Online research in philosophy

After clarifying the probabilistic conception of causality suggested by Good (1961-2), Suppes (1970), Cartwright (1979), and Skyrms (1980), we prove a sufficient condition for transitivity of causal chains. The bearing of these considerations on the units of selection problem in evolutionary theory and on the Newcomb paradox in decision theory is then discussed.

Comienzo este artículo mostrando que las teorías neohumeanas de la causalidad probabilista basadas en la noción de relevancia estadlstica (como la teoria de Suppes, 1970) se encuentran con múltiples e insuperables dificultades. Luego analizo brevemente algunas versiones de la causalidad probabilista que relativizan o prescinden de dicha noción: la de Cartwright, que postula la existencia de capacidades causales, y las de Salmon y Dowe, quienes, aunque se proponen no abandonar el suelo humeano, creen necesario introducir una ontología de propensiones. Y concluyo que el análisis de estas versiones demuestra que la causalidad probabilista constituye un nuevo y serio obstáculo para el enfoque humeano o neohumeano de la causalidad.In this paper I first show that the neohumean theories of probabilistic causality based on the notion of statistical relevance (as that of Suppes, 1970) run into many and unsolvable difficulties. Then I briefty analyze some accounts of probabilistic causality which relativize or avoid this notion: the Cartwright’s account, claiming the existence of causal capacities, and those of Salmon and Dowe, though trying to remain on a Humean ground, believe that the introduction of an ontology of propensities is required. I finally conclude that the analysis of these accounts shows that probabilistic causality constitutes a new and serious obstacle to the Humean or neohumean view of causality.

This paper argues that if the world is irreducibly stochastic, then both Salmon's S-R model of explanation and Fetzer's C-R model of explanation have the following undesirable consequence: the objective probability (associated with the model's relevance condition) of any actual macro-event is either undefined or else, if defined, it equals one--so that the event is not even a candidate for a probabilistic explanation. This result follows from the temporal ambiguity of ontic probability in an irreducibly stochastic world. It is argued further that an analogous difficulty faces those theories of probabilistic causality which depend upon the notions of contributing and counteracting causes. Because of the problem of temporal ambiguity, it is not possible to objectively label a particular event as a contributing (or a counteracting) cause of some subsequent event. The argument is carried through in detail for a recent theory of probabilistic causality proposed by Paul Humphreys.

Probabilistic accounts of causality have long had trouble with ‘spurious’ evidential correlations. Such correlations are also central to the case for causal decision theory—the argument that evidential decision theory is inadequate to cope with certain sorts of decision problem. However, there are now several strong defences of the evidential theory. Here I present what I regard as the best defence, and apply it to the probabilistic approach to causality. I argue that provided a probabilistic theory appeals to the notions of agency and effective strategy, it can avoid the problem of spurious causes. I show that such an appeal has other advantages; and argue that it is not illegitimate, even for a causal realist.

The investigation of probabilistic causality has been plagued by a variety of misconceptions and misunderstandings. One has been the thought that the aim of the probabilistic account of causality is the reduction of causal claims to probabilistic claims. Nancy Cartwright (1979) has clearly rebutted that idea. Another ill-conceived idea continues to haunt the debate, namely the idea that contextual unanimity can do the work of objective homogeneity. It cannot. We argue that only objective homogeneity in combination with a causal interpretation of Bayesian networks can provide the desired criterion of probabilistic causality.

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.

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.

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.

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.