Federica Russo

Causal analysis in the social sciences takes advantage of a variety of methods and of a multi-fold source of information and evidence. This pluralistic methodology and source of information raises the question of whether we should accordingly have a pluralistic metaphysics and epistemology. This paper focuses on epistemology and argues that a pluralistic methodology and evidence don’t entail a pluralistic epistemology. It will be shown that causal models employ a single rationale of testing, based on the notion of variation. Further, I shall argue that this monistic epistemology is also involved in alternative philosophical theories of causation

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.

The Agency and the Manipulability theory of causation, in spite of significant differences, share at least three claims. First, that manipulation – roughly, that by manipulating causes we bring about effects – is a central notion for causation; second, that such a notion of manipulation allows a reductive – i.e. general and comprehensive – account of causation; third, that this view has its forefathers in the works of Collingwood, Gasking and von Wright. This paper mainly challenges the third claim and argues that the misreading of those authors leads to a more dangerous consequence: a confusion between epistemological, metaphysical and methodological issues about causation

The Recursive Bayesian Net (RBN) formalism was originally developed for modelling nested causal relationships. In this paper we argue that the formalism can also be applied to modelling the hierarchical structure of mechanisms. The resulting network contains quantitative information about probabilities, as well as qualitative information about mechanistic structure and causal relations. Since information about probabilities, mechanisms and causal relations is vital for prediction, explanation and control respectively, an RBN can be applied to all these tasks. We show in particular how a simple two-level RBN can be used to model a mechanism in cancer science. The higher level of our model contains variables at the clinical level, while the lower level maps the structure of the cell's mechanism for apoptosis

This article addresses the contributions of the literature on the new mechanistic philosophy of science for the scientific practice of model building in ecology. This is reflected in a one-to-one interdisciplinary collaboration between an ecologist and a philosopher of science during science-in-the-making. We argue that the identification, reconstruction and understanding of mechanisms is context-sensitive, and for this case study mechanistic modeling did not present a normative role but a heuristic one. We expect our study to provides useful epistemic tools for the improvement of empirically-riven work in the debates about mechanistic explanation of ecological phenomena.

The term ‘scientism’ has not attracted consensus about its meaning or about its scope of application. In this paper, we consider Mizrahi’s suggestion to distinguish ‘Strong’ and ‘Weak’ scientism, and the consequences this distinction may have for philosophical methodology. While we side with Mizrahi that his definitions help advance the debate, by avoiding verbal dispute and focussing on questions of method, we also have concerns about his proposal as it defends a hierarchy of knowledge production. Mizrahi’s position is that Weak Scientism should be adopted, stating that “of all the knowledge we have, scientific knowledge is the best knowledge”. This version of scientism, however, has consequences for philosophical methodology. In particular, if one conceives of philosophy as an a priori discipline and holds Weak Scientism, the introduction of empirical methods in philosophy may threaten its very essence or soul. In this chapter, we will defend the move to adopt empirical methods in philosophy and argue that, rather than threatening its essence or soul, these methods put philosophy in a better position to contribute to knowledge production, an endeavor shared with the sciences, and in a very interdisciplinary spirit. Our point of disagreement with Mizrahi is that we should avoid any hierarchy of knowledge, and instead focus on what each perspective -- scientific, philosophical, historical, or other -- can contribute to understanding phenomena.

A careful analysis of Salmon’s Theoretical Realism and van Fraassen’s Constructive Empiricism shows that both share a common origin: the requirement of literal construal of theories inherited by the Standard View. However, despite this common starting point, Salmon and van Fraassen strongly disagree on the existence of unobservable entities. I argue that their different ontological commitment towards the existence of unobservables traces back to their different views on the interpretation of probability via different conceptions of induction. In fact, inferences to statements claiming the existence of unobservable entities are inferences to probabilistic statements, whence the crucial importance of the interpretation of probability.

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

This paper addresses questions about how the levels of causality (generic and single-case causality) are related. One question is epistemological: can relationships at one level be evidence for relationships at the other level? We present three kinds of answer to this question, categorised according to whether inference is top-down, bottom-up, or the levels are independent. A second question is metaphysical: can relationships at one level be reduced to relationships at the other level? We present three kinds of answer to this second question, categorised according to whether single-case relations are reduced to generic, generic relations are reduced to single-case, or the levels are independent. We then explore causal inference in autopsy. This is an interesting case study, we argue, because it refutes all three epistemologies and all three metaphysics. We close by sketching an account of causality that survives autopsy—the epistemic theory

The paper addresses the question of how different types of evidence ought to inform public health policy. By analysing case studies on obesity, the paper draws lessons about the different roles that different types of evidence play in setting up public health policies. More specifically, it is argued that evidence of difference-making supports considerations about ‘what works for whom in what circumstances’, and that evidence of mechanisms provides information about the ‘causal pathways’ to intervene upon

Causal claims in biomedical contexts are ubiquitous albeit they are not always made explicit. This paper addresses the question of what causal claims mean in the context of disease. It is argued that in medical contexts causality ought to be interpreted according to the epistemic theory. The epistemic theory offers an alternative to traditional accounts that cash out causation either in terms of “difference-making” relations or in terms of mechanisms. According to the epistemic approach, causal claims tell us about which inferences (e.g., diagnoses and prognoses) are appropriate, rather than about the presence of some physical causal relation analogous to distance or gravitational attraction. It is shown that the epistemic theory has important consequences for medical practice, in particular with regard to evidence-based causal assessment

The paper examines definitions of ‘cause’ in the epidemiological literature. Those definitions all describe causes as factors that make a difference to the distribution of disease or to individual health status. In the philosophical jargon, causes in epidemiology are difference-makers. Two claims are defended. First, it is argued that those definitions underpin an epistemology and a methodology that hinge upon the notion of variation, contra the dominant Humean paradigm according to which we infer causality from regularity. Second, despite the fact that causes be defined in terms of ‘difference-making’, this cannot fixes the causal metaphysics. Causality in epidemiology ought to be interpreted according to the epistemic theory. In this approach relations are deemed causal depending on the evidence and on the available methods. Indeed, evidence to establish causal claims requires difference-making considerations; furthermore, those definitions of cause reflect the ‘variational’ epistemology and methodology of epidemiology.

