.

A probabilistic theory of causation is a theory which holds that the central feature of causation is that causes (usually) raise the probability of their effects. In this dissertation, I defend Hans Reichenbach's original (1953) version of the probabilistic theory of causation, which analyses causal relations in terms of a three place statistical betweenness relation. Unlike most discussions of this theory, I hold that the statistical relation should be taken as a sufficient, but not as necessary, condition for causal betweenness. With this difference in interpretation, Reichenbach's theory is shown to be immune to all of the criticisms which have been raised against it in the last..

This paper examines a promising probabilistic theory of singular causation developed by David Lewis. I argue that Lewis' theory must be made more sophisticated to deal with certain counterexamples involving pre-emption. These counterexamples appear to show that in the usual case singular causation requires an unbroken causal process to link cause with effect. I propose a new probabilistic account of singular causation, within the framework developed by Lewis, which captures this intuition.

The starting point in the development of probabilistic analyses of token causation has usually been the naïve intuition that, in some relevant sense, a cause raises the probability of its effect. But there are well-known examples both of non-probability-raising causation and of probability-raising non-causation. Sophisticated extant probabilistic analyses treat many such cases correctly, but only at the cost of excluding the possibilities of direct non-probability-raising causation, failures of causal transitivity, action-at-a-distance, prevention, and causation by absence and omission. I show that an examination of the structure of these problem cases suggests a different treatment, one which avoids the costs of extant probabilistic analyses.

“Probabilistic Causation” designates a group of theories that aim to characterize the relationship between cause and effect using the tools of probability theory. The central idea behind these theories is that causes change the probabilities of their effects. This article traces developments in probabilistic causation, including recent developments in causal modeling. A variety of issues within, and objections to, probabilistic theories of causation will also be discussed.

I argue that the orthodox account of probabilistic causation, on which probabilistic causes determine the probability of their effects, is inconsistent with certain ontological assumptions implicit in scientific practice. In particular, scientists recognize the possibility that properties of populations can cause the behavior of members of the populations. Such emergent population level causation is metaphysically impossible on the orthodoxy.

Larry Wright and others have advanced causal accounts of functional explanation, designed to alleviate fears about the legitimacy of such explanations. These analyses take functional explanations to describe second order causal relations. These second order relations are conceptually puzzling. I present an account of second order causation from within the framework of Eells' probabilistic theory of causation; the account makes use of the population-relativity of causation that is built into this theory.