Jon Williamson

Causal claims in biomedical contexts are ubiquitous albeit they are not always made explicit. This paper addresses the question of what causal claims mean in the context of disease. It is argued that in medical contexts causality ought to be interpreted according to the epistemic theory. The epistemic theory offers an alternative to traditional accounts that cash out causation either in terms of “difference-making” relations or in terms of mechanisms. According to the epistemic approach, causal claims tell us about which inferences (e.g., diagnoses and prognoses) are appropriate, rather than about the presence of some physical causal relation analogous to distance or gravitational attraction. It is shown that the epistemic theory has important consequences for medical practice, in particular with regard to evidence-based causal assessment.

The paper considers the legal tools that have been developed in German pharmaceutical regulation as a result of the precautionary attitude inaugurated by the Contergan decision (1970). These tools are (i) the notion of "well-founded suspicion", which attenuates the requirements for safety intervention by relaxing the requirement of a proved causal connection between danger and source, and the introduction of (ii) the reversal of proof burden in liability norms. The paper focuses on the first and proposes seeing the precautionary principle as an instance of the requirement that one should maximise expected utility. In order to maximise expected utility certain probabilities are required and it is argued that objective Bayesianism offers the most plausible means to determine the optimal decision in cases where evidence supports diverging choices.

Mechanisms have become much-discussed, yet there is still no consensus on how to characterise them. In this paper, we start with something everyone is agreed on – that mechanisms explain – and investigate what constraints this imposes on our metaphysics of mechanisms. We examine two widely shared premises about how to understand mechanistic explanation: (1) that mechanistic explanation offers a welcome alternative to traditional laws-based explanation and (2) that there are two senses of mechanistic explanation that we call ‘epistemic explanation’ and ‘physical explanation’. We argue that mechanistic explanation requires that mechanisms are both real and local. We then go on to argue that real, local mechanisms require a broadly active metaphysics for mechanisms, such as a capacities metaphysics.

Russo and Williamson (Int Stud Philos Sci 21(2):157–170, 2007) put forward the thesis that, at least in the health sciences, to establish the claim that C is a cause of E, one normally needs evidence of an underlying mechanism linking C and E as well as evidence that C makes a difference to E. This epistemological thesis poses a problem for most current analyses of causality which, in virtue of analysing causality in terms of just one of mechanisms or difference making, cannot account for the need for the other kind of evidence. Weber (Int Stud Philos Sci 23(2):277–295, 2009) has suggested to the contrary that Giere’s probabilistic analysis of causality survives this criticism. In this paper, we look in detail at the case of medical imaging technology, which, we argue, supports the thesis of Russo and Williamson, and we respond to Weber’s suggestion, arguing that Giere’s account does not survive the criticism.

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.

The Recursive Bayesian Net (RBN) formalism was originally developed for modelling nested causal relationships. In this paper we argue that the formalism can also be applied to modelling the hierarchical structure of mechanisms. The resulting network contains quantitative information about probabilities, as well as qualitative information about mechanistic structure and causal relations. Since information about probabilities, mechanisms and causal relations is vital for prediction, explanation and control respectively, an RBN can be applied to all these tasks. We show in particular how a simple two-level RBN can be used to model a mechanism in cancer science. The higher level of our model contains variables at the clinical level, while the lower level maps the structure of the cell's mechanism for apoptosis.

Objective Bayesianism has been criticised on the grounds that objective Bayesian updating, which on a finite outcome space appeals to the maximum entropy principle, differs from Bayesian conditionalisation. The main task of this paper is to show that this objection backfires: the difference between the two forms of updating reflects negatively on Bayesian conditionalisation rather than on objective Bayesian updating. The paper also reviews some existing criticisms and justifications of conditionalisation, arguing in particular that the diachronic Dutch book justification fails because diachronic Dutch book arguments are subject to a reductio: in certain circumstances one can Dutch book an agent however she changes her degrees of belief. One may also criticise objective Bayesianism on the grounds that its norms are not compulsory but voluntary, the result of a stance. It is argued that this second objection also misses the mark, since objective Bayesian norms are tied up in the very notion of degrees of belief.