A shared problem across the sciences is to make sense of correlational data coming from observations and/or from experiments. Arguably, this means establishing when correlations are causal and when they are not. This is an old problem in philosophy. This paper, narrowing down the scope to quantitative causal analysis in social science, reformulates the problem in terms of the validity of statistical models. Two strategies to make sense of correlational data are presented: first, a 'structural strategy', the goal of which is to model and test causal structures that explain correlational data; second, a 'manipulationist or interventionist strategy', that hinges upon the notion of invariance under intervention. It is argued that while the former can offer a solution the latter cannot

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.

The notion of ‘causal web’ emerged in the epidemiological literature in the early Sixties and had to wait until the Nineties for a thorough critical appraisal. Famously, Nancy Krieger argued that such a notion isn’t helpful unless we specify what kind of spiders create the webs. This means, according to Krieger, (i) that the role of the spiders is to provide an explanation of the yarns of the web and (ii) that the sought spiders have to be biological and social. This paper contributes to the development of the notion of causal web, elaborating on the two following points: (i) to catch the spiders we need multi-fold evidence—specifically, mechanistic and difference-making—and (ii) for the eco-social to be explanatory, the web has to be mechanistic in a sense to be specified.

In social science, one objection to causal analysis is that the assumption of the closure of the system makes the analysis too narrow in scope, that is, it considers only 'closed' and 'hermetic' systems thus neglecting many other external influences. On the contrary, system analysis deals with complex structures where every element is interrelated with everything else in the system. The question arises as to whether the two approaches can be compatible and whether causal analysis can be integrated into the broader framework of system analysis. This article attempts a negative answer on the grounds of fundamental differences in their assumptions and suggests using system analysis as a post-hoc comparative tool

Current research in molecular epidemiology uses biomarkers to model the different disease phases from environmental exposure, to early clinical changes, to development of disease. The hope is to get a better understanding of the causal impact of a number of pollutants and chemicals on several diseases, including cancer and allergies. In a recent paper Russo and Williamson address the question of what evidential elements enter the conceptualisation and modelling stages of this type of biomarkers research. Recent research in causality has examined Ned Hall’s distinction between two concepts of causality: production and dependence. In another recent paper, Illari examined the relatively under-explored production approach to causality, arguing that at least one job of an account of causal production is to illuminate our inferential practices concerning causal linking. Illari argued that an informational account solves existing problems with traditional accounts. This paper follows up this previous work by investigating the nature of the causal links established in biomarkers research. We argue that traditional accounts of productive causality are unable to provide a sensible account of the nature of the causal link in biomarkers research, while an informational account is very promising

Social research, from economics to demography and epidemiology, makes extensive use of statistical models in order to establish causal relations. The question arises as to what guarantees the causal interpretation of such models. In this paper we focus on econometrics and advance the view that causal models are ‘augmented’ statistical models that incorporate important causal information which contributes to their causal interpretation. The primary objective of this paper is to argue that causal claims are established on the basis of a plurality of evidence. We discuss the consequences of ‘evidential pluralism’ in the context of econometric modelling.

Evidence and CausalityCausality is a vibrant and thriving topic in philosophy of science. It is closely related to many other challenging scientific concepts, such as probability and mechanisms, which arise in many different scientific contexts, in different fields. For example, probability and mechanisms are relevant to both causal inference (finding out what causes what) and causal explanation (explaining how a cause produces its effect). They are also of interest to fields as diverse as astrophysics, biochemistry, biomedical and social sciences. At the same time, there has been an explosion of interest in evidence, most obviously in biomedical contexts with the rise of ‘evidence-based medicine’, but also elsewhere, such as in social science. What is evidence? How do we decide what our best sources of evidence are?This topos examines the relation between causality and evidence in different scientific areas. This involves questions about the foundations of the sciences, e.g. what is e ..

The Recursive Bayesian Net formalism was originally developed for modelling nested causal relationships. In this paper we argue that the formalism can also be applied to modelling the hierarchical structure of mechanisms. The resulting network contains quantitative information about probabilities, as well as qualitative information about mechanistic structure and causal relations. Since information about probabilities, mechanisms and causal relations is vital for prediction, explanation and control respectively, an RBN can be applied to all these tasks. We show in particular how a simple two-level RBN can be used to model a mechanism in cancer science. The higher level of our model contains variables at the clinical level, while the lower level maps the structure of the cell's mechanism for apoptosis.

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

Econometrics applies statistical methods to study economic phenomena. Roughly, by means of equations, econometricians typically account for the response variable in terms of a number of explanatory variables. The question arises under what conditions econometric models can be given a causal interpretation. By drawing the distinction between associational models and causal models, the paper argues that a proper use of background knowledge, three distinct types of assumptions (statistical, extra-statistical, and causal), and the hypothetico-deductive methodology provide sufficient conditions for a causal interpretation of econometric models.