Reichenbach's 'principle of the common cause' is a foundational assumption of some important recent contributions to quantitative social science methodology but no similar principle appears in econometrics. Reiss (2005) has argued that the principle is necessary for instrumental variables methods in econometrics, and Pearl (2009) builds a framework using it that he proposes as a means of resolving an important methodological dispute among econometricians. We aim to show, through analysis of the main problem instrumental variables methods are used to resolve, (...) that the relationship of the principle to econometric methods is more nuanced than implied by previous work, but nevertheless may make a valuable contribution to the coherence and validity of existing methods. (shrink)

When evaluating the success of causal theories of explanation the focus has typically been on the legitimacy of causal relations and on putative examples of explanations that we cannot capture in causal terms. Here I motivate the existence of a third kind of problem: the difficulty of accounting for explanatory disputes. Moreover, I argue that this problem remains even if the first two are settled and that it threatens to undercut one of the central motivations for causal accounts of explanation, (...) namely, the causal account of the directionality of scientific explanation. (shrink)

It is widely held that it is difficult, if not impossible, to apply causal theory to the domain of quantum mechanics. However, there are several recent scientific explanations that appeal crucially to quantum processes, and which are most naturally construed as causal explanations. They come from two relatively new fields: quantum biology and quantum technology. We focus on two examples, the explanation for the optical interferometer LIGO and the explanation for the avian magneto-compass. We analyse the explanation for the avian (...) magneto-compass from the perspective of Woodward's interventionist theory and provide a causal model. Furthermore, we show how worries expressed by Woodward about quantum causation are circumvented in these cases, concluding that these kinds of explanations are most naturally construed as causal. (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 many biological experiments, due to gene-redundancy or distributed backup mechanisms, there are no visible effects on the functionality of the organism when a gene is knocked out or down. In such cases there is apparently no counterfactual dependence between the gene and the phenotype in question, although intuitively the gene is causally relevant. Due to relativity of causal relations to causal models, we suggest that such cases can be handled by changing the resolution of the causal model that represents (...) the system. By decreasing the resolution of our causal model, counterfactual dependencies can be established at a higher level of abstraction. By increasing the resolution, stepwise causal dependencies of the right kind can serve as a sufficient condition for causal relevance. Finally, we discuss how introducing a temporal dimension in causal models can account for causation in cases of non-modular systems dynamics. (shrink)

Jaegwon Kim (1998a, 2005) claims that his exclusion problem follows a priori for the non-reductive physicalist given her commitment to five apparently inconsistent theses: mental causation, non-identity, supervenience, causal closure and non-overdetermination. For Kim, the combination of these theses entails that mental properties are a priori excluded as causes, forcing the non-reductive physicalist to accept either epiphenomenalism, or some form of reduction. In this thesis, I argue that Kim’s exclusion problem depends on a particular conception of causation, namely sufficient production, (...) and that when causation is understood in interventionist terms, the non-reductive physicalist can avoid the exclusion problem. I argue that Woodward’s (2003, 2008a, 2011a) version of interventionism not only provides an account of mental causation that avoids the exclusion problem, but argue that it also upholds all of the minimal commitments of non-reductive physicalism, thereby providing a successful non-reductive physicalist solution to the exclusion problem. In Chapter 2, I argue that all five theses are minimal commitments of non-reductive physicalism that cannot be rejected in order to avoid the exclusion problem. Chapter 3 identifies the assumptions that I take to underlie the exclusion problem. Chapter 4 introduces and outlines the central features of Woodward’s (2003) interventionism and Chapter 5 argues that Woodward’s interventionist account of mental causation provides a solution to the exclusion problem. I examine two alternative interventionist accounts of mental causation[1] that fail to provide satisfactory solutions to the exclusion problem and conclude that Woodward’s account therefore provides the only satisfactory account of mental causation and solution to the exclusion problem. Chapter 6 addresses some challenges proposed by Michael Baumgartner (2009, 2010) and argues that the interventionist is able to defend her position against these objections and uphold the interventionist solution to the exclusion problem outlined in this thesis. [1. Proposed by List and Menzies (2009) and Campbell (2007, 2008a, 2008b, 2010).]. (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)

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)

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)

