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. (shrink)

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. (shrink)

According to Russo and Williamson (Int Stud Philos Sci 21(2):157–170, 2007, Hist Philos Life Sci 33:389–396, 2011a, Philos Sci 1(1):47–69, 2011b ), in order to establish a causal claim of the form, ‘_C_ is a cause of _E_’, one typically needs evidence that there is an underlying mechanism between _C_ and _E_ as well as evidence that _C_ makes a difference to _E_. This thesis has been used to argue that hierarchies of evidence, as championed by evidence-based movements, tend to (...) give primacy to evidence of difference making over evidence of mechanisms and are flawed because the two sorts of evidence are required and they should be treated on a par. An alternative approach gives primacy to evidence of mechanism over evidence of difference making. In this paper, we argue that this alternative approach is equally flawed, again because both sorts of evidence need to be treated on a par. As an illustration of this parity, we explain how scientists working in the ‘EnviroGenomarkers’ project constantly make use of the two evidential components in a dynamic and intertwined way. We argue that such an interplay is needed not only for causal assessment but also for policy purposes. (shrink)

According to the Russo-Williamson Thesis, causal claims in the health sciences need to be supported by both difference-making and mechanistic evidence. In this article, we attempt to determine whether Evidence-based Medicine can be improved through the consideration of mechanistic evidence. We discuss the practical composition and function of each RWT evidence type and propose that exposure-outcome evidence provides associations that can be explained through a hypothesis of causation, while mechanistic evidence provides finer-grained associations and knowledge of entities that ultimately explains (...) a causal hypothesis. We suggest that mechanistic evidence holds untapped potential to add value to the assessment of evidence quality in EBM and propose initial recommendations for the integration of mechanistic and exposure-outcome evidence to improve EBM by robustly leveraging available evidence in support of good medical decisions. (shrink)

Evidence-based medicine (EBM) makes use of explicit procedures for grading evidence for causal claims. Normally, these procedures categorise evidence of correlation produced by statistical trials as better evidence for a causal claim than evidence of mechanisms produced by other methods. We argue, in contrast, that evidence of mechanisms needs to be viewed as complementary to, rather than inferior to, evidence of correlation. In this paper we first set out the case for treating evidence of mechanisms alongside evidence of correlation in (...) explicit protocols for evaluating evidence. Next we provide case studies which exemplify the ways in which evidence of mechanisms complements evidence of correlation in practice. Finally, we put forward some general considerations as to how the two sorts of evidence can be more closely integrated by EBM. (shrink)

This paper seeks to analyse the effects on Economics of Research Assessment Systems, such as the Research Assessment Exercise (or RAE) which was carried out in the UK between 1986 and 2008. The paper begins by pointing out that, in the 2008 RAE, economics turned out to be the research area which was accorded the highest valuation of any subject in the UK, even though economists were then under attack for failing to predict the global financial crash which had occurred (...) a few months earlier. One aim of the paper is to explain this economics anomaly in research assessment. The paper goes on to point out a key difference between economics and the natural sciences. Most areas of the natural sciences are dominated for most of the time by a single, generally accepted, paradigm, whereas there are always in economics different schools of thought which have different and highly conflicting paradigms. Given this situation, it is argued that the effect of research assessment systems in economics is to strengthen the majority school in the subject (whatever that is), and weaken the minority schools. This conclusion is supported by empirical data collected by Frederic Lee for the UK. It is then shown that the greater the dominance of the majority school, the higher the overall valuation of the subject is likely to be, and this is used to explain the anomaly noted earlier. It is argued that research in economics flourishes better in a situation in which there are a number of different schools treated equally, than in one in which a single school dominates. The conclusion is that research assessment systems have a negative effect on research in economics and give misleading results. Instead of such systems, an attempt should be made to encourage pluralism in the subject. (shrink)

In this thesis I investigate causal inquiry in the social sciences, drawing on examples from various disciplines and in particular from conflict studies. In a backlash against the pervasiveness of statistical methods, in the last decade certain social scientists have focused on finding the causal mechanisms behind observed correlations. To provide evidence for such mechanisms, researchers increasingly rely on ‘process tracing’, a method which attempts to give evidence for causal relations by specifying the chain of events connecting a putative cause (...) and effect of interest. I will ask whether the causal claims process tracers make are defensible, and where they are not defensible I will ask how we can improve the method. Throughout these investigations, I show that the conclusions of process tracing are constrained both by the causal structure ofthe social world and by social scientists’ aims and values. My central argument is this: all instances of social phenomena have causally relevant differences, which implies that any research design that requires some comparison between cases is limited by how we systematize these phenomena. Moreover, such research cannot rely on stable regularities. Nevertheless, to forego causal conclusions altogether is not the right response to these limitations; by carefully outlining our epistemic assumptions we can make progress in causal inquiry. While I use philosophical theories of causation to comment on the feasibility of a social scientific method, I also do the reverse: by investigating a popular contemporary method in the social sciences, I show to what extent our philosophical theories of causation are workable in practice. Thus, this thesis is both a methodological and a philosophical work. Every chapter discusses both a fundamental philosophical position on the social sciences and a relevant case study from the social sciences. (shrink)