What happens to the causal structure of a world when time is reversed? At first glance it seems there are two possible answers: the causal relations are reversed, or they are not. I argue that neither of these answers is correct: we should either deny that time-reversed worlds have causal relations at all, or deny that causal concepts developed in the actual world are reliable guides to the causal structure of time-reversed worlds. The first option is motivated by the instability (...) of time-reversed dynamical evolutions under interventions. The second option is motivated by a recognition of how contingent structural features of the actual world shape our causal concepts and reasoning strategies. (shrink)

We propose a formal framework for interpretable machine learning. Combining elements from statistical learning, causal interventionism, and decision theory, we design an idealised explanation game in which players collaborate to find the best explanation for a given algorithmic prediction. Through an iterative procedure of questions and answers, the players establish a three-dimensional Pareto frontier that describes the optimal trade-offs between explanatory accuracy, simplicity, and relevance. Multiple rounds are played at different levels of abstraction, allowing the players to explore overlapping causal (...) patterns of variable granularity and scope. We characterise the conditions under which such a game is almost surely guaranteed to converge on a optimal explanation surface in polynomial time, and highlight obstacles that will tend to prevent the players from advancing beyond certain explanatory thresholds. The game serves a descriptive and a normative function, establishing a conceptual space in which to analyse and compare existing proposals, as well as design new and improved solutions. (shrink)

We propose a formal framework for interpretable machine learning. Combining elements from statistical learning, causal interventionism, and decision theory, we design an idealisedexplanation gamein which players collaborate to find the best explanation(s) for a given algorithmic prediction. Through an iterative procedure of questions and answers, the players establish a three-dimensional Pareto frontier that describes the optimal trade-offs between explanatory accuracy, simplicity, and relevance. Multiple rounds are played at different levels of abstraction, allowing the players to explore overlapping causal patterns of (...) variable granularity and scope. We characterise the conditions under which such a game is almost surely guaranteed to converge on a (conditionally) optimal explanation surface in polynomial time, and highlight obstacles that will tend to prevent the players from advancing beyond certain explanatory thresholds. The game serves a descriptive and a normative function, establishing a conceptual space in which to analyse and compare existing proposals, as well as design new and improved solutions. (shrink)

I argue that the Causal Markov Condition (CMC) is in principle applicable to the Einstein–Podolsky–Rosen (EPR) correlations. This is in line with my defence in the past of the applicability of the Principle of Common Cause to quantum mechanics. I first review a contrary claim by Dan Hausman and Jim Woodward, who endeavour to preserve the CMC against a possible counterexample by asserting that the conditions for the application of the CMC are not met in the EPR experiment. In their (...) view the CMC is inapplicable to the EPR correlations—i.e. it neither obtains nor fails. The view is grounded upon the non-separability of the quantum state, and the consequent unavailability of interventions. I urge that whether interventions are available in EPR—and why—is a complex and contextual question that does not have a unique or uniform answer. Instead, I argue that different combinations of causal hypotheses under test and interpretations of quantum mechanics yield different answers to the question. (shrink)

Woodward present an argument for the Causal Markov Condition (CMC) on the basis of a principle they dub ‘modularity’ ([1999, 2004]). I show that the conclusion of their argument is not in fact the CMC but a substantially weaker proposition. In addition, I show that their argument is invalid and trace this invalidity to two features of modularity, namely, that it is stated in terms of pairwise independence and ‘arrow-breaking’ interventions. Hausman & Woodward's argument can be rendered valid through a (...) reformulation of modularity, but it is doubtful that the argument so revised provides any substantially new insight regarding the basis of the CMC. Introduction The CMC versus Hausman & Woodward's conclusion Hausman & Woodward's argument Modularity and independent error terms Conclusion Appendix: D-separation. (shrink)

