Online research in philosophy

In order to motivate the thesis that there is no single concept of causation that can do justice to all of our core intuitions concerning that concept, Ned Hall has argued that there is a conflict between a counterfactual criterion of causation and the condition of causal locality. In this paper I critically examine Hall’s argument within the context of a more general discussion of the role of locality constraints in a causal conception of the world. I present two strategies that defenders of counterfactual accounts of causation can pursue to respond to Hall’s challenge—including the adoption of a counterfactual condition that is sufficient for causal action-at-a-distance in place of Hall’s ‘process’ condition—and conclude that Hall’s argument against counterfactual accounts of causation is unsuccessful.

Nancy Cartwright offers an account of causal powers, and argues that it explains some important general features of scientific method. Patricia Cheng argues that this theory is superior as a psychological theory of learning to standard models of conditioning. I extend and develop the theory, and argue that it provides the best explanation of a number of problem cases for philosophical theories of causation, including preemption, overdetermination and puzzles about transitivity. Hitchcock and Halpern & Pearl on ‘actual causes’ Problems and morals 2.1 Puzzles about prevention 2.2 Counterfactuals Causal powers 3.1 Generative causal power 3.2 Preventative causal power Net and component powers ‘Actual’ or ‘successful’ causes Solutions to puzzle cases Conclusion.

Polygenic effects have more than one cause. They testify to the fact that several causal contributors are sometimes simultaneously involved in causation. The importance of polygenic causation was noticed early on by Mill (1893). It has since been shown to be a problem for causal-law approaches to causation and accounts of causation cast in terms of capacities. However, polygenic causation needs to be examined more thoroughly in the emerging literature on causal mechanisms. In this paper I examine whether an influential theory of mechanisms proposed by Peter Machamer, Lindley Darden and Carl Craver can accommodate polygenic effects and other forms of causal interaction. This theory is problematic, I will argue, because it ascribes a central role to activities. In it, activities are needed not only to constitute mechanisms but also to perform the causal role of mechanisms. Any such mechanism-as-activity will be incompatible with causal situations where either no or merely another kind of activity occurs. But, as I will try to illustrate in this paper, both kinds of situation may be frequent. If I am right, the view that Machamer and colleagues suggest leads to an impoverished conception of mechanism.

In a recent paper Causal Asymmetry, Douglas Ehring has proposed an intriguing solution to the vexing problem of causal asymmetry. The aim of this paper is to show that his theory is not satisfactory. Moreover, the examples that I use in showing the defect of Ehring's theory also indicate that the counterfactual analysis of causation has a problem that cannot be remedied by Marshall Swain's suggested refinement of the counterfactual analysis of causation in Causation and Distinct Events.

I defend what may loosely be called an eliminativist account of causation by showing how several of the main features of causation, namely asymmetry, transitivity, and necessitation (or sometimes probability-raising), arise from the combination of fundamental dynamical laws and a special constraint on the macroscopic structure of matter in the past. At the microscopic level, the causal features of necessitation and transitivity are grounded, but not the asymmetry. At the coarse-grained level of the macroscopic physics, the causal asymmetry is grounded, but not the necessitation or transitivity. Thus, at no single level of description does the physics justify the conditions that are taken to be constitutive of causation. Nevertheless, if we mix our reasoning about the microscopic and macroscopic descriptions, the structure provided by the dynamics and special initial conditions can justify the folk concept of causation to a significant extent. I explain why our causal concept works so well even though at bottom it is comprised of a patchwork of principles that don't mesh well.

Counterfactual theories of causation of the sort presented in Mackie, 1974, and Lewis, 1973 are a familiar part of the philosophical landscape. Such theories are typically advanced primarily as accounts of the metaphysics of causation. But they also raise empirical psychological issues concerning the processes and representations that underlie human causal reasoning. For example, do human subjects internally represent causal claims in terms of counterfactual judgments and when they engage in causal reasoning, does this involves reasoning about counterfactual claims? This paper explores several such issues from a broadly interventionist perspective.

Causation is a deeply intuitive and familiar relation, gripped powerfully by common sense. Or so it seems. But as is typical in philosophy, deep intuitive familiarity has not led to any philosophical account of causation that is at once clean, precise, and widely agreed upon. Not for lack of trying: the last 30 years or so have seen dozens of attempts to provide such an account, and the pace of development is, if anything, accelerating. (See Collins, Hall and Paul 2003a for a comprehensive sampling of the latest work.) It is safe to say that none has yet succeeded. It is also safe to say that the effort put into their development has yielded a wealth of insights into causation. And it is, arguably, from the study of causal preemption—cases that feature multiple competing candidates for the title of “cause” of some given effect—that the greatest such wealth has flowed. These cases come in a number of varieties: so-called early and late preemption, symmetric overdetermination, and trumping preemption. Collectively, they place extremely severe constraints on any philosophical account of causation that can successfully handle them. One of the lessons they have to teach, then, is a lesson about the form that a successful analysis of causation must have. There is a deeper lesson, a lesson about the nature of causation itself, or if you like, about the workings of our causal concept. It emerges from close study of the struggles that extant accounts face in trying to provide even remotely attractive treatments of causal preemption. It is this: There appears to be a significant and perhaps intractable tension between one strand in our thinking about causation—a strand that emphasizes the need for causes to be connected to their effects via intervening processes with the right intrinsic character—and another—one that emphasizes the claim that effects in some sense depend on their causes. By the end of this essay, this tension will be vividly apparent..

We currently have on offer a variety of different theories of causation. Many are strikingly good, providing detailed and plausible treatments of exemplary cases; and all suffer from clear counterexamples. I argue that, contra Hume and Kant, this is because causation is not a single, monolithic concept. There are different kinds of causal relations imbedded in different kinds of systems, readily described using thick causal concepts. Our causal theories pick out important and useful structures that fit some familiar cases—cases we discover and ones we devise to fit.

When is a cause of a cause of an effect also a cause of that effect? The right answer is either Sometimes or Always . In favour of Always , transitivity is considered by some to be necessary for distinguishing causes from redundant non-causal events. Moreover transitivity may be motivated by an interest in an unselective notion of causation, untroubled by principles of invidious discrimination. And causal relations appear to add up like transitive relations, so that the obtaining of the overarching relation is not independent of the obtaining of the intermediaries. On the other hand, in favour of Sometimes , often we seem not to treat events that are very spatiotemporally remote from an effect as its causes, even when connected to the effect in question by a chain of counterfactual or chance-raising dependence. Moreover cases of double prevention provide counterexamples to causal transitivity even over short chains. According to the argument of this paper, causation is non-transitive. Transitizing causation provides no viable account of causal redundancy. An unselective approach to causation may motivate resisting the distance counterexamples to transitivity, but it does not help with double prevention, and even makes it more intractable. The strongest point in favour of transitivity is the adding up of causal relations, and this is the point that extant non-transitizing analyses have not adequately addressed. I propose a necessary condition on causation that explains the adding up phenomenon. In doing so it also provides a unifying explanation of distance and double prevention counterexamples to transitivity.

Counter factual theories of Causation have had problems with cases of probabilistic causation and preemption. I put forward a counterfactual theory that seems to deal with these problematic cases and also has the virtue of providing an account of the alleged asymmetry between hasteners and delayers: the former usually being counted as causes, the latter not. I go on to consider a new type of problem case that has not received so much attention in the literature, those I dub catalysts and anti-catalysts, and show how my account needs to be adjusted to deliver the right verdicts in these cases. The net result is a particular conception of a cause that I try to spell out in the closing section of the paper. In that section, I also briefly discuss causal asymmetry and the purpose behind providing a counterfactual theory of causation.