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. (shrink)

What are scientific theories and how should they be represented? In this article, I propose a causal–structural account, according to which scientific theories are to be represented as sets of interrelated causal and credal nets. In contrast with other accounts of scientific theories (such as Sneedian structuralism, Kitcher’s unificationist view, and Darden’s theory of theoretical components), this leaves room for causality to play a substantial role. As a result, an interesting account of explanation is provided, which sheds light on explanatory (...) unification within a causalist framework. The theory of classical genetics is used as a case study. 1 Introduction2 The Theory of Classical Genetics3 Three Philosophical Accounts of the Theory of Classical Genetics3.1 The structuralist account3.2 Kitcher’s unificationism3.3 Darden and theory change in science4 A Common Lacuna: Where is Causality?5 Woodward’s Interventionist Account of Causation6 Causal Bayes Nets and Their Interrelations6.1 Causal Bayes nets6.2 Relations among causal nets6.3 Credal nets and their interrelations7 The Theory of the Gene and its Causal Graph8 A First Exemplar: Stem Length in Pea Plants8.1 Three crosses on stem length in pea plants8.2 The causal graph for stem length in pea plants8.3 Morgan’s explanatory principles and the credal net for stem length in pea plants9 Explaining Mendel’s Crosses: A Causal–Structural Account10 Monohybrid Crosses with Complete Dominance11 Exemplars,Explanatory Patterns, Generic Credal Nets, and Mechanism Schemas12 Incomplete Dominance13 Anomalies14 Multi-hybrid Crosses with Independent Assortment15 Multi-hybrid Crosses with Linkage and Crossing-Over16 Double Crossing-Over and the Linear Order of the Gene17 Causal–Structural Explanation18 Explanatory Unification19 Concluding Remarks. (shrink)

Highly idealized models may serve various epistemic functions, notably explanation, in virtue of representing the world. Inferentialism provides a prima facie compelling characterization of what constitutes the representation relation. In this paper, I argue that what I call factive inferentialism does not provide a satisfactory solution to the puzzle of model-based—factive—explanation. In particular, I show that making explanatory counterfactual inferences is not a sufficient guide for accurate representation, factivity, or realism. I conclude by calling for a more explicit specification of (...) model-world mismatches and properties imputation. (shrink)

The failure to recognize a correlation as spurious can lead people to adopt strategies to bring about a specific outcome that manipulate something other than a cause of the outcome. However, in a 2008 paper appearing in the journal Analysis, Bert Leuridan, Erik Weber and Maarten Van Dyck suggest that knowledge of spurious correlations can, at least sometimes, justify adopting a strategy aiming at bringing about some change. This claim is surprising and, if true, throws into question the claim of (...) Nancy Cartwright and others that knowledge of laws of association is insufficient for distinguishing effective and ineffective strategies. This paper examines the nature of spurious correlations and their value in crafting strategies for change. The conclusion of the paper is that while knowledge of a spurious correlation may have practical value, the value depends on either having knowledge of the causal structure underlying the correlation or it depends on the use of ‘causal criteria’. (shrink)