We clarify the status of the so-called causal minimality condition in the theory of causal Bayesian networks, which has received much attention in the recent literature on the epistemology of causation. In doing so, we argue that the condition is well motivated in the interventionist (or manipulability) account of causation, assuming the causal Markov condition which is essential to the semantics of causal Bayesian networks. Our argument has two parts. First, we show that the causal minimality condition, rather than an (...) add-on methodological assumption of simplicity, necessarily follows from the substantive interventionist theses, provided that the actual probability distribution is strictly positive. Second, we demonstrate that the causal minimality condition can fail when the actual probability distribution is not positive, as is the case in the presence of deterministic relationships. But we argue that the interventionist account still entails a pragmatic justification of the causal minimality condition. Our argument in the second part exemplifies a general perspective that we think commendable: when evaluating methods for inferring causal structures and their underlying assumptions, it is relevant to consider how the inferred causal structure will be subsequently used for counterfactual reasoning. (shrink)

This article considers interventionist arguments for downward causation and non-fundamental level causal explanation from the point of view of inferring causation from experiments. Several authors have utilised the interventionist theory of causal explanation to argue that the causal exclusion argument is moot and that higher-level as well as downward causation is real. I show that this argument can be made when levels are understood as levels of grain, leaving us with a choice between causal explanations pitched at different levels. Causal (...) proportionality has been suggested as a principle for choosing the correct level of description for causal explanations, but this suggestion has serious problems. I offer an alternative principle, based on the idea that explanations should track actual difference-makers. I then consider claims about systems causally influencing their own parts. Such claims risk conceptual confusion for the same reason as the exclusion argument, by conflating causal and constitutive dependencies. The distinction between causation and constitution is used to give criteria for the correct use of the idea of downward causation. (shrink)

The most serious candidates for common causes that fail to screen off and thus violate the causal Markov condition refer to quantum phenomena. In her seminal debate with Hausman and Woodward, Cartwright early on focussed on unfortunate non-quantum examples. Especially, Hausman and Woodward’s redescriptions of quantum cases saving the CMC remain unchallenged. This paper takes up this lose end of the discussion and aims to resolve the debate in favour of Cartwright’s position. It systematically considers redescriptions of ICC structures, including (...) those by Hausman and Woodward, and explains why these are inappropriate, when quantum mechanics is true. It first shows that all cases of purported quantum ICCs are cases of entanglement and then, using the tools of causal modelling, it provides an analysis of the quantum mechanical formalism for the case that the collapse of entangled systems is best described as a causal model with an ICC. (shrink)

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. (shrink)

It is common to assume that the problem of induction arises only because of small sample sizes or unreliable data. In this paper, I argue that the piecemeal collection of data can also lead to underdetermination of theories by evidence, even if arbitrarily large amounts of completely reliable experimental and observational data are collected. Specifically, I focus on the construction of causal theories from the results of many studies (perhaps hundreds), including randomized controlled trials and observational studies, where the studies (...) focus on overlapping, but not identical, sets of variables. Two theorems reveal that, for any collection of variables V, there exist fundamentally different causal theories over V that cannot be distinguished unless all variables are simultaneously measured. Underdetermination can result from piecemeal measurement, regardless of the quantity and quality of the data. Moreover, I generalize these results to show that, a priori, it is impossible to choose a series of small (in terms of number of variables) observational studies that will be most informative with respect to the causal theory describing the variables under investigation. This final result suggests that scientific institutions may need to play a larger role in coordinating differing research programs during inquiry. (shrink)

In medicine and the social sciences, researchers must frequently integrate the findings of many observational studies, which measure overlapping collections of variables. For instance, learning how to prevent obesity requires combining studies that investigate obesity and diet with others that investigate obesity and exercise. Recently developed causal discovery algorithms provide techniques for integrating many studies, but little is known about what can be learned from such algorithms. This article argues that there are causal facts that one could learn by conducting (...) a large study but which could not be learned by combining many smaller studies. Moreover, I characterize the frequency with which combining many studies increases underdetermination and exactly how much information is lost. 1 Introduction2 Causal Inference from Observational Data3 Piecemeal Causal Inference4 The Extent and Frequency of the Problem of Piecemeal Induction5 Conclusion. (shrink)

