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- Jon Williamson (2006). Dispositional Versus Epistemic Causality. Minds and Machines 16 (3).I put forward several desiderata that a philosophical theory of causality should satisfy: it should account for the objectivity of causality, it should underpin formalisms for causal reasoning, it should admit a viable epistemology, it should be able to cope with the great variety of causal claims that are made, and it should be ontologically parsimonious. I argue that Nancy Cartwright’s dispositional account of causality goes part way towards meeting these criteria but is lacking in important respects. I go on to argue that my epistemic account, which ties causal relationships to an agent’s knowledge and ignorance, performs well in the light of the desiderata. Such an account, I claim, is all we require from a theory of causality.No categories
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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.
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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.
This paper addresses questions about how the levels of causality (generic and single-case causality) are related. One question is epistemological: can relationships at one level be evidence for relationships at the other level? We present three kinds of answer to this question, categorised according to whether inference is top-down, bottom-up, or the levels are independent. A second question is metaphysical: can relationships at one level be reduced to relationships at the other level? We present three kinds of answer to this second question, categorised according to whether single-case relations are reduced to generic, generic relations are reduced to single-case, or the levels are independent. We then explore causal inference in autopsy. This is an interesting case study, we argue, because it refutes all three epistemologies and all three metaphysics. We close by sketching an account of causality that survives autopsy—the epistemic theory.
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In this paper I offer an anti-Humean critique to Williamson and Russo’s approach to medical mechanisms. I focus on one of the specific claims made by Williamson and Russo, namely the claim that micro-structural ‘mechanisms’ provide evidence for the stability across populations of causal relationships ascertained at the (macro-) level of (test) populations. This claim is grounded in the epistemic account of causality developed by Williamson, an account which—while not relying exclusively on mechanistic evidence for justifying causal judgements—appeals nevertheless to mechanisms, and rejects their anti-Humean interpretation in terms of capacities, powers, potencies, etc. By using (and expanding on) Cartwright’s basic critique against Humean mechanisms, I suggest that, in order to move beyond the level of plausibility, Williamson and Russo’s position is in need of a clarification as to the occurent reading of the components, functioning and interferences of mechanisms. Relatedly, as concerns Williamson’s epistemic account of causation, I argue that this account is in need of a more straightforward answer as to what truth-makers its causal claims should have.
It is tempting to analyse causality in terms of just one of the indicators of causal relationships, e.g., mechanisms, probabilistic dependencies or independencies, counterfactual conditionals or agency considerations. While such an analysis will surely shed light on some aspect of our concept of cause, it will fail to capture the whole, rather multifarious, notion. So one might instead plump for pluralism: a different analysis for a different occasion. But we do not seem to have lots of different kinds of cause—just one eclectic notion. The resolution of this conundrum, I think, requires us to accept that our causal beliefs are generated by a wide variety of indicators, but to deny that this variety of indicators yields a variety of concepts of cause. This focus on the relation between evidence and causal beliefs leads to what I call epistemic causality. Under this view, certain causal beliefs are appropriate or rational on the basis of observed evidence; our notion of cause can be understood purely in terms of these rational beliefs. Causality, then, is a feature of our epistemic representation of the world, rather than of the world itself. This yields one, multifaceted notion of cause.
This chapter provides an overview of a range of probabilistic theories of causality, including those of Reichenbach, Good and Suppes, and the contemporary causal net approach. It discusses two key problems for probabilistic accounts: counterexamples to these theories and their failure to account for the relationship between causality and mechanisms. It is argued that to overcome the problems, an epistemic theory of causality is required.
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.
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This chapter addresses two questions: what are causal relationships? how can one discover causal relationships? I provide a survey of the principal answers given to these questions, followed by an introduction to my own view, epistemic causality, and then a comparison of epistemic causality with accounts provided by Judea Pearl and Huw Price.
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Discussion of Jon Williamson, Dispositional versus epistemic causality
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