Philosophical discussions on causal inference in medicine are stuck in dyadic camps, each defending one kind of evidence or method rather than another as best support for causal hypotheses. Whereas Evidence Based Medicine advocates the use of Randomised Controlled Trials and systematic reviews of RCTs as gold standard, philosophers of science emphasise the importance of mechanisms and their distinctive informational contribution to causal inference and assessment. Some have suggested the adoption of a pluralistic approach to causal inference, and an inductive (...) rather than hypothetico-deductive inferential paradigm. However, these proposals deliver no clear guidelines about how such plurality of evidence sources should jointly justify hypotheses of causal associations. We here develop such guidelines by first giving a philosophical analysis of the underpinnings of Hill’s viewpoints on causality. We then put forward an evidence-amalgamation framework adopting a Bayesian net approach to model causal inference in pharmacology for the assessment of harms. Our framework accommodates a number of intuitions already expressed in the literature concerning the EBM vs. pluralist debate on causal inference, evidence hierarchies, causal holism, relevance, and reliability. (shrink)

Amalgamating evidence from heterogeneous sources and across levels of inquiry is becoming increasingly important in many pure and applied sciences. This special issue provides a forum for researchers from diverse scientific and philosophical perspectives to discuss evidence amalgamation, its methodologies, its history, its pitfalls, and its potential. We situate the contributions therein within six themes from the broad literature on this subject: the variety-of-evidence thesis, the philosophy of meta-analysis, the role of robustness/sensitivity analysis for evidence amalgamation, its bearing on questions (...) of extrapolation and external validity of experiments, its connection with theory development, and its interface with causal inference, especially regarding causal theories of cancer. (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)

In Nozick’s rendition of the decision situation given in Newcomb’s Paradox dominance and the principle of maximum expected utility recommend different strategies. While evidential decision theory seems to be split over which principle to apply and how to interpret the principles in the first place, causal decision theory seems to go for the solution recommended by dominance. As a reply to the CDT proposal by Wolfgang Spohn, who opts for “one-boxing” by employing reflexive decision graphs, I will draw on the (...) framework of causal knowledge patterns, i.e., Bayes net causal models, augmented by non-causal knowledge, to finally arrive at “one-boxing” – more intuitively and more closely to what actually is in Nozick’s story. This proposal allows the careful re-examination of all relevant concepts in the original story and might cast new light on the following questions: How may causality in general be understood to allow causal inference from hybrid patterns encoding subjective knowledge? How can the notion of prediction be analyzed – philosophically and formally? And what’s the decision-maker’s conceptualization of the situation he will act upon? (shrink)

In their paper "How Fundamental Physics represents Causality", Andreas Bartels and Daniel Wohlfarth maintain that there is place for causality in General Relativity. Their argument contains two steps: First they show that there are time-asymmetric models in General Relativity, then they claim to derive that two events are causally connected if and only if there is a time-asymmetric energy flow from one event to the other. In our comment we first give a short summary of their paper followed by a (...) section introducing and pondering different conceptions of causation since Bartels and Wohlfarth don’t explicitly declare which notion of causation they build on in the paper. In order to analyze their argument in detail we formalize their crucial step in logical terms. This helps to pose the question whether their proposed derivation is not just a definition in a more precise way. (shrink)

If well-designed, the results of a Randomised Clinical Trial can justify a causal claim between treatment and effect in the study population; however, additional information might be needed to carry over this result to another population. RCTs have been criticized exactly on grounds of failing to provide this sort of information Evidence, inference and enquiry. Oxford University Press, New York, 2011), as well as to black-box important details regarding the mechanisms underpinning the causal law instantiated by the RCT result. On (...) the other side, so-called In Silico Clinical Trials face the same criticisms addressed against standard modelling and simulation techniques, and cannot be equated to experiments Philosophy of molecular medicine: foundational issues in research and practice, Routledge, New York, 2017; Parker in Synthese 169:483–496, 2009; Parke in Philos Sci 81:516–536, 2014; Diez Roux in Am J Epidemiol 181:100–102, 2015 and related discussions in Frigg and Reiss in Synthese 169:593–613, 2009; Winsberg in Synthese 169:575–592, 2009; Beisbart and Norton in Int Stud Philos Sci 26:403–422, 2012). We undertake a formal analysis of both methods in order to identify their distinct contribution to causal inference in the clinical setting. Britton et al.’s study :E2098–E2105, 2013) on the impact of ion current variability on cardiac electrophysiology is used for illustrative purposes. We deduce that, by predicting variability through interpolation, ISCTs aid with problems regarding extrapolation of RCTs results, and therefore in assessing their external validity. Furthermore, ISCTs can be said to encode “thick” causal knowledge —as opposed to “thin” difference-making information inferred from RCTs. Hence, ISCTs and RCTs cannot replace one another but rather, they are complementary in that the former provide information about the determinants of variability of causal effects, while the latter can, under certain conditions, establish causality in the first place. (shrink)