Currently, two frameworks of causal reasoning compete: Whereas dependency theories focus on dependencies between causes and effects, dispositional theories model causation as an interaction between agents and patients endowed with intrinsic dispositions. One important finding providing a bridge between these two frameworks is that failures of causes to generate their effects tend to be differentially attributed to agents and patients regardless of their location on either the cause or the effect side. To model different types of error attribution, we augmented (...) a causal Bayes net model with separate error sources for causes and effects. In several experiments, we tested this new model using the size of Markov violations as the empirical indicator of differential assumptions about the sources of error. As predicted by the model, the size of Markov violations was influenced by the location of the agents and was moderated by the causal structure and the type of causal variables. (shrink)

In this paper I analyze the process by which modelers in systems biology arrive at an adequate representation of the biological structures thought to underlie data gathered from high-throughput experiments. Contrary to views that causal claims and explanations are rare in systems biology, I argue that in many studies of gene regulatory networks modelers aim at a representation of causal structure. In addressing modeling challenges, they draw on assumptions informed by theory and pragmatic considerations in a manner that is guided (...) by an interventionist conception of causal structure. While doubts have been raised about the applicability of this notion of causality to complex biological systems, it is here seen to be an adequate guide to inquiry. (shrink)

What are scientific theories and how should they be represented? In this article, I propose a causal–structural account, according to which scientific theories are to be represented as sets of interrelated causal and credal nets. In contrast with other accounts of scientific theories (such as Sneedian structuralism, Kitcher’s unificationist view, and Darden’s theory of theoretical components), this leaves room for causality to play a substantial role. As a result, an interesting account of explanation is provided, which sheds light on explanatory (...) unification within a causalist framework. The theory of classical genetics is used as a case study. 1 Introduction2 The Theory of Classical Genetics3 Three Philosophical Accounts of the Theory of Classical Genetics3.1 The structuralist account3.2 Kitcher’s unificationism3.3 Darden and theory change in science4 A Common Lacuna: Where is Causality?5 Woodward’s Interventionist Account of Causation6 Causal Bayes Nets and Their Interrelations6.1 Causal Bayes nets6.2 Relations among causal nets6.3 Credal nets and their interrelations7 The Theory of the Gene and its Causal Graph8 A First Exemplar: Stem Length in Pea Plants8.1 Three crosses on stem length in pea plants8.2 The causal graph for stem length in pea plants8.3 Morgan’s explanatory principles and the credal net for stem length in pea plants9 Explaining Mendel’s Crosses: A Causal–Structural Account10 Monohybrid Crosses with Complete Dominance11 Exemplars,Explanatory Patterns, Generic Credal Nets, and Mechanism Schemas12 Incomplete Dominance13 Anomalies14 Multi-hybrid Crosses with Independent Assortment15 Multi-hybrid Crosses with Linkage and Crossing-Over16 Double Crossing-Over and the Linear Order of the Gene17 Causal–Structural Explanation18 Explanatory Unification19 Concluding Remarks. (shrink)

In this article, I present two conceptual problems for Craver's mutual manipulability account of constitutive relevance in mechanisms. First, constitutive relevance threatens to imply causal relevance despite Craver (and Bechtel)'s claim that they are strictly distinct. Second, if (as is intuitively appealing) parthood is defined in terms of spatio-temporal inclusion, then the mutual manipulability account is prone to counterexamples, as I show by a case of endosymbiosis. I also present a methodological problem (a case of experimental underdetermination) and formulate two (...) partial, but fallible solutions based on the notions of parthood and synchronicity. (shrink)

Economics prefers complete explanations: general over partial equilibrium, microfoundational over aggregate. Similarly, probabilistic accounts of causation frequently prefer greater detail to less as in typical resolutions of Simpson’s paradox. Strategies of causal refinement equally aim to distinguish direct from indirect causes. Yet, there are countervailing practices in economics. Representative-agent models aim to capture economic motivation but not to reduce the level of aggregation. Small structural vector-autoregression and dynamic stochastic general-equilibrium models are practically preferred to larger ones. The distinction between exogenous (...) and endogenous variables suggests partitioning the world into distinct subsystems. The tension in these practices is addressed within a structural account of causation inspired by the work of Herbert Simon’s, which defines cause with reference to complete systems adapted to deal with incomplete systems and piecemeal evidence. The focus is on understanding the constraints that a structural account of causation places on the freedom to model complex or lower-order systems as simpler or higher-order systems and on to what degree piecemeal evidence can be incorporated into a structural account. (shrink)

