Causal reasoning is an aspect of learning, reasoning, and decision-making that involves the cognitive ability to discover relationships between causal relata, learn and understand these causal relationships, and make use of this causal knowledge in prediction, explanation, decision-making, and reasoning in terms of counterfactuals. Can we fully automate causal reasoning? One might feel inclined, on the basis of certain groundbreaking advances in causal epistemology, to reply in the affirmative. The aim of this paper is to demonstrate that one still has (...) good skeptical grounds for resisting any conclusions in favour of the automation of causal reasoning. If by causal reasoning is meant the entirety of the process through which we discover causal relationships and make use of this knowledge in prediction, explanation, decision-making, and reasoning in terms of counterfactuals, then one relies besides on tacit knowledge, as might be constituted by or derived from the epistemic faculty virtues and abilities of the causal reasoner, the value systems and character traits of the causal reasoner, the implicit knowledge base available to the causal reasoner, and the habits that sustain our causal reasoning practices. While certain aspects of causal reasoning may be axiomatized and formalized and algorithms may be implemented to approximate causal reasoning, one has to remain skeptical about whether causal reasoning may be fully automated. This demonstration will involve an engagement with Meno’s Paradox. (shrink)

Crispin Wright’s discussion of the notion of ‘transmission-failure’ promises to have important philosophical ramifications, both in epistemology and beyond. This paper offers a precise, formal characterisation of the concept within a Bayesian framework. The interpretation given avoids the serious shortcomings of a recent alternative proposal due to Samir Okasha.

This paper defends the need for evidential diversity and the mix of methods that that can in train require. The focus is on causal claims, especially ‘singular’ claims about the effects of causes in a specific setting—either what will happen or what has happened. I do so by offering a template that categorises kinds of evidence that can support these claims. The catalogue is generated by considering what needs to happen for a causal process to carry through from putative cause (...) at the start to the targeted effect at the end. The usual call for mixed methods focusses on a single overall claim and argues that we increase certainty by the use of different methods with compensating strengths and weaknesses. My proposals instead focus on the evidence that supports the great many subsidiary claims that must hold if the overall one is to be true. As is typical for singular causal claims, the mix of methods that will generally be required to collect the kinds of evidence I urge will usually have little claim to the kind of rigour that is now widely demanded in evidencing causal claims, especially those for policy/treatment effectiveness. So I begin with an exploration of what seems to be intended by ‘rigour’ in such discussions, since it is seldom made clear just what makes the favoured methods especially rigorous. I then argue that the emphasis on rigour can be counterproductive. Rigour is often the enemy of evidential diversity, and evidential diversity—lots of it—can make for big improvements in the reliability of singular causal predictions and post hoc evaluations. I illustrate with the paragon of rigour for causal claims, randomised controlled trials (RCTs), rehearsing at some length what they can and cannot do to make it easier to assess the importance of rigour in warranting singular causal claims. (shrink)

An important question for the causal modeling approach is how to integrate non‐causal dependence relations such as asymmetric supervenience into the approach. The most prominent proposal to that effect (due to Gebharter) is to treat those dependence relationships as formally analogous to causal relationships. We argue that this proposal neglects some crucial differences between causal and non‐causal dependencies, and that in the context of causal modeling non‐causal dependence relationships should be represented as mutual dependence relationships. We develop a new kind (...) of model – “hybrid models” ‐ based on this suggestion, and formulate a set of axioms for those models. Our formalism has important implications for Kim's exclusion problem: whereas Gebharter's framework vindicates Kim's causal exclusion objection against nonreductive physicalism, our framework has no such implication, and can help non‐reductive physicalists vindicate the efficacy of high‐level properties. A further benefit of our formalism is that it yields a natural and plausible way of thinking about interventions in multi‐level contexts. (shrink)

Causation appears to present us with an interpretative difficulty. While arguably a redundant relation given fundamental physics, it is nevertheless apparently pragmatically indispensable. This chapter revisits certain arguments made previously by the author for these claims with the benefit of hindsight, starting with the role of causal models in the human sciences, and attempting to explain why it is not possible to straightforwardly ground such models in fundamental physics. This suggests that further constraints, going beyond physics, are needed to legitimate (...) such models. These supplementary constraints could be reified, but that would seem to conflict with the completeness of physics. A response is to emphasize the practical role of causal talk, and the author suggests that a fictionalist approach might be worth exploring. After clarifying fictionalism as a general approach, they carry out in some detail the project of clarifying what a fictionalist attitude to causation would involve. (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)

