Online research in philosophy

Using Bayesian network causal models, we provide a simple general account of probabilistic causal interaction. We also detail problems in the leading accounts by Ellery Eells, and any others which require valence reversals, contextual unanimity, or average effects.

Sober 2011 argues that, contrary to Hume, some causal statements can be known a priori to be true?notably, some ?would promote? statements figuring in causal models of natural selection. We find Sober's argument unconvincing. We regard the Humean thesis as denying that causal explanations contain any a priori knowable statements specifying certain features of events to be causally relevant. We argue that not every ?would promote? statement is genuinely causal, and we suggest that Sober has not shown that his examples of ?would promote? statements manage to achieve a priori status without sacrificing their causal character.

A theory of causality based upon physical processes is developed. Causal processes are distinguished from pseudo-processes by means of a criterion of mark transmission. Causal interactions are characterized as those intersections of processes in which the intersecting processes are mutually modified in ways which persist beyond the point of intersection. Causal forks of three kinds (conjunctive, interactive, and perfect) are introduced to explicate the principle of the common cause. Causal forks account for the production of order and modifications of order; causal processes account for the propagation of causal influence.

A graphical model is a graph that represents a set of conditional independence relations among the vertices (random variables). The graph is often given a causal interpretation as well. I describe how graphical causal models can be used in an algorithm for constructing partial information about causal graphs from observational data that is reliable in the large sample limit, even when some of the variables in the causal graph are unmeasured. I also describe an algorithm for estimating from observational data (in some cases) the total effect of a given variable on a second variable, and theoretical insights into fundamental limitations on the possibility of certain causal inferences by any algorithm whatsoever, and regardless of sample size.

Econometrics applies statistical methods to study economic phenomena. Roughly, by means of equations, econometricians typically account for the response variable in terms of a number of explanatory variables. The question arises under what conditions econometric models can be given a causal interpretation. By drawing the distinction between associational models and causal models, the paper argues that a proper use of background knowledge, three distinct types of assumptions (statistical, extra-statistical, and causal), and the hypothetico-deductive methodology provide sufficient conditions for a causal interpretation of econometric models.

The invariance under interventions –account of causal explanation imposes a modularity constraint on causal systems: a local intervention on a part of the system should not change other causal relations in that system. This constraint has generated criticism against the account, since many ordinary causal systems seem to break this condition. This paper answers to this criticism by noting that explanatory models are always models of specific causal structures, not causal systems as a whole, and that models of causal structures can have different modularity properties which determine what can and what cannot be explained with the model.

In an influential article published in 1982, Bas Van Fraassen developed an argument against causal realism on the basis of an analysis of the Einstein-Podolsky-Rosen correlations of quantum mechanics. Several philosophers of science and experts in causal inference -including some causal realists like Wesley Salmon- have accepted Van Fraassen’s argument, interpreting it as a proof that the quantum correlations cannot be given any causal model. In this paper I argue that Van Fraassen’s article can also be interpreted as a good guide to the different causal models available for the EPR correlations, and their relative virtues. These models in turn give us insight into some of the unusual features that quantum propensicies might have.

Learning to understand a single causal system can be an achievement, but humans must learn about multiple causal systems over the course of a lifetime. We present a hierarchical Bayesian framework that helps to explain how learning about several causal systems can accelerate learning about systems that are subsequently encountered. Given experience with a set of objects, our framework learns a causal model for each object and a causal schema that captures commonalities among these causal models. The schema organizes the objects into categories and specifies the causal powers and characteristic features of these categories and the characteristic causal interactions between categories. A schema of this kind allows causal models for subsequent objects to be rapidly learned, and we explore this accelerated learning in four experiments. Our results confirm that humans learn rapidly about the causal powers of novel objects, and we show that our framework accounts better for our data than alternative models of causal learning.

We further develop the mathematical theory of causal interventions, extending earlier results of Korb, Twardy, Handfield, & Oppy, (2005) and Spirtes, Glymour, Scheines (2000). Some of the skepticism surrounding causal discovery has concerned the fact that using only observational data can radically underdetermine the best explanatory causal model, with the true causal model appearing inferior to a simpler, faithful model (cf. Cartwright, (2001). Our results show that experimental data, together with some plausible assumptions, can reduce the space of viable explanatory causal models to one.

Wesley Salmon has developed a theory of causation which makes use of the concepts of a "causal process" and a "causal interaction." Roughly, a causal process is a process which transmits its own structure, and a causal interaction is an intersection of processes which transforms the character of these processes. The cause-effect relation is analyzed as a causal interaction followed by a causal process which terminates in a further causal interaction. In this paper I present a series of problem cases which run "counter" to Salmon's account.