Philosophical analyses of causation have been centred on the question of what causation is. More precisely speaking, philosophers tend to address four different issues: metaphysical (what is causation out there?), epistemological (how can a causal claim be established and assessed?), conceptual (what does the word ‘cause’ mean?), and methodological (what methods ought one to use in order to establish and assess causal claims?). This chapter argues that the practical issue of causation (what is a causal claim for in practice?) is (...) highly relevant to the metaphysical, epistemological, conceptual, and methodological issues of causation. Any philosophical enquiry into causation without an examination of this practical issue is incomplete. In other words, a promising approach to causation ought to take all of the metaphysical, epistemological, conceptual, methodological, and practical issues into account. (shrink)

The interventionist theory of causation has been advertised as an empirically informed and more nuanced approach to causality than the competing theories. However, previous literature has not yet analyzed the regression discontinuity (hereafter, RD) and the difference-in-differences (hereafter, DD) within an interventionist framework. In this paper, I point out several drawbacks of using the interventionist methodology for justifying the DD and RD designs. However, I argue that the first step towards enhancing our understanding of the DD and RD designs from (...) an interventionist perspective is to take advantage of the assumptions of common trend and continuity. (shrink)

There is a tension between, on the one hand, the view that natural selection refers to individual-level causes, and on the other hand, the view that it refers to a population-level cause. In this article, I make the case for the individual-level cause view. I respond to recent claims made by McLoone that the individual-level cause view is inconsistent. I show that if one were to follow his arguments, any causal claim in any context would have to be regarded as (...) vindicating a form of population-level cause view. I show why this is implausible and how a consistent individual-level cause position can be held within the interventionist account of causation. Finally, I argue that there is one sense in which natural selection might be said to refer to population-level causes of evolutionary change. The upshot is that, as noted by others, natural selection can be regarded as referring to a population-level cause in the context of frequency-dependent selection and other situations of fitness-altering interactions between the individuals of a population. But whether this statement is true will depend on the empirical case investigated, not some a priori conceptual distinction. Thus, even though situations of frequency dependence might be ubiquitous, it is orthogonal to the conceptual question of whether frequency-independent natural selection—McLoone’s target—refers to individual- or population-level causes. (shrink)

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. (shrink)

There are three questions associated with Simpson’s Paradox (SP): (i) Why is SP paradoxical? (ii) What conditions generate SP?, and (iii) What should be done about SP? By developing a logic-based account of SP, it is argued that (i) and (ii) must be divorced from (iii). This account shows that (i) and (ii) have nothing to do with causality, which plays a role only in addressing (iii). A counterexample is also presented against the causal account. Finally, the causal and logic-based (...) approaches are compared by means of an experiment to show that SP is not basically causal. (shrink)

Many researchers consider cancer to have molecular causes, namely mutated genes that result in abnormal cell proliferation (e.g. Weinberg 1998). For others, the causes of cancer are to be found not at the molecular level but at the tissue level where carcinogenesis consists of disrupted tissue organization with downward causation effects on cells and cellular components (e.g. Sonnenschein and Soto 2008). In this contribution, I ponder how to make sense of such downward causation claims. Adopting a manipulationist account of causation (...) (Woodward 2003), I propose a formal definition of downward causation and discuss further requirements (in light of Baumgartner 2009). I then show that such an account cannot be mobilized in support of non-reductive physicalism (contrary to Raatikainen 2010). However, I also argue that such downward causation claims might point at particularly interesting dynamic properties of causal relationships that might prove salient in characterizing causal relationships (following Woodward 2010). (shrink)

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)

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. (shrink)

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. (shrink)