While probabilistic logics in principle might be applied to solve a range of problems, in practice they are rarely applied --- perhaps because they seem disparate, complicated, and computationally intractable. This programmatic book argues that several approaches to probabilistic logic fit into a simple unifying framework in which logically complex evidence is used to associate probability intervals or probabilities with sentences. Specifically, Part I shows that there is a natural way to present a question posed in probabilistic logic, and that various inferential procedures provide semantics for that question, while Part II shows that there is the potential to develop computationally feasible methods to mesh with this framework. The book is intended for researchers in philosophy, logic, computer science and statistics. A familiarity with mathematical concepts and notation is presumed, but no advanced knowledge of logic or probability theory is required.

In this paper, we compare the mechanisms of protein synthesis and natural selection. We identify three core elements of mechanistic explanation: functional individuation, hierarchical nestedness or decomposition, and organization. These are now well understood elements of mechanistic explanation in fields such as protein synthesis, and widely accepted in the mechanisms literature. But Skipper and Millstein have argued (2005) that natural selection is neither decomposable nor organized. This would mean that much of the current mechanisms literature does not apply to the mechanism of natural selection. We take each element of mechanistic explanation in turn. Having appreciated the importance of functional individuation, we show how decomposition and organization should be better understood in these terms. We thereby show that mechanistic explanation by protein synthesis and natural selection are more closely analogous than they appear—both possess all three of these core elements of a mechanism widely recognized in the mechanisms literature.

The theory of belief revision and merging has recently been applied to judgement aggregation. In this paper I argue that judgements are best aggregated by merging the evidence on which they are based, rather than by directly merging the judgements themselves. This leads to a three-step strategy for judgement aggregation. First, merge the evidence bases of the various agents using some method of belief merging. Second, determine which degrees of belief one should adopt on the basis of this merged evidence base, by applying objective Bayesian theory. Third, determine which judgements are appropriate given these degrees of belief by applying a decision-theoretic account of rational judgement formation.

This paper develops connections between objective Bayesian epistemology - which holds that the strengths of an agent's beliefs should be representable by probabilities, should be calibrated with evidence of empirical probability, and should otherwise be equivocal - and probabilistic logic. After introducing objective Bayesian epistemology over propositional languages, the formalism is extended to handle predicate languages. A rather general probabilistic logic is formulated and then given a natural semantics in terms of objective Bayesian epistemology. The machinery of objective Bayesian nets and objective credal nets is introduced and this machinery is applied to provide a calculus for probabilistic logic that meshes with the objective Bayesian semantics.

We present a new framework for combining logic with probability, and demonstrate the application of this framework to breast cancer prognosis. Background knowledge concerning breast cancer prognosis is represented using logical arguments. This background knowledge and a database are used to build a Bayesian net that captures the probabilistic relationships amongst the variables. Causal hypotheses gleaned from the Bayesian net in turn generate new arguments. The Bayesian net can be queried to help decide when one argument attacks another. The Bayesian net is used to perform the prognosis, while the argumentation framework is used to provide a qualitative explanation of the prognosis.

Determining a prior probability function via the maximum entropy principle can be a computationally intractable task. However one can easily determine - in advance of entropy maximisation - a list of conditional independencies that the maximum entropy function will satisfy. These independencies can be used to reduce the complexity of the entropy maximisation task. In particular, one can use these independencies to construct a direct acyclic graph in a Bayesian network, and then maximise entropy with respect to the numerical parameters of this network. This can result in an efficient representation of a prior probability function, and one that may allow efficient updating and marginalisation. The computational complexity of maximising entropy can be further reduced when knowledge of causal relationships is available. Moreover, the proposed simplification of the entropy maximisation task may be exploited to construct a proof theory for probabilistic logic.

How ought we learn causal relationships? While Popper advocated a hypothetico-deductive logic of causal discovery, inductive accounts are currently in vogue. Many inductive approaches depend on the causal Markov condition as a fundamental assumption. This condition, I maintain, is not universally valid, though it is justifiable as a default assumption. In which case the results of the inductive causal learning procedure must be tested before they can be accepted. This yields a synthesis of the hypothetico-deductive and inductive accounts, which forms the focus of this paper. I discuss the justification of this synthesis and draw an analogy between objective Bayesianism and the account of causal learning presented here.

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.

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 concepts 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.