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

In this thesis, I give a metascientific account of causality in medicine. I begin with two historical cases of causal discovery. These are the discovery of the causation of Burkitt’s lymphoma by the Epstein-Barr virus, and of the various viral causes suggested for cervical cancer. These historical cases then support a philosophical discussion of causality in medicine. This begins with an introduction to the Russo- Williamson thesis (RWT), and discussion of a range of counter-arguments against it. Despite these, I argue (...) that the RWT is historically workable, given a small number of modifications. I then expand Russo and Williamson’s account. I first develop their suggestion that causal relationships in medicine require some kind of evidence of mechanism. I begin with a number of accounts of mechanisms and produce a range of consensus features of them. I then develop this consensus position by reference to the two historical case studies with an eye to their operational competence. In particular, I suggest that it is mechanistic models and their representations which we are concerned with in medicine, rather than the mechanism as it exists in the world. -/- I then employ these mechanistic models to give an account of the sorts of evidence used in formulating and evaluating causal claims. Again, I use the two human viral oncogenesis cases to give this account. I characterise and distinguish evidence of mechanism from evidence of difference-making, and relate this to mechanistic models. I then suggest the relationship between types of evidence presents us with a means of tackling the reference-class problem. This sets the scene for the final chapter. Here, I suggest the manner in which these two different classes of evidence become integrated is also reflected in the way that developing research programmes change as their associated causal claims develop. (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)

To evaluate Hume's thesis that causal claims are always empirical, I consider three kinds of causal statement: ?e1 caused e2 ?, ?e1 promoted e2 ?, and ?e1 would promote e2 ?. Restricting my attention to cases in which ?e1 occurred? and ?e2 occurred? are both empirical, I argue that Hume was right about the first two, but wrong about the third. Standard causal models of natural selection that have this third form are a priori mathematical truths. Some are obvious, others (...) less so. Empirical work on natural selection takes the form of defending causal claims of the first two types. I provide biological examples that illustrate differences among these three kinds of causal claim. (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)

It is still a matter of controversy whether the Principle of the Common Cause (PCC) can be used as a basis for sound causal inference. It is thus to be expected that its application to quantum mechanics should be a correspondingly controversial issue. Indeed the early 90’s saw a flurry of papers addressing just this issue in connection with the EPR correlations. Yet, that debate does not seem to have caught up with the most recent literature on causal inference generally, (...) which has moved on to consider the virtues of a generalised PCC-inspired condition, the so-called Causal Markov Condition (CMC). In this paper we argue that the CMC is an appropriate benchmark for debating possible causal explanations of the EPR correlations. But we go on to take issue with some pronouncements on EPR by defenders of the CMC. (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)

This paper attempts to elucidate three characteristics of causal relationships that are important in biological contexts. Stability has to do with whether a causal relationship continues to hold under changes in background conditions. Proportionality has to do with whether changes in the state of the cause “line up” in the right way with changes in the state of the effect and with whether the cause and effect are characterized in a way that contains irrelevant detail. Specificity is connected both to (...) David Lewis’ notion of “influence” and also with the extent to which a causal relation approximates to the ideal of one cause–one effect. Interrelations among these notions and their possible biological significance are also discussed. (shrink)

Non-reductive interventionist theories of causation and methodologies of causal reasoning embedded in that theoretical framework have become increasingly popular in recent years. This paper argues that one variant of an interventionist account of causation, viz. the one presented, for example, in Woodward (2003 ), is unsuited as a theoretical fundament of interventionist methodologies of causal reasoning, because it renders corresponding methodologies incapable of uncovering a causal structure in a finite number of steps. This finding runs counter to Woodward's own assessment (...) and to other recent studies which presume that Woodward's version of interventionism is effectively applicable to uncover causal structures, e.g. Campbell (2007 ) or Shapiro and Sober (2007 ). (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.

