Jon Williamson

This paper highlights the role of Lewis’ Principal Principle and certain auxiliary conditions on admissibility as serving to explicate normal informal standards of what is reasonable. These considerations motivate the presuppositions of the argument that the Principal Principle implies the Principle of Indifference, put forward by Hawthorne et al.. They also suggest a line of response to recent criticisms of that argument, due to Pettigrew and Titelbaum and Hart, 621–632, 2020). The paper also shows that related concerns of Hart and Titelbaum, 252–262, 2015) do not undermine the argument of Hawthorne et al..

The EBM+ programme is an attempt to improve the way in which present-day evidence-based medicine (EBM) assesses causal claims: according to EBM+, mechanistic studies should be scrutinised alongside association studies. This paper addresses two worries about EBM+: (i) that it is not feasible in practice, and (ii) that it is too malleable, i.e., its results depend on subjective choices that need to be made in order to implement the procedure. Several responses to these two worries are considered and evaluated. The paper also discusses the question of whether we should have confidence in medical interventions, in the light of Stegenga's arguments for medical nihilism.

The maximum entropy principle is widely used to determine non-committal probabilities on a finite domain, subject to a set of constraints, but its application to continuous domains is notoriously problematic. This paper concerns an intermediate case, where the domain is a first-order predicate language. Two strategies have been put forward for applying the maximum entropy principle on such a domain: applying it to finite sublanguages and taking the pointwise limit of the resulting probabilities as the size n of the sublanguage increases; selecting a probability function on the language as a whole whose entropy on finite sublanguages of size n is not dominated by that of any other probability function for sufficiently large n. The entropy-limit conjecture says that, where these two approaches yield determinate probabilities, the two methods yield the same probabilities. If this conjecture is found to be true, it would provide a boost to the project of seeking a single canonical inductive logic—a project which faltered when Carnap's attempts in this direction succeeded only in determining a continuum of inductive methods. The truth of the conjecture would also boost the project of providing a canonical characterisation of normal or default models of first-order theories. Hitherto, the entropy-limit conjecture has been verified for languages which contain only unary predicate symbols and also for the case in which the constraints can be captured by a categorical statement of quantifier complexity. This paper shows that the entropy-limit conjecture also holds for categorical statements of complexity, for various non-categorical constraints, and in certain other general situations.

This paper poses a problem for Lewis’ Principal Principle in a subjective Bayesian framework: we show that, where chances inform degrees of belief, subjective Bayesianism fails to validate normal informal standards of what is reasonable. This problem points to a tension between the Principal Principle and the claim that conditional degrees of belief are conditional probabilities. However, one version of objective Bayesianism has a straightforward resolution to this problem, because it avoids this latter claim. The problem, then, offers some support to this version of objective Bayesianism.

While the importance of mechanisms in determining causality in medicine is currently the subject of active debate, the role of mechanistic reasoning in clinical practice has received far less attention. In this paper we look at this question in the context of the treatment of a particular individual, and argue that evidence of mechanisms is indeed key to various aspects of clinical practice, including assessing population-level research reports, diagnostic as well as therapeutic decision making, and the assessment of treatment effects. We use the pulmonary condition bronchiectasis as a source of examples of the importance of mechanistic reasoning to clinical practice.

The use of evidence in medicine is something we should continuously seek to improve. This book seeks to develop our understanding of evidence of mechanism in evaluating evidence in medicine, public health, and social care; and also offers tools to help implement improved assessment of evidence of mechanism in practice. In this way, the book offers a bridge between more theoretical and conceptual insights and worries about evidence of mechanism and practical means to fit the results into evidence assessment procedures.

The teratogenicity of the Zika virus was considered established in 2016, and is an interesting case because three different sets of causal criteria were used to assess teratogenicity. This paper appeals to the thesis of Russo and Williamson (2007) to devise an epistemological framework that can be used to compare and evaluate sets of causal criteria. The framework can also be used to decide when enough criteria are satisfied to establish causality. Arguably, the three sets of causal criteria considered here offer only a rudimentary assessment of mechanistic studies, and some suggestions are made as to alternative ways to establish causality.