Bell appealed to the theory of relativity in formulating his principle of local causality. But he maintained that quantum field theories do not conform to that principle, even when their field equations are relativistically covariant and their observable algebras satisfy a relativistically motivated microcausality condition. A pragmatist view of quantum theory and an interventionist approach to causation prompt the reevaluation of local causality and microcausality. Local causality cannot be understood as a reasonable requirement on relativistic quantum field theories: it is (...) unmotivated even if applicable to them. But microcausality emerges as a sufficient condition for the consistent application of a relativistic quantum field theory. (shrink)

This survey presents some of the main principles involved in discovering causal relations. They belong to a large array of possible assumptions and conditions about causal relations, whose various combinations limit the possibilities of acquiring causal knowledge in different ways. How much and in what detail the causal structure can be discovered from what kinds of data depends on the particular set of assumptions one is able to make. The assumptions considered here provide a starting point to explore further the (...) foundations of causal discovery procedures, and how they can be improved. (shrink)

The literature on causal discovery has focused on interventions that involve randomly assigning values to a single variable. But such a randomized intervention is not the only possibility, nor is it always optimal. In some cases it is impossible or it would be unethical to perform such an intervention. We provide an account of ‘hard' and ‘soft' interventions and discuss what they can contribute to causal discovery. We also describe how the choice of the optimal intervention(s) depends heavily on the (...) particular experimental setup and the assumptions that can be made. ‡The first author is funded by the Causal Learning Collaborative Initiative supported by the James S. McDonnell Foundation. Many aspects of this paper were inspired by discussions with members of the collaborative. †To contact the authors, please write to: Department of Philosophy, Carnegie Mellon University, Pittsburgh, PA 15213; e-mail: [email protected] and [email protected]. (shrink)

In this paper, I focus on life-threatening medical conditions and argue that from the point of view of natural properties, induction(s), and participation in laws, at least some of the ill organisms dealt with in somatic medicine form natural kinds in the same sense in which the kinds in the exact sciences are thought of as natural. By way of comparing two ‘divisions of nature’, viz., a ‘classical’ exact science kind (gold) and a kind of disease (Graves disease), I show (...) that there is no justifiable ‘ontological gap’ between disease kinds and exact sciences kinds. We have instead a difference of degree. (shrink)

It is common to defend the Homeostatic Property Cluster ( HPC ) view as a third way between conventionalism and essentialism about natural kinds ( Boyd , 1989, 1991, 1997, 1999; Griffiths , 1997, 1999; Keil , 2003; Kornblith , 1993; Wilson , 1999, 2005; Wilson , Barker , & Brigandt , forthcoming ). According to the HPC view, property clusters are not merely conventionally clustered together; the co-occurrence of properties in the cluster is sustained by a similarity generating ( (...) or homeostatic ) mechanism . I argue that conventional elements are involved partly but ineliminably in deciding which mechanisms define kinds , for deciding when two mechanisms are mechanisms of the same type, and for deciding where one particular mechanism ends and another begins. This intrusion of conventional perspective into the idea of a mechanism raises doubts as to whether the HPC view is sufficiently free of conventional elements to serve as an objective arbiter in scientific disputes about what the kinds of the special sciences should be. (shrink)

Mechanistic philosophy of science views a large part of scientific activity as engaged in modelling mechanisms. While science textbooks tend to offer qualitative models of mechanisms, there is increasing demand for models from which one can draw quantitative predictions and explanations. Casini et al. (Theoria 26(1):5–33, 2011) put forward the Recursive Bayesian Networks (RBN) formalism as well suited to this end. The RBN formalism is an extension of the standard Bayesian net formalism, an extension that allows for modelling the hierarchical (...) nature of mechanisms. Like the standard Bayesian net formalism, it models causal relationships using directed acyclic graphs. Given this appeal to acyclicity, causal cycles pose a prima facie problem for the RBN approach. This paper argues that the problem is a significant one given the ubiquity of causal cycles in mechanisms, but that the problem can be solved by combining two sorts of solution strategy in a judicious way. (shrink)