The distinction between distributive and non-distributive profiles figures prominently in current evaluations of the ethical and epistemological risks that are associated with automated profiling practices. The diagnosis that non-distributive profiles may coincidentally situate an individual in the wrong category is often perceived as the central shortcoming of such profiles. According to this diagnosis, most risks can be retraced to the use of non-universal generalisations and various other statistical associations. This article develops a top-down analysis of non-distributive profiles in which this (...) fallibility of non-distributive profiles is no longer central. Instead, it focuses on how profiling creates various asymmetries between an individual data-subject and a profiler. The emergence of informational, interest, and perspectival asymmetries between data-subject and profiler explains how non-distributive profiles weaken the epistemic position of a profiled individual. This alternative analysis provides a more balanced assessment of the epistemic risks associated with non-distributive profiles. (shrink)

It is widely agreed that social factors are related to health outcomes: much research served to establish correlations between classes of social factors on the one hand and classes of disease on the other hand. However, why and how social factors are an active part in the aetiology of disease development is something that is gaining attention only recently in the health sciences and in the medical humanities. In this paper, we advance the view that, just as bio-markers help trace (...) the causal continuum from exposure to disease development at the biological level, socio-markers ought to be introduced and studied in order to trace the social continuum from exposure to disease development. We explain how socio-markers differ from social indicators and how they can be used in combination with bio-markers in order to reconstruct the mixed mechanisms of health and disease, namely mechanisms in which both biological and social factors have an active causal role. (shrink)

A difference-making account of causality is proposed that is based on a counterfactual definition, but differs from traditional counterfactual approaches to causation in a number of crucial respects: it introduces a notion of causal irrelevance; it evaluates the truth-value of counterfactual statements in terms of difference-making; it renders causal statements background-dependent. On the basis of the fundamental notions 'causal relevance' and 'causal irrelevance', further causal concepts are defined including causal factors, alternative causes, and importantly inus-conditions. Problems and advantages of the (...) proposed account are discussed. Finally, it is shown how the account can shed new light on three classic problems in epistemology, the problem of induction, the logic of analogy, and the framing of eliminative induction. (shrink)

Manipulationism holds that information about the results of interventions is of utmost importance for scientific practices such as causal assessment or explanation. Specifically, manipulation provides information about the stability, or invariance, of the relationship between X and Y: were we to wiggle the cause X, the effect Y would accordingly wiggle and, additionally, the relation between the two will not be disrupted. This sort of relationship between variables are called 'invariant empirical generalisations'. The paper focuses on questions about causal assessment (...) and analyses the status of manipulation. It is argued that manipulationism is trapped in a dilemma. If manipulationism is read as providing a conceptual analysis of causation, then it fails to provide a story about the methods for causal assessment. If, instead, manipulationism is read as providing a method for causal assessment, then it is at an impasse concerning causal assessment in areas where manipulations are not performed. Empirical generalisations are then reassessed, in such a way that manipulation is not taken as methodologically fundamental. The paper concludes that manipulation is the appropriate tool for some scientific contexts, but not for all. (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)

One way social scientists explain phenomena is by building structural models. These models are explanatory insofar as they manage to perform a recursive decomposition on an initial multivariate probability distribution, which can be interpreted as a mechanism. Explanations in social sciences share important aspects that have been highlighted in the mechanisms literature. Notably, spelling out the functioning the mechanism gives it explanatory power. Thus social scientists should choose the variables to include in the model on the basis of their function (...) in the mechanism. This paper examines the notion of ‘function’ within structural modelling. We argue that ‘functions’ ought to be understood as the theoretical underpinnings of the causes, namely as the role that causes play in the functioning of the mechanism. (shrink)

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. (shrink)

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. (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)

In this paper, we compare the mechanisms of protein synthesis and natural selection. We identify three core elements of mechanistic explanation: functional individuation, hierarchical nestedness or decomposition, and organization. These are now well understood elements of mechanistic explanation in fields such as protein synthesis, and widely accepted in the mechanisms literature. But Skipper and Millstein have argued that natural selection is neither decomposable nor organized. This would mean that much of the current mechanisms literature does not apply to the mechanism (...) of natural selection.We take each element of mechanistic explanation in turn. Having appreciated the importance of functional individuation, we show how decomposition and organization should be better understood in these terms. We thereby show that mechanistic explanation by protein synthesis and natural selection are more closely analogous than they appear—both possess all three of these core elements of a mechanism widely recognized in the mechanisms literature. (shrink)

