Jon Williamson

In this paper, we examine what is to be said in defence of Machamer, Darden and Craver’s (MDC) controversial dualism about activities and entities (Machamer, Darden and Craver’s in Philos Sci 67:1–25, 2000). We explain why we believe the notion of an activity to be a novel, valuable one, and set about clearing away some initial objections that can lead to its being brushed aside unexamined. We argue that substantive debate about ontology can only be effective when desiderata for an ontology are explicitly articulated. We distinguish three such desiderata. The first is a more permissive descriptive ontology of science, the second a more reductive ontology prioritising understanding, and the third a more reductive ontology prioritising minimalism. We compare MDC’s entities-activities ontology to its closest rival, the entities-capacities ontology, and argue that the entities-activities ontology does better on all three desiderata

According to current hierarchies of evidence for EBM, evidence of correlation (e.g., from RCTs) is always more important than evidence of mechanisms when evaluating and establishing causal claims. We argue that evidence of mechanisms needs to be treated alongside evidence of correlation. This is for three reasons. First, correlation is always a fallible indicator of causation, subject in particular to the problem of confounding; evidence of mechanisms can in some cases be more important than evidence of correlation when assessing a causal claim. Second, evidence of mechanisms is often required in order to obtain evidence of correlation (for example, in order to set up and evaluate RCTs). Third, evidence of mechanisms is often required in order to generalise and apply causal claims. While the EBM movement has been enormously successful in making explicit and critically examining one aspect of our evidential practice, i.e., evidence of correlation, we wish to extend this line of work to make explicit and critically examine a second aspect of our evidential practices: evidence of mechanisms.

1, . . . , n | ≈ ψ ? Here 1, . . . , n, ψ are premisses of some formal language, such as a propositional language or a predicate language. | ≈ is an entailment relation: the entailment holds if all models of the premisses also satisfy the conclusion, where the logic provides some suitable notion of ‘model’ and ‘satisfy’. Proof theory is normally invoked to answer a question of this form: one tries to prove the conclusion from the premisses in a finite sequence of steps, where at each step one invokes an axiom or applies a rule of inference

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.

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 need for a coherent answer to this question has become increasingly urgent in the past few years, particularly in the field of artificial intelligence. There, both logical and probabilistic techniques are routinely applied in an attempt to solve complex problems such as parsing natural language and determining the way proteins fold. The hope is that some combination of logic and probability will produce better solutions. After all, both natural language and protein molecules have some structure that admits logical representation and reasoning; yet inherent uncertainties also demand the use of probabilistic methods: this structure is only partially known and does not in any case fully determine a solution—context or environment also play a role.

Objective Bayesian epistemology invokes three norms: the strengths of our beliefs should be probabilities, they should be calibrated to our evidence of physical probabilities, and they should otherwise equivocate sufficiently between the basic propositions that we can express. The three norms are sometimes explicated by appealing to the maximum entropy principle, which says that a belief function should be a probability function, from all those that are calibrated to evidence, that has maximum entropy. However, the three norms of objective Bayesianism are usually justified in different ways. In this paper we show that the three norms can all be subsumed under a single justification in terms of minimising worst-case expected loss. This, in turn, is equivalent to maximising a generalised notion of entropy. We suggest that requiring language invariance, in addition to minimising worst-case expected loss, motivates maximisation of standard entropy as opposed to maximisation of other instances of generalised entropy. Our argument also provides a qualified justification for updating degrees of belief by Bayesian conditionalisation. However, conditional probabilities play a less central part in the objective Bayesian account than they do under the subjective view of Bayesianism, leading to a reduced role for Bayes’ Theorem.

Evidence can be complex in various ways: e.g., it may exhibit structural complexity, containing information about causal, hierarchical or logical structure as well as empirical data, or it may exhibit combinatorial complexity, containing a complex combination of kinds of information. This paper examines evidential complexity from the point of view of Bayesian epistemology, asking: how should complex evidence impact on an agent’s degrees of belief? The paper presents a high-level overview of an objective Bayesian answer: it presents the objective Bayesian norms concerning the relation between evidence and degrees of belief, and goes on to show how evidence of causal, hierarchical and logical structure lead to natural constraints on degrees of belief. The objective Bayesian network formalism is presented, and it is shown how this formalism can be used to handle both kinds of evidential complexity—structural complexity and combinatorial complexity.

this paper we argue that the formalism can also be applied to modelling the hierarchical structure of physical 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 are vital for prediction, explanation and control respectively, a recursive Bayesian net can be applied to all these tasks. We show how a Recursive Bayesian Net can be used to model mechanisms in cancer science. The highest level of the proposed model will contain variables at the clinical level, while a middle level will map the structure of the DNA damage response mechanism and the lowest level will contain information about gene expression.

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.

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