Jon Williamson

The mechanistic and causal accounts of explanation are often conflated to yield a ‘causal-mechanical’ account. This paper prizes them apart and asks: if the mechanistic account is correct, how can causal explanations be explanatory? The answer to this question varies according to how causality itself is understood. It is argued that difference-making, mechanistic, dualist and inferentialist accounts of causality all struggle to yield explanatory causal explanations, but that an epistemic account of causality is more promising in this regard.

This introduction to the volume begins with a manifesto that puts forward two theses: first, that the sciences are the best place to turn in order to understand causality; second, that scientifically-informed philosophical investigation can bring something to the sciences too. Next, the chapter goes through the various parts of the volume, drawing out relevant background and themes of the chapters in those parts. Finally, the chapter discusses the progeny of the papers and identifies some next steps for research into causality in the sciences.

How is probability related to logic? Should probability and logic be combined? If so, how? Bayesianism tells us we ought to reason probabilistically. In that sense, probability theory is logic. How then does probability theory relate to classical logic and the various non-classical logics that also stake a claim on normative reasoning? Is probability theory to be preferred over other logics or vice versa? Is probability theory to be used in some situations, and the other logics in other situations? Or should probability be combined with other logics?

I present a formalism that combines two methodologies: objective Bayesianism and Bayesian nets. According to objective Bayesianism, an agent’s degrees of belief (i) ought to satisfy the axioms of probability, (ii) ought to satisfy constraints imposed by background knowledge, and (iii) should otherwise be as non-committal as possible (i.e. have maximum entropy). Bayesian nets offer an efficient way of representing and updating probability functions. An objective Bayesian net is a Bayesian net representation of the maximum entropy probability function.

This paper presents the progicnet programme. It proposes a general framework for probabilistic logic that can guide inference based on both logical and probabilistic input. After an introduction to the framework as such, it is illustrated by means of a toy example from psychometrics. It is shown that the framework can accommodate a number of approaches to probabilistic reasoning: Bayesian statistical inference, evidential probability, probabilistic argumentation, and objective Bayesianism. The framework thus provides insight into the relations between these approaches, it illustrates how the results of different approaches can be combined, and it provides a basis for doing efficient inference in each of the approaches.

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.

Objective Bayesianism has been criticised for not allowing learning from experience: it is claimed that an agent must give degree of belief ½ to the next raven being black, however many other black ravens have been observed. I argue that this objection can be overcome by appealing to objective Bayesian nets, a formalism for representing objective Bayesian degrees of belief. Under this account, previous observations exert an inductive influence on the next observation. I show how this approach can be used to capture the Johnson-Carnap continuum of inductive methods, as well as the Nix-Paris continuum, and show how inductive influence can be measured

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

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

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.

Mechanistic philosophy of science views a large part of scientific activity as engaged in modelling mechanisms. While science textbooks tend to offer qualitative models of mechanisms, there is increasing demand for models from which one can draw quantitative predictions and explanations. Casini et al. (Theoria 26(1):5–33, 2011) put forward the Recursive Bayesian Networks (RBN) formalism as well suited to this end. The RBN formalism is an extension of the standard Bayesian net formalism, an extension that allows for modelling the hierarchical nature of mechanisms. Like the standard Bayesian net formalism, it models causal relationships using directed acyclic graphs. Given this appeal to acyclicity, causal cycles pose a prima facie problem for the RBN approach. This paper argues that the problem is a significant one given the ubiquity of causal cycles in mechanisms, but that the problem can be solved by combining two sorts of solution strategy in a judicious way.

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 threestep 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

Metabolism is a set of chemical reactions, used by living organisms to process chemical compounds in order to take energy and eliminate toxic compounds, for example. Its processes are referred as metabolic pathways. Understanding metabolism is imperative to biology, toxicology and medicine, but the number and complexity of metabolic pathways makes this a difficult task. In our paper, we investigate the use of causal Bayesian networks to model the pathways of yeast saccharomyces cerevisiae metabolism: such a network can be used to draw predictions about the levels of metabolites and enzymes in a particular specimen. We propose a two-stage methodology for causal networks, as follows. First construct a causal network from the network of metabolic pathways. The viability of this causal network depends on the validity of the causal Markov condition. If this condition fails, however, the principle of the common cause motivates the addition of a new causal arrow or a new `hidden' common cause to the network (stage 2 of the model formation process). Algorithms for adding arrows or hidden nodes have been developed separately in a number of papers, and in this paper we combine them, showing how the resulting procedure can be applied to the metabolic pathway problem. Our general approach was tested on neural cell morphology data and demonstrated noticeable improvements in both prediction and network accuracy.

Causal inference is perhaps the most important form of reasoning in the sciences. A panoply of disciplines, ranging from epidemiology to biology, from econometrics to physics, make use of probability and statistics to infer causal relationships. The social and health sciences analyse population-level data using statistical methods to infer average causal relations. In diagnosis of disease, probabilistic statements are based on population-level causal knowledge combined with knowledge of a particular person’s symptoms. For the physical sciences, the Salmon-Dowe account develops an analysis of causation based on the notion of process and interaction. In artificial intelligence, the development of graphical methods has leant impetus to a probabilistic analysis of causality. The biological sciences use probabilistic methods to look for evolutionary causes of the state of a current species and to look for genetic causal factors. This variegated situation raises at least two fundamental philosophical issues: about the relation between causality and probability, and about the interpretation of probability in causal analysis. In this book we bring philosophers and scientists together to discuss the relation between causality and probability, and the applications of these concepts within the sciences.

Expert probability forecasts can be useful for decision making . But levels of uncertainty escalate: however the forecaster expresses the uncertainty that attaches to a forecast, there are good reasons for her to express a further level of uncertainty, in the shape of either imprecision or higher order uncertainty . Bayesian epistemology provides the means to halt this escalator, by tying expressions of uncertainty to the propositions expressible in an agent’s language . But Bayesian epistemology comes in three main varieties. Strictly subjective Bayesianism and empirically-based subjective Bayesianism have difficulty in justifying the use of a forecaster’s probabilities for decision making . On the other hand, objective Bayesianism can justify the use of these probabilities, at least when the probabilities are consistent with the agent’s evidence . Hence objective Bayesianism offers the most promise overall for explaining how testimony of uncertainty can be useful for decision making. Interestingly, the objective Bayesian analysis provided in Sect. 5 can also be used to justify a version of the Principle of Reflection.

Objective Bayesianism says that the strengths of one’s beliefs ought to be probabilities, calibrated to physical probabilities insofar as one has evidence of them, and otherwise sufficiently equivocal. These norms of belief are often explicated using the maximum entropy principle. In this paper we investigate the extent to which one can provide a unified justification of the objective Bayesian norms in the case in which the background language is a first-order predicate language, with a view to applying the resulting formalism to inductive logic. We show that the maximum entropy principle can be motivated largely in terms of minimising worst-case expected loss.