Combining physics, mathematics and computer science, quantum computing and its sister discipline of quantum information have developed in the past few decades from visionary ideas to two of the most fascinating areas of quantum theory. General interest and excitement in quantum computing was initially triggered by Peter Shor (1994) who showed how a quantum algorithm could exponentially “speed-up” classical computation and factor large numbers into primes far more efficiently than any (known) classical algorithm. Shor’s algorithm was soon followed by several (...) other algorithms that aimed to solve combinatorial and algebraic problems, and in the years since theoretical study of quantum systems serving as computational devices has achieved tremendous progress. Common belief has it that the implementation of Shor’s algorithm on a large scale quantum computer would have devastating consequences for current cryptography protocols which rely on the premise that all known classical worst-case algorithms for factoring take time exponential in the length of their input (see, e.g., Preskill 2005). Consequently, experimentalists around the world are engaged in attempts to tackle the technological difficulties that prevent the realisation of a large scale quantum computer. But regardless whether these technological problems can be overcome (Unruh 1995; Ekert and Jozsa 1996; Haroche and Raimond 1996), it is noteworthy that no proof exists yet for the general superiority of quantum computers over their classical counterparts. -/- The philosophical interest in quantum computing is manifold. From a social-historical perspective, quantum computing is a domain where experimentalists find themselves ahead of their fellow theorists. Indeed, quantum mysteries such as entanglement and nonlocality were historically considered a philosophical quibble, until physicists discovered that these mysteries might be harnessed to devise new efficient algorithms. But while the technology for harnessing the power of 50–100 qubits (the basic unit of information in the quantum computer) is now within reach (Preskill 2018), only a handful of quantum algorithms exist, and the question of whether these can truly outperform any conceivable classical alternative is still open. From a more philosophical perspective, advances in quantum computing may yield foundational benefits. For example, it may turn out that the technological capabilities that allow us to isolate quantum systems by shielding them from the effects of decoherence for a period of time long enough to manipulate them will also allow us to make progress in some fundamental problems in the foundations of quantum theory itself. Indeed, the development and the implementation of efficient quantum algorithms may help us understand better the border between classical and quantum physics (Cuffaro 2017, 2018a; cf. Pitowsky 1994, 100), and perhaps even illuminate fundamental concepts such as measurement and causality. Finally, the idea that abstract mathematical concepts such as computability and complexity may not only be translated into physics, but also re-written by physics bears directly on the autonomous character of computer science and the status of its theoretical entities—the so-called “computational kinds”. As such it is also relevant to the long-standing philosophical debate on the relationship between mathematics and the physical world. (shrink)

There has been an intense discussion, albeit largely an implicit one, concerning the inference of causal hypotheses from statistical correlations in quantum mechanics ever since John Bell’s first statement of his notorious theorem in 1966. As is well known, its focus has mainly been the so-called Einstein-Podolsky-Rosen (“EPR”) thought experiment, and the ensuing observed correlations in real EPR like experiments. But although implicitly the discussion goes as far back as Bell’s work, it is only in the last two decades that (...) it has become recognizably and explicitly a debate about causal inference in the quantum realm. The bulk of this paper is devoted to a review of three influential arguments in the philosophical literature that aim to show that causal models for the EPR correlations are impossible, due to Bas Van Fraassen, Daniel Hausman and Huw Price. I contend that all these arguments are inconclusive since they contain premises or presuppositions that are false, unwarranted, or at least controversial. Five different common cause models are outlined that seem perfectly viable for the EPR correlations. These models are then employed to illustrate various difficulties with the premises and presuppositions underlying Van Fraassen’s, Hausman’s and Price’s arguments. In all these cases it is argued that the difficulties cut deep against these authors’ own theories of causation and causal inference. My conclusions are that causal models for the EPR correlations remain viable, that philosophical work is still required to assess their relative virtues, and that in any case the mere theoretical conceivability and empirical possibility of these models sheds doubts over Van Fraassen’s, Hausman’s and (important elements in) Price’s theories of causation and causal inference. (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)

Much of the recent work on the epistemology of causation has centered on two assumptions, known as the Causal Markov Condition and the Causal Faithfulness Condition. Philosophical discussions of the latter condition have exhibited situations in which it is likely to fail. This paper studies the Causal Faithfulness Condition as a conjunction of weaker conditions. We show that some of the weaker conjuncts can be empirically tested, and hence do not have to be assumed a priori. Our results lead to (...) two methodologically significant observations: (1) some common types of counterexamples to the Faithfulness condition constitute objections only to the empirically testable part of the condition; and (2) some common defenses of the Faithfulness condition do not provide justification or evidence for the testable parts of the condition. It is thus worthwhile to study the possibility of reliable causal inference under weaker Faithfulness conditions. As it turns out, the modification needed to make standard procedures work under a weaker version of the Faithfulness condition also has the practical effect of making them more robust when the standard Faithfulness condition actually holds. This, we argue, is related to the possibility of controlling error probabilities with finite sample size (“uniform consistency”) in causal inference. (shrink)