The role of mechanistic evidence tends to be under-appreciated in current evidencebased medicine (EBM), which focusses on clinical studies, tending to restrict attention to randomized controlled studies (RCTs) when they are available. The EBM+ programme seeks to redress this imbalance, by suggesting methods for evaluating mechanistic studies alongside clinical studies. Drug approval is a problematic case for the view that mechanistic evidence should be taken into account, because RCTs are almost always available. Nevertheless, we argue that mechanistic evidence is central to all the key tasks in the drug approval process: in drug discovery and development; assessing pharmaceutical quality; devising dosage regimens; assessing efficacy, harms, external validity, and cost-effectiveness; evaluating adherence; and extending product licences. We recommend that, when preparing for meetings in which any aspect of drug approval is to be discussed, mechanistic evidence should be systematically analysed and presented to the committee members alongside analyses of clinical studies.

Systems medicine is a promising new paradigm for discovering associations, causal relationships and mechanisms in medicine. But it faces some tough challenges that arise from the use of big data: in particular, the problem of how to integrate evidence and the problem of how to structure the development of models. I argue that objective Bayesian models offer one way of tackling the evidence integration problem. I also offer a general methodology for structuring the development of models, within which the objective Bayesian approach fits rather naturally.

This paper presents a new argument for the Principle of Indifference. This argument can be thought of in two ways: as a pragmatic argument, justifying the principle as needing to hold if one is to minimise worst-case expected loss, or as an epistemic argument, justifying the principle as needing to hold in order to minimise worst-case expected inaccuracy. The question arises as to which interpretation is preferable. I show that the epistemic argument contradicts Evidentialism and suggest that the relative plausibility of Evidentialism provides grounds to prefer the pragmatic interpretation. If this is right, it extends to a general preference for pragmatic arguments for the Principle of Indifference, and also to a general preference for pragmatic arguments for other norms of Bayesian epistemology.

This paper presents a new argument for the Principle of Indifference. This argument can be thought of in two ways: as a pragmatic argument, justifying the principle as needing to hold if one is to minimise worst-case expected loss, or as an epistemic argument, justifying the principle as needing to hold in order to minimise worst-case expected inaccuracy. The question arises as to which interpretation is preferable. I show that the epistemic argument contradicts Evidentialism and suggest that the relative plausibility of Evidentialism provides grounds to prefer the pragmatic interpretation. If this is right, it extends to a general preference for pragmatic arguments for the Principle of Indifference, and also to a general preference for pragmatic arguments for other norms of Bayesian epistemology.

Russo and Williamson put forward the following thesis: in order to establish a causal claim in medicine, one normally needs to establish both that the putative cause and putative effect are appropriately correlated and that there is some underlying mechanism that can account for this correlation. I argue that, although the Russo-Williamson thesis conflicts with the tenets of present-day evidence-based medicine, it offers a better causal epistemology than that provided by present-day EBM because it better explains two key aspects of causal discovery. First, the thesis better explains the role of clinical studies in establishing causal claims. Second, it yields a better account of extrapolation.

We consider the use of interventions for resolving a problem of unidentified statistical models. The leading examples are from latent variable modelling, an influential statistical tool in the social sciences. We first explain the problem of statistical identifiability and contrast it with the identifiability of causal models. We then draw a parallel between the latent variable models and Bayesian networks with hidden nodes. This allows us to clarify the use of interventions for dealing with unidentified statistical models. We end by discussing the philosophical and methodological import of our result.

The Recursive Bayesian Net 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.

Inductive logic admits a variety of semantics (Haenni et al., 2011, Part 1). This paper develops semantics based on the norms of Bayesian epistemology (Williamson, 2010, Chapter 7). §1 introduces the semantics and then, in §2, the paper explores methods for drawing inferences in the resulting logic and compares the methods of this paper with the methods of Barnett and Paris (2008). §3 then evaluates this Bayesian inductive logic in the light of four traditional critiques of inductive logic, arguing (i) that it is language independent in a key sense, (ii) that it admits connections with the Principle of Indifference but these connections do not lead to paradox, (iii) that it can capture the phenomenon of learning from experience, and (iv) that while the logic advocates scepticism with regard to some universal hypotheses, such scepticism is not problematic from the point of view of scientific theorising

Practical reasoning requires decision—making in the face of uncertainty. Xenelda has just left to go to work when she hears a burglar alarm. She doesn’t know whether it is hers but remembers that she left a window slightly open. Should she be worried? Her house may not be being burgled, since the wind or a power cut may have set the burglar alarm off, and even if it isn’t her alarm sounding she might conceivably be being burgled. Thus Xenelda can not be certain that her house is being burgled, and the decision that she takes must be based on her degree of certainty, together with the possible outcomes of that decision.

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 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

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