In recent years, Reichenbach's 1920 conception of the principles of coordination has attracted increased attention after Michael Friedman's attempt to revive Reichenbach's idea of a "relativized a priori". This paper follows the origin and development of this idea in the framework of Reichenbach's distinction between the axioms of coordination and the axioms of connection. It suggests a further differentiation among the coordinating axioms and accordingly proposes a different account of Reichenbach's "relativized a priori".

When does it make sense to act randomly? A persuasive argument from Bayesian decision theory legitimizes randomization essentially only in tie-breaking situations. Rational behaviour in humans, non-human animals, and artificial agents, however, often seems indeterminate, even random. Moreover, rationales for randomized acts have been offered in a number of disciplines, including game theory, experimental design, and machine learning. A common way of accommodating some of these observations is by appeal to a decision-maker’s bounded computational resources. Making this suggestion both precise (...) and compelling is surprisingly difficult. Toward this end, I propose two fundamental rationales for randomization, drawing upon diverse ideas and results from the wider theory of computation. The first unifies common intuitions in favour of randomization from the aforementioned disciplines. The second introduces a deep connection between randomization and memory: access to a randomizing device is provably helpful for an agent burdened with a finite memory. Aside from fit with ordinary intuitions about rational action, the two rationales also make sense of empirical observations in the biological world. Indeed, random behaviour emerges more or less where it should, according to the proposal. (shrink)

Cohen and Meskin 2006 recently offered a counterfactual theory of information to replace the standard probabilistic theory of information. They claim that the counterfactual theory fares better than the standard account on three grounds: first, it provides a better framework for explaining information flow properties; second, it requires a less expensive ontology; and third, because it does not refer to doxastic states of the information-receiving organism, it provides an objective basis. In this paper, I show that none of these is (...) really an advantage. Moreover, the counterfactual theory fails to satisfy one of the basic properties of information flow, namely the Conjunction principle. Thus, I conclude, there is no reason to give up the standard probabilistic theory for the counterfactual theory of information. (shrink)

Abstract: According to Laurence BonJour, the problem of induction can be solved by recognizing the a priori necessity that inductive conclusions constitute the best explanations of inductive premises. I defend an interpretation of the key probability claims BonJour makes about inductive premises and show that they are not susceptible to many of the objections that have been lodged against them. I then argue that these purportedly necessary probability claims nevertheless remain deeply problematic and that, as a result, BonJour's proposal fails (...) to provide a satisfactory resolution of the problem of induction. (shrink)

How should probabilities be interpreted in causal models in the social and health sciences? In this paper we take a step towards answering this question by investigating the case of cancer in epidemiology and arguing that the objective Bayesian interpretation is most appropriate in this domain.

In this thesis, I give a metascientific account of causality in medicine. I begin with two historical cases of causal discovery. These are the discovery of the causation of Burkitt’s lymphoma by the Epstein-Barr virus, and of the various viral causes suggested for cervical cancer. These historical cases then support a philosophical discussion of causality in medicine. This begins with an introduction to the Russo- Williamson thesis (RWT), and discussion of a range of counter-arguments against it. Despite these, I argue (...) that the RWT is historically workable, given a small number of modifications. I then expand Russo and Williamson’s account. I first develop their suggestion that causal relationships in medicine require some kind of evidence of mechanism. I begin with a number of accounts of mechanisms and produce a range of consensus features of them. I then develop this consensus position by reference to the two historical case studies with an eye to their operational competence. In particular, I suggest that it is mechanistic models and their representations which we are concerned with in medicine, rather than the mechanism as it exists in the world. -/- I then employ these mechanistic models to give an account of the sorts of evidence used in formulating and evaluating causal claims. Again, I use the two human viral oncogenesis cases to give this account. I characterise and distinguish evidence of mechanism from evidence of difference-making, and relate this to mechanistic models. I then suggest the relationship between types of evidence presents us with a means of tackling the reference-class problem. This sets the scene for the final chapter. Here, I suggest the manner in which these two different classes of evidence become integrated is also reflected in the way that developing research programmes change as their associated causal claims develop. (shrink)