This paper describes an alternative to the common view that explanation in the special sciences involves subsumption under laws. According to this alternative, whether or not a generalization can be used to explain has to do with whether it is invariant rather than with whether it is lawful. A generalization is invariant if it is stable or robust in the sense that it would continue to hold under a relevant if it is stable or robust in the sense that it (...) would continue to hold under a relevant class of changes. Unlike lawfulness, invariance comes in degrees and has other features that are well suited to capture the characteristics of explanatory generalizations in the special sciences. For example, a generalization can be invariant even if it has exceptions or holds only over a limited spatio-temporal interval. The notion of invariance can be used to resolve a number of dilemmas that arise in standard treatments of explanatory generalizations in the special sciences. (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)

Russell famously argued that causation should be dispensed with. He gave two explicit arguments for this conclusion, both of which can be defused if we loosen the ties between causation and determinism. I show that we can define a concept of causation which meets Russell’s conditions but does not reduce to triviality. Unfortunately, a further serious problem is implicit beneath the details of Russell’s arguments, which I call the causal exclusion problem. Meeting this problem involves deploying a minimalist pragmatic account (...) of the nature and function of modal language. Russell’s scruples about causation can be accommodated, even as we partially legitimise the pervasive causal explanations in folk and scientific practice. (shrink)

expose some gaps and difficulties in the argument for the causal Markov condition in our essay ‘Independence, Invariance and the Causal Markov Condition’ ([1999]), and we are grateful for the opportunity to reformulate our position. In particular, Cartwright disagrees vigorously with many of the theses we advance about the connection between causation and manipulation. Although we are not persuaded by some of her criticisms, we shall confine ourselves to showing how our central argument can be reconstructed and to casting doubt (...) on Cartwright's claim that the causal Markov condition typically fails when there are indeterministic by-products. Why believe the causal Markov condition? Causation and manipulation The argument Indeterministic by-products and the causal Markov condition The chemical factory counterexample and PM2 Conclusions: causation and manipulability. (shrink)

In their rich and intricate paper ‘Independence, Invariance, and the Causal Markov Condition’, Daniel Hausman and James Woodward ([1999]) put forward two independent theses, which they label ‘level invariance’ and ‘manipulability’, and they claim that, given a specific set of assumptions, manipulability implies the causal Markov condition. These claims are interesting and important, and this paper is devoted to commenting on them. With respect to level invariance, I argue that Hausman and Woodward's discussion is confusing because, as I point out, (...) they use different senses of ‘intervention’ and ‘invariance’ without saying so. I shall remark on these various uses and point out that the thesis is true in at least two versions. The second thesis, however, is not true. I argue that in their formulation, the manipulability thesis is patently false and that a modified version does not fare better. Furthermore, I think their proof that manipulability implies the causal Markov condition is not conclusive. In the deterministic case it is valid but vacuous, whereas it is invalid in the probabilistic case. 1 Introduction 2 Intervention, invariance and modularity 3 The causal Markov condition: CM1 and CM2 4 From MOD to the causal Markov condition and back 5 A second argument for CM2 6 The proof of the causal Markov condition for probabilistic causes 7 ‘Cartwright's objection’ defended 8 Metaphysical defenses of the causal Markov condition 9 Conclusion. (shrink)

This article defends the use of interventionist counterfactuals to elucidate causal and explanatory claims against criticisms advanced by James Bogen and Peter Machamer. Against Bogen, I argue that counterfactual claims concerning what would happen under interventions are meaningful and have determinate truth values, even in a deterministic world. I also argue, against both Machamer and Bogen, that we need to appeal to counterfactuals to capture the notions like causal relevance and causal mechanism. Contrary to what both authors suppose, counterfactuals are (...) not "unscientific" - a substantial tradition within statistics and the causal modelling literature makes heavy use of them. (shrink)