Glennan appeals to interventions to solve the ontological and explanatory regresses that threaten his mechanistic account of causality . I argue that Glennan’s manoeuvre fails. The appeal to interventions is not able to address the ontological regress, and it blocks the explanatory regress only at the cost of making the account inapplicable to non-modular mechanisms. I offer a solution to the explanatory regress that makes use of dynamic Bayesian networks. My argument is illustrated by a case study from systems biology, (...) namely, the mechanism for the irreversibility of apoptosis. I conclude by pointing out the implications of my argument for Glennan’s mechanistic account of causality and, more generally, for accounts of mechanistic explanation based on interventions. 1 Introduction2 Glennan’s Account of Causality3 Objections to Glennan’s Account4 Glennan’s Replies5 Ontological Symmetry?6 Explanatory Symmetry?7 A Solution to the Explanatory Regress8 The Prospects of Glennan’s Account. (shrink)

Daniel Hausman and James Woodward claim to prove that the causal Markov condition, so important to Bayes-nets methods for causal inference, is the ‘flip side’ of an important metaphysical fact about causation—that causes can be used to manipulate their effects. This paper disagrees. First, the premise of their proof does not demand that causes can be used to manipulate their effects but rather that if a relation passes a certain specific kind of test, it is causal. Second, the proof is (...) invalid. Third, the kind of testability they require can easily be had without the causal Markov condition. Introduction Earlier views: manipulability v testability Increasingly weaker theses The proof is invalid MOD* is implausible Two alternative claims and their defects A true claim and a valid argument Indeterminism Overall conclusion. (shrink)

I present three reasons why philosophers of science should be more concerned about violations of causal faithfulness (CF). In complex evolved systems, mechanisms for maintaining various equilibrium states are highly likely to violate CF. Even when such systems do not precisely violate CF, they may nevertheless generate precisely the same problems for inferring causal structure from probabilistic relationships in data as do genuine CF-violations. Thus, potential CF-violations are particularly germane to experimental science when we rely on probabilistic information to uncover (...) the DAG, rather than already knowing the DAG from which we could predict the right experiments to ‘catch out’ the hidden causal relationships. (shrink)

The reduction of grounding to causation, or each to a more general relation of which they are species, has sometimes been justified by the impressive inferential capacity of structural equation modelling, causal Bayes nets, and interventionist causal modelling. Many criticisms of this assimilation focus on how causation is inadequate for grounding. Here, I examine the other direction: how treating grounding in the image of causation makes the resulting view worse for causation. The distinctive features of causal modelling that make this (...) connection appealing are distorted beyond use by forcing them to fit onto grounding. The very inferential strength that makes causation attractive is only possible because of a narrow construal of what counts as a causal relation; as soon as that broadens, the inferential capacity markedly diminishes. Making causation suitable for application to grounding spoils what was appealing about causation for this task in the first place. However, grounding need not appeal to causation: causal modelling does not have exclusive claim to structural equation modeling or other formal techniques of modelling structure. I offer a case in favour of a different kind of metaphysical frugality, which tend towards narrow, more restrictive construals of relations like causation or grounding, because then each relation behaves more homogenously. This more homogenous behavior delivers stronger inferential power per relation even though there may be more relations to which one is committed. (shrink)

