The development of causal modelling since the 1950s has been accompanied by a number of controversies, the most striking of which concerns the Markov condition. Reichenbach's conjunctive forks did satisfy the Markov condition, while Salmon's interactive forks did not. Subsequently some experts in the field have argued that adequate causal models should always satisfy the Markov condition, while others have claimed that non-Markovian causal models are needed in some cases. This paper argues for the second position by considering the multi-causal (...) forks, which are widespread in contemporary medicine (Section 2). A non-Markovian causal model for such forks is introduced and shown to be mathematically tractable (Sections 6, 7, and 8). The paper also gives a general discussion of the controversy about the Markov condition (Section 1), and of the related controversy about probabilistic causality (Sections 3, 4, and 5). (shrink)

Emergence is interpreted in a non-dualist framework of thought. No metaphysical distinction between the higher and basic levels of organization is supposed, but only a duality of modes of access. Moreover, these modes of access are not construed as mere ways of revealing intrinsic patterns of organization: They are supposed to be constitutive of them, in Kant’s sense. The emergent levels of organization, and the inter-level causations as well, are therefore neither illusory nor ontologically real: They are objective in the (...) sense of transcendental epistemology. This neo-Kantian approach defuses several paradoxes associated with the concept of downward causation, and enables one to make good sense of it independently of any prejudice about the existence (or inexistence) of a hierarchy of levels of being. (shrink)

Over the past two decades, modal epistemology has turned its attention to ordinary modal knowledge. This paper brings to the fore a neglected but central form of ordinary modal knowledge: knowledge of agentive modality, and in particular of our own abilities, which I call ‘ability knowledge’. I argue that modal epistemology as it is does not account for ability knowledge, by looking at the most promising candidate theories: perception-based, counterfactual-based, and similarity-based modal epistemologies. I then outline a more promising epistemology (...) for our ability knowledge, which relies on the experience of our own agency, and draw out some lessons for modal epistemology in general. (shrink)

Concrete Causation centers about theories of causation, their interpretation, and their embedding in metaphysical-ontological questions, as well as the application of such theories in the context of science and decision theory. The dissertation is divided into four chapters, that firstly undertake the historical-systematic localization of central problems (chapter 1) to then give a rendition of the concepts and the formalisms underlying David Lewis' and Judea Pearl's theories (chapter 2). After philosophically motivated conceptual deliberations Pearl's mathematical-technical framework is drawn on for (...) an epistemic interpretation and for emphasizing the knowledge-organizing aspect of causality in an extension of the interventionist Bayes net account of causation (chapter 3). Integrating causal and non-causal knowledge in unified structures ultimately leads to an approach towards solving problems of (causal) decision theory and at the same time facilitates the representation of logical-mathematical, synonymical, as well as reductive relationships in efficiently structured, operational nets of belief propagation (chapter 4). (shrink)

We argue that current discussions of criteria for actual causation are ill-posed in several respects. (1) The methodology of current discussions is by induction from intuitions about an infinitesimal fraction of the possible examples and counterexamples; (2) cases with larger numbers of causes generate novel puzzles; (3) "neuron" and causal Bayes net diagrams are, as deployed in discussions of actual causation, almost always ambiguous; (4) actual causation is (intuitively) relative to an initial system state since state changes are relevant, but (...) most current accounts ignore state changes through time; (5) more generally, there is no reason to think that philosophical judgements about these sorts of cases are normative; but (6) there is a dearth of relevant psychological research that bears on whether various philosophical accounts are descriptive. Our skepticism is not directed towards the possibility of a correct account of actual causation; rather, we argue that standard methods will not lead to such an account. A different approach is required. (shrink)

In the philosophy of causation, manipulationist literature is broadly divided into agency and interventionist accounts. The division between these accounts is partially due to a dispute regarding the meaning of “manipulation”, which specifically questions, “Must one analyse manipulation by appealing to human agency?” This paper attempts to clarify the notion of manipulation and defends the thesis that agency theorists and interventionists analyse manipulation by appealing to human agency. However, following Collingwood's work, I argue that there are two ways to interpret (...) “human agency”. With an extended notion of agency in place, I reveal a pathway towards a consensus between the agency and interventionist accounts. Further, I highlight the alleged discrepancies between agency and interventionist accounts, including the issues of scope and objectivity, and suggest additional pathways towards a consensus. (shrink)

Causal assessment is the problem of establishing whether a relation between (variable) X and (variable) Y is causal. This problem, to be sure, is widespread across the sciences. According to accredited positions in the philosophy of causality and in social science methodology, invariance under intervention provides the most reliable test to decide whether X causes Y. This account of invariance (under intervention) has been criticised, among other reasons, because it makes manipulations on the putative causal factor fundamental for the causal (...) methodology; consequently, the argument goes, the account is ill-suited to those contexts where manipulations are not performed, for instance, the social sciences. The article aims to extend the account of invariance (under intervention), in a way that manipulations on the putative causal factors are not methodologically fundamental, and yet invariance remains key for causal assessment both in experimental and non-experimental contexts. (shrink)

The notion of causal evidence in medicine has been the subject of wide philosophical debate in recent years. The notion of evidence has been discussed mostly in connection with Evidence Based Medicine and, more in general, with the assessment of causal nexus in medical, and especially research contexts. “Manipulative evidence” is one of the notions of causal evidence that has stimulated much debate. It has been defined in slightly different ways, attributed different relevance, and recently placed at the core of (...) Gillies’ “action-related theory of causality”, a view specifically meant to address causation in medicine. While in general sympathetic to Gillies’ account, and totally convinced of the relevance of manipulative evidence and different sorts of interventions in the biomedical sciences, we believe that some further qualifications are needed to allow the notion of manipulative evidence to better express features of medical practice. In particular, we provide some qualification of the role of “interventional evidence” proposed by Gillies, suggesting a distinction between “interventional evidence” and “evidence for interventions”. A case study from research on rare diseases is analyzed in depth and a multifaceted notion of manipulative evidence put forward that allows better understanding of what manipulations in medical contexts amount to and what their targets are. (shrink)

This paper begins by developing a causal theory of mechanisms in medicine, and illustrates the theory with the example of the mechanism of the disease anthrax as elucidated by Koch. The causal approach to mechanisms is then compared to the Machamer, Darden, Craver approach. At first sight the two approaches appear to be very different, but it is argued that the divergence is less than it initially seems. There are some differences, however, and it is argued that, where these differences (...) occur, the causal approach to mechanisms is superior. (shrink)