Is the common cause principle merely one of a set of useful heuristics for discovering causal relations, or is it rather a piece of heavy duty metaphysics, capable of grounding the direction of causation itself? Since the principle was introduced in Reichenbach’s groundbreaking work The Direction of Time (1956), there have been a series of attempts to pursue the latter program—to take the probabilistic relationships constitutive of the principle of the common cause and use them to ground the direction of (...) causation. These attempts have not all explicitly appealed to the principle as originally formulated; it has also appeared in the guise of independence conditions, counterfactual overdetermination, and, in the causal modelling literature, as the causal markov condition. In this paper, I identify a set of difficulties for grounding the asymmetry of causation on the principle and its descendents. The first difficulty, concerning what I call the vertical placement of causation, consists of a tension between considerations that drive towards the macroscopic scale, and considerations that drive towards the microscopic scale—the worry is that these considerations cannot both be comfortably accommodated. The second difficulty consists of a novel potential counterexample to the principle based on the familiar Einstein Podolsky Rosen (EPR) correlations in quantum mechanics. (shrink)

I highlight a metaphysical concern that stands in the way of more widespread adoption of causal modeling techniques such as causal Bayes nets. Researchers in some fields may resist adoption due to concerns that they don't 'really' understand what they are saying about a system when they apply such techniques. Students in these fields are repeated exhorted to be cautious about application of statistical techniques to their data without a clear understanding of the conditions required for those techniques to yield (...) genuine insight into the data. They are acutely aware that anyone can chuck some data into a software package and get what looks like an answer, even though these tests may not be well-defined for the data on which they can apparently be run. This is thus a healthy skepticism for uptake of causal modeling methods, which points directly to the need for a metaphysical understanding of causation in order to successfully use the modeling methods. Without a clear understanding of what the methods are committing to, including what it means to say that there exists a causal relationship, researchers have limited ability to identify potentially bad output, or to independently verify results. (shrink)

This paper argues that the interventionist account of causation faces a dilemma concerning macroscopic causation – i.e., causation by composite objects. Interventionism must either require interventions on a composite object to hold the behavior of its parts fixed, or allow such interventions to vary the behavior of those parts. The first option runs the risk of making wholes causally excluded by their parts, while the second runs the risk of mistakenly ascribing to wholes causal abilities that belong to their parts (...) only. Using as starting point Baumgartner’s well-known argument that interventionism leads to causal exclusion of multiply realized properties, I first show that a similar interventionist exclusion argument can be mounted against the causal efficacy of composite objects. I then show that Woodward’s (2015) updated interventionist account (explicitly designed to address exclusion worries) avoids this problem, but runs into an opposite issue of over-inclusion: it grants to composites causal abilities that belong to their parts only. Finally, I examine two other interventionist accounts designed to address Baumgartner’s argument, and show that when applied to composites, they too fall on one horn (exclusion) or the other (over-inclusion) of the dilemma. I conclude that the dilemma constitutes an open and difficult issue for interventionism. (shrink)

Causal representations are distinguished from non-causal ones by their ability to predict the results of interventions. This widely-accepted view suggests the following adequacy condition for causal models: a causal model is adequate only if it does not contain variables regarding which it makes systematically false predictions about the results of interventions. Here I argue that this condition should be rejected. For a class of equilibrium systems, there will be two incompatible causal models depending on whether one intervenes upon a certain (...) variable to fix its value, or ‘lets go’ of the variable and allows it to vary. The latter model will fail to predict the result of interventions on the let-go-of variable. I argue that there is no basis for preferring one of these models to the other, and thus that models failing to predict interventions on particular variables can be just as adequate as those making no such false predictions. This undermines a key argument (Dash in Caveats for causal reasoning with equilibrium models. University of Pittsburgh. PhD thesis, 2003) against relying upon causal models inferred from equilibrium data. (shrink)

Philosophy and statistics have studied two causal species, deterministic and probabilistic. There's a third species, however, hitherto unanalysed: underdeterministic causal phenomena, which are non-deterministic yet non-probabilistic. Here, I formulate a framework for modelling them. -/- Consider a simple case. If I go out, I may stumble into you but also may miss you. If I don’t go out, we won't meet. I go out. We meet. My going out is a cause of our encounter even if there was no determinate (...) probability of us meeting conditional on my going out. The cause is neither deterministic (it didn't necessitate the effect) nor probabilistic (the relevant conditional probabilities are undefined). Rather, it's underdeterministic: it raises the modal status of the effect from causally impossible to possible. -/- Here, I won't offer a theory of such token causes but develop the prerequisite for any such theory: the underdeterministic framework. The framework is like the deterministic structural-equations framework but with one consequential difference---an equation can return multiple values. This change allows me to define causal possibility and necessity, and corresponding notions of interventionist might- and would-counterfactuals. I also define conditional independence, which obeys the graphoid axioms, and prove that underdeterministic models satisfy the causal Markov condition. The framework can causally model situations that other frameworks cannot: decision-making under bounded uncertainty, games with multiple equilibria, infinite fair lotteries, and any other non-deterministic situation where indeterminacies are essentially non-probabilistic, or where we have a reason not to use probabilities. (shrink)