The anti-causal prophecies of last century have been disproved. Causality is neither a ‘relic of a bygone’ nor ‘another fetish of modern science’; it still occupies a large part of the current debate in philosophy and the sciences. This investigation into causal modelling presents the rationale of causality, i.e. the notion that guides causal reasoning in causal modelling. It is argued that causal models are regimented by a rationale of variation, nor of regularity neither invariance, thus breaking down the dominant (...) Human paradigm. The notion of variation is shown to be embedded in the scheme of reasoning behind various causal models: e.g. Rubin’s model, contingency tables, and multilevel analysis. It is also shown to be latent – yet fundamental – in many philosophical accounts. Moreover, it has significant consequences for methodological issues: the warranty of the causal interpretation of causal models, the levels of causation, the characterisation of mechanisms, and the interpretation of probability. This book offers a novel philosophical and methodological approach to causal reasoning in causal modelling and provides the reader with the tools to be up to date about various issues causality rises in social science. (shrink)

Questions about the metaphysics of causation may be usefully divided as follows. First, there are questions about the nature of the causal relata, including (1.1) whether they are in spacetime immanence), (1.2) how fine grained they are individuation), and (1.3) how many there are adicity). Second, there are questions about the metaphysics of the causal relation, including (2.1) what is the difference between causally related and causally unrelated sequences connection), (2.2) what is the difference between sequences related as cause to (...) effect, and those related as effect to cause or as joint effects of a common cause direction), and (2.3) what is the difference between sequences involving the cause, and those involving mere conditions selection). (shrink)

“Probabilistic Causation” designates a group of theories that aim to characterize the relationship between cause and effect using the tools of probability theory. The central idea behind these theories is that causes change the probabilities of their effects. This article traces developments in probabilistic causation, including recent developments in causal modeling. A variety of issues within, and objections to, probabilistic theories of causation will also be discussed.

This chapter provides an introduction to the study of the philosophical notions of mechanisms and causality in biology and economics. This chapter sets the stage for this volume, Mechanism and Causality in Biology and Economics, in three ways. First, it gives a broad review of the recent changes and current state of the study of mechanisms and causality in the philosophy of science. Second, consistent with a recent trend in the philosophy of science to focus on scientific practices, it in (...) turn implies the importance of studying the scientific methods employed by researchers. Finally, by way of providing an overview of each chapter in the volume, this chapter demonstrates that biology and economics are two fertile fields for the philosophy of science and shows how biological and economic mechanisms and causality can be synthesized. (shrink)

N. Cartwright's recent results on invariance under intervention and causality (2003) are reconsidered. Procedural approach to causality elicited in this paper and contrasted with Cartwright's apparently philosophical one unravels certain ramifications of her results. The procedural approach seems to license only a constrained notion of intervention and in consequence the "correctness to invariance" part of Cartwright's first theorem fails for a class of cases. The converse "invariance to correctness" part of the theorem relies heavily on modeling assumptions which prove to (...) be difficult to validate in practice and are often buttressed by independently acquired evidence. (shrink)

These preprints were automatically compiled into a PDF from the collection of papers deposited in PhilSci-Archive in conjunction with the PSA 2012.

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)

Pearl and Woodward are both well-known advocates of interventionist causation. What is less well-known is the interesting relationship between their respective accounts. In this paper we discuss the different perspectives of causation these two accounts present and show that they are two sides of the same coin. Pearl’s focus is on leveraging global network constraints to correctly identify local causal relations. The rules by which global causal structures are composed from distinct causal relations are precisely defined by the global constraints. (...) Woodward’s focus, however, is on the use of local manipulation to identify single causal relations that then compose into global causal structures. The rules by which this composition takes place emerge as a result of local interventionist constraints. We contend that the complete picture of causality to be found between these two perspectives from the interventionist tradition must recognise both the global constraints of the sort identified by Pearl and the local constraints of the sort identified by Woodward, and the interplay between them: Pearl requires the possibility of local interventions and Woodward requires a global statistical framework within which to build composite causal structures. (shrink)

In the following we will apply the manipulability theory of causation of Woodward 2003 to physical systems, and show that, in the latter context, the theory can be simplified. Elaborating on an argument by Cartwright, we will argue that the notions of ‘modularity’ and ‘intervention’ of the cited work should be adapted for typical physical systems, in order to take coupling of system equations into account. We will show that this allows to reduce all cause types discussed in Woodward 2003 (...) to only one, namely that of ‘total cause’. (shrink)