Online research in philosophy

Allow me to recapitulate some territory that will be familiar to most readers. Here is how the problem of mental causation has typically been set up since shortly after the onset of non-reductive physicalism. It is now widely assumed that the realm of the physical is causally closed: every physical event has a complete physical cause, a cause that is sufficient for the event’s occurrence. This apparently leaves us with a limited number of options concerning psychological causation, none of which appear hugely attractive. Either: (a) the psychological is epiphenomenal and can have no causal impact on the physical, or (b) the psychological is identical with the physical, or (c) thoughts and actions are all over-determined, each one having two distinct sufficient causes. Option (b) subdivides into two further options. Either (b1) the psychological reduces to the physical and every psychological property is identical with some physical property, or (b2) token psychological events are identical with or constituted from token physical events but psychological properties are not identical with physical properties. (b1) is widely held to be inconsistent with the multiple realisation of the psychological by the physical. And (b2) appears to bring us back to the original problematic, with the properties as the locus of tension. If one event causes another it does so in virtue some of its properties and not others. If I throw a stone at a window and the window breaks, it is because the stone was hard and heavy that it broke the window and not, say, because it was grey and millions of years old. The properties in virtue of which an event has a particular effect are typically called the ‘causally efficacious properties of the cause with respect to the effect.’ Suppose, then that token neural event causes an action. We can ask ‘Does it do so in virtue of its physical properties or its psychological properties?’ and we are back to choosing between options (a) and (c) or returning to (b1)..

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.

Argument for Epiphenomenalism [I]: (A) Mental event-tokens are identical with physical event-tokens. (B) The causal powers of a physical event are determined only by its physical properties; and (C) mental properties are not reducible to physical properties.

This paper examines the relationship between physical theories of causation and theories of difference-making. It is plausible to think that such theories are compatible with one another as they are aimed at different targets: the former, an empirical account of actual causal relations; the latter, an account that will capture the truth of most of our ordinary causal claims. The question then becomes: what is the relationship between physical causation and difference-making? Is one kind of causal fact more fundamental than the other? This paper defends causal foundationalism: the view that facts about difference-making are dependent on the obtaining of facts about physical causation. However, the paper's main goal is to clarify the structure of the debate. At the end of the paper, it is shown how settling the issue about the relationship between physical theories of causation and theories of difference-making has more than mere intrinsic interest in unifying the very different pursuits that have been undertaken in the philosophy of causation. It can help to break a stalemate that has arisen in the current debate about mental causation.

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.

Yablo suggests that we can understand the possibility of mental causation by supposing that mental properties determine physical properties, in the classic sense of determination according to which red determines scarlet. Determinates and their determinables do not compete for causal relevance, so if mental and physical properties are related as determinable and determinates, they should not compete for causal relevance either. I argue that this solution won''t work. I first construct a more adequate account of determination than that provided by Yablo. I then consider two common accounts of the mental, token identity theories and dispositional theories, and argue that on neither do mental and physical properties satisfy the requirements for determination.

One part of the true theory of actual causation is a set of conditions responsible for eliminating all of the non-causes of an effect that can be discerned at the level of counterfactual structure. I defend a proposal for this part of the theory.

Process theories of causality seek to explicate causality as a property of individual causal processes. This paper examines the capacity of such theories to account for the asymmetry of causation. Three types of theories of asymmetry are discussed; the subjective, the temporal, and the physical, the third of these being the preferred approach. Asymmetric features of the world, namely the entropic and Kaon arrows, are considered as possible sources of causal asymmetry and a physical theory of asymmetry is subsequently developed with special reference to the questions of objectivity and backwards causation.

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.