In the Origin, Darwin forwards two incompatible lines of attack on special creationism. First, he argues that imperfect or functionless traits are evidence against design. Second, he argues that since special creationism can be made compatible with any observation, it is unscientific and explanatorily vacuous. In later works, Darwin shifts to an argument that he finds much more persuasive and which would undermine theistic evolutionism as well. He argues that variation is random with respect to selection and that this demonstrates (...) that there is no design in the biological world. I examine why Darwin found the argument from independence of variation and selection more compelling than the argument from imperfection. I argue that Darwin utilized general principles of causal inference, akin to those used in modern causal modeling, to rule out any unified cause behind the evolutionary process. (shrink)

Most philosophers of physics are eliminativists about causation. Following Bertrand Russell’s lead, they think that causation is a folk concept that cannot be rationally reconstructed within a worldview informed by contemporary physics. Against this thesis, I argue that physics contributes to shaping the concept of causation, in two ways. (1) Special Relativity is a physical theory that expresses causal constraints. (2) The physical concept of a conserved quantity can be used in the functional reduction of the notion of causation. The (...) empirical part of this reduction makes the hypothesis that the transference of an amount of a conserved quantity is a necessary and sufficient condition for causation. This hypothesis is defended against several objections from physics: that amounts of energy do not possess the appropriate identity conditions required for being able to be transmitted, that there is no universal principle of the conservation of energy in General Relativity, and that there are at least two types of physical systems in which causation does not involve any transference: entangled systems in quantum mechanics and the Aharonov–Bohm effect. In order to show that physics provides means to elaborate the concept of causation it is important to avoid certain misunderstandings. In particular, the claim that there is causation in a physical world does not mean that causation is an additional ingredient of the “furniture” of the world, over and above the ingredients identified by physics. (shrink)

This paper aims to provide an answer to James Woodward’s article “Flagpoles anyone? Causal and explanatory asymmetries”. It will be conjectured that, when causal directionality depends on the experimental design, it is because the variables involved are capable of producing changes in each other. This will be exemplified using the case of ideal gases as opposed to the flagpole-shadow scenario.

Causation is a macroscopic phenomenon. The temporal asymmetry displayed by causation must somehow emerge along with other asymmetric macroscopic phenomena like entropy increase and the arrow of radiation. I shall approach this issue by considering ‘causal inference’ techniques that allow causal relations to be inferred from sets of observed correlations. I shall show that these techniques are best explained by a reduction of causation to structures of equations with probabilistically independent exogenous terms. This exogenous probabilistic independence imposes a recursive order (...) on these equations and a consequent distinction between dependent and independent variables that lines up with the temporal asymmetry of causation. (shrink)

It is often said that the world is explained by laws of nature together with initial conditions. But does that mean initial conditions don’t require further explanation? And does the explanatory role played by initial conditions entail or require that time has a preferred direction? This chapter looks at the use of the ‘initialness defence’ in physics, the idea that initial conditions are intrinsically special in that they don’t require further explanation, unlike the state of the world at other times. (...) Such defences commonly assume a primitive directionality of time to distinguish between initial and final conditions. Using the case study of the time-asymmetry of thermodynamics and the so-called ‘past hypothesis’ — the hypothesis that the early universe was in a state of very low entropy —, I outline and support a deflationary account of the initialness defence that does not pre- suppose a basic directionality of time, and argue that there is a relevant explanatory asymmetry between initial conditions and the state of systems at other times only if certain causal conditions are satisfied. Hence, the initialness defence is available to those who reject a fundamental direction of time. (shrink)