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. (shrink)

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. (shrink)

This paper deals with causal analysis in the social sciences. We first present a conceptual framework according to which causal analysis is based on a rationale of variation and invariance, and not only on regularity. We then develop a formal framework for causal analysis by means of structural modelling. Within this framework we approach causality in terms of exogeneity in a structural conditional model based which is based on (i) congruence with background knowledge, (ii) invariance under a large variety of (...) environmental changes, and (iii) model fit. We also tackle the issue of confounding and show how latent confounders can play havoc with exogeneity. This framework avoids making untestable metaphysical claims about causal relations and yet remains useful for cognitive and action-oriented goals. (shrink)

I argue for the causal character of modeling in data-intensive science, contrary to widespread claims that big data is only concerned with the search for correlations. After discussing the concept of data-intensive science and introducing two examples as illustration, several algorithms are examined. It is shown how they are able to identify causal relevance on the basis of eliminative induction and a related difference-making account of causation. I then situate data-intensive modeling within a broader framework of an epistemology of scientific (...) knowledge. In particular, it is shown to lack a pronounced hierarchical, nested structure. The significance of the transition to such “horizontal” modeling is underlined by the concurrent emergence of novel inductive methodology in statistics such as non-parametric statistics. Data-intensive modeling is well equipped to deal with various aspects of causal complexity arising especially in the higher level and applied sciences. (shrink)

After a decade of intense debate about mechanisms, there is still no consensus characterization. In this paper we argue for a characterization that applies widely to mechanisms across the sciences. We examine and defend our disagreements with the major current contenders for characterizations of mechanisms. Ultimately, we indicate that the major contenders can all sign up to our characterization.

The regulation of chemicals is undergoing drastic changes with the use of computational models to predict environmental toxicity. This particular issue has not attracted much attention, despite its major impacts on the regulation of chemicals. This raises the problem of causality at the crossroads between data and regulatory sciences, particularly in the case models known as quantitative structure–activity relationship models. This paper shows that models establish correlations and not scientific facts, and it engages anew the way regulators deal with uncertainties. (...) It does so by exploring the tension and problems raised by the possibility of causal explanation afforded by quantitative structure–activity relationship models. It argues that the specificity of predictive modelling promotes rethinking of the regulation of chemicals. (shrink)

Newcomb’s problem involves a decision-maker faced with a choice and a predictor forecasting this choice. The agents’ interaction seems to generate a choice dilemma once the decision-maker seeks to apply two basic principles of rational choice theory : maximize expected utility ; adopt the dominant strategy. We review unsuccessful attempts at pacifying the dilemma by excluding Newcomb’s problem as an RCT-application, by restricting MEU and ADS, and by allowing for backward causation. A probability approach shows that Newcomb’s original problem-formulation lacks (...) causal information. This makes it impossible to specify the probability structure of Newcomb’s univocally. Once missing information is added, Newcomb’s problem and RCT re-align, thus explaining Newcomb’s problem as a seeming dilemma. Building on Wolpert and Benford :1637–1646, 2013), we supply additional details and offer a crucial correction to their formal proof. (shrink)

Probabilistic phenomena are often perceived as being problematic targets for contrastive explanation. It is usually thought that the possibility of contrastive explanation hinges on whether or not the probabilistic behaviour is irreducibly indeterministic, and that the possible remaining contrastive explananda are token event probabilities or complete probability distributions over such token outcomes. This paper uses the invariance-under-interventions account of contrastive explanation to argue against both ideas. First, the problem of contrastive explanation also arises in cases in which the probabilistic behaviour (...) of the explanandum is due to unobserved causal heterogeneity. Second, it turns out that, in contrast to the case of pure indeterminism, the plausible contrastive explananda under causal heterogeneity are not token event probabilities, but population-level statistical facts. (shrink)