Causal representations are distinguished from non-causal ones by their ability to predict the results of interventions. This widely-accepted view suggests the following adequacy condition for causal models: a causal model is adequate only if it does not contain variables regarding which it makes systematically false predictions about the results of interventions. Here I argue that this condition should be rejected. For a class of equilibrium systems, there will be two incompatible causal models depending on whether one intervenes upon a certain (...) variable to fix its value, or ‘lets go’ of the variable and allows it to vary. The latter model will fail to predict the result of interventions on the let-go-of variable. I argue that there is no basis for preferring one of these models to the other, and thus that models failing to predict interventions on particular variables can be just as adequate as those making no such false predictions. This undermines a key argument against relying upon causal models inferred from equilibrium data. (shrink)

Functional robustness refers to a system’s ability to maintain a function in the face of perturbations to the causal structures that support performance of that function. Modularity, a crucial element of standard methods of causal inference and difference-making accounts of causation, refers to the independent manipulability of causal relationships within a system. Functional robustness appears to be at odds with modularity. If a function is maintained despite manipulation of some causal structure that supports that function, then the relationship between that (...) structure and function fails to be manipulable independent of other causal relationships within the system. Contrary to this line of reasoning, I argue that functional robustness often attends feedback control, rather than failures of modularity. Feedback control poses its own challenges to causal explanation and inference, but those challenges do not undermine modularity—and indeed, modularity is crucial to grappling with them. (shrink)

If the laws are deterministic, then standard theories of counterfactuals are forced to reject at least one of the following conditionals: 1) had you chosen differently, there would not have been a violation of the laws of nature; and 2) had you chosen differently, the initial conditions of the universe would not have been different. On the relevant readings—where we hold fixed factors causally independent of your choice—both of these conditionals appear true. And rejecting either one leads to trouble for (...) philosophical theories which rely upon counterfactual conditionals—like, for instance, causal decision theory. Here, I outline a semantics for counterfactual conditionals which allows us to accept both (1) and (2). And I discuss how this semantics deals with objections to causal decision theory from Arif Ahmed. (shrink)

Is psychopathy born or made? Contemporary psychopathy research shows that there is much wrong with this question. It is increasingly accepted that the development of psychopathy is dependent on multiple causal factors interacting with one another. However, there remains the major theoretical challenge of understanding the relations between these multiple causal factors in the developmental process. In this paper, I argue that the conventional picture of gene-environment interactionism does not offer an adequate account of psychopathy development. Instead, I propose that (...) a theoretical framework from the philosophy of biology, namely developmental systems theory, can facilitate a better understanding of psychopathy development that captures the contingent and dynamic relations between multiple causal factors. Some practical implications of a developmental systems theory approach to psychopathy are also explored. (shrink)

Proponents of various causal exclusion arguments claim that for any given event, there is often a unique level of granularity at which that event is caused. Against these causal exclusion arguments, causal ecumenists argue that the same event or phenomenon can be caused at multiple levels of granularity. This paper argues that the Bayesian network approach to representing the causal structure of target systems is consistent with causal ecumenism. Given the ubiquity of Bayesian networks as a tool for representing causal (...) structure in both philosophy of science and science itself, this result speaks in favor of the ecumenical view, and against rival exclusionary accounts. Gebharter’s (Philos Phenomenol Res 95(2):353–375, 2017) argument that the Bayes nets formalism is consistent with causal exclusion is considered and rebutted. (shrink)

Most philosophers of physics are eliminativists about causation. Following Bertrand Russell’s lead, they think that causation is a folk concept that cannot be rationally reconstructed within a worldview informed by contemporary physics. Against this thesis, I argue that physics contributes to shaping the concept of causation, in two ways. 1. Special Relativity is a physical theory that expresses causal constraints. 2. The physical concept of a conserved quantity can be used in the functional reduction of the notion of causation. The (...) empirical part of this reduction makes the hypothesis that the transference of an amount of a conserved quantity is a necessary and sufficient condition for causation. This hypothesis is defended against several objections from physics: that amounts of energy do not possess the appropriate identity conditions required for being able to be transmitted, that there is no universal principle of the conservation of energy in General Relativity, and that there are at least two types of physical systems in which causation does not involve any transference: entangled systems in quantum mechanics and the Aharanov-Bohm effect. In order to show that physics provides means to elaborate the concept of causation it is important to avoid certain misunderstandings. In particular, the claim that there is causation in a physical world does not mean that causation is an additional ingredient of the "furniture" of the world, over and above the ingredients identified by physics. (shrink)