The framework of causal Bayes nets, currently influential in several scientific disciplines, provides a rich formalism to study the connection between causality and probability from an epistemological perspective. This article compares three assumptions in the literature that seem to constrain the connection between causality and probability in the style of Occam's razor. The trio includes two minimality assumptions—one formulated by Spirtes, Glymour, and Scheines (SGS) and the other due to Pearl—and the more well-known faithfulness or stability assumption. In terms of (...) logical strength, it is fairly obvious that the three form a sequence of increasingly stronger assumptions. The focus of this article, however, is to investigate the nature of their relative strength. The comparative analysis reveals an important sense in which Pearl's minimality assumption is as strong as the faithfulness assumption and identifies a useful condition under which it is as safe as SGS's relatively secure minimality assumption. Both findings have notable implications for the theory and practice of causal inference. 1 Introduction2 Background: Inference of Causal Structure in Markovian Causal Models3 Three Assumptions of Simplicity4 A Comparison of P-minimality and Faithfulness5 A Comparison of P-minimality and SGS-minimality6 Methodological Formulations and Prior Knowledge of Causal Order7 Conclusion. (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)

The evidence from randomized controlled trials (RCTs) is widely regarded as supplying the ‘gold standard’ in medicine—we may sometimes have to settle for other forms of evidence, but this is always epistemically second-best. But how well justified is the epistemic claim about the superiority of RCTs? This paper adds to my earlier (predominantly negative) analyses of the claims produced in favour of the idea that randomization plays a uniquely privileged epistemic role, by closely inspecting three related arguments from leading contributors (...) to the burgeoning field of probabilistic causality—Papineau, Cartwright and Pearl. It concludes that none of these further arguments supplies any practical reason for thinking of randomization as having unique epistemic power. IntroductionWhy the issue is of great practical importance—the ECMO casePapineau on the ‘virtues of randomization’Cartwright on causality and the ‘ideal’ randomized experimentPearl on randomization, nets and causesConclusion. (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)

A cause may influence its effect via multiple paths. Paradigmatically (Hesslow [1974]), taking birth control pills both decreases one’s risk of thrombosis by preventing pregnancy and increases it by producing a blood chemical. Building on Pearl ([2001]), I explicate the notion of a path-specific effect. Roughly, a path-specific effect of C on E via path P is the degree to which a change in C would change E were they to be transmitted only via P. Facts about such effects may (...) be gleaned from the structural equations commonly used to represent the causal relationships among variables. I contrast my analysis of the Hesslow case with those given by theorists of probabilistic causality, who mistakenly link it to issues of causal heterogeneity, token-causation and indeterminism. The reason probabilistic theories misdiagnose this case is that they pay inadequate attention to the structural relationships among variables. (shrink)

I analyse critically what I regard as the most accomplished empiricist account of propensities, namely the long run propensity theory developed by Donald Gillies . Empiricist accounts are distinguished by their commitment to the ‘identity thesis’: the identification of propensities and objective probabilities. These theories are intended, in the tradition of Karl Popper’s influential proposal, to provide an interpretation of probability that renders probability statements directly testable by experiment. I argue that the commitment to the identity thesis leaves empiricist theories, (...) including Gillies’ version, vulnerable to a variant of what is known as Humphreys’ paradox. I suggest that the tension may be resolved only by abandoning the identity thesis, and by adopting instead an understanding of propensities as explanatory properties of chancy objects. (shrink)

Though common sense says that causes must temporally precede their effects, the hugely influential interventionist account of causation makes no reference to temporal precedence. Does common sense lead us astray? In this paper, I evaluate the power of the commonsense assumption from within the interventionist approach to causal modeling. I first argue that if causes temporally precede their effects, then one need not consider the outcomes of interventions in order to infer causal relevance, and that one can instead use temporal (...) and probabilistic information to infer exactly when X is causally relevant to Y in each of the senses captured by Woodward’s interventionist treatment. Then, I consider the upshot of these findings for causal decision theory, and argue that the commonsense assumption is especially powerful when an agent seeks to determine whether so-called “dominance reasoning” is applicable. (shrink)

In a recent article (Sober 1982), I criticized an account of causation proposed by Giere (1979, 1980) by describing a series of examples concerning natural selection. Collier (1983) has criticized my criticisms, saying that I misapplied Giere's proposal and misconstrued the biology. More recently, Giere (1984) has defended his theory against my criticisms. Here I argue that my criticisms still stand.

This paper outlines a general theory of efficient causation, a theory that deals in a unified way with traditional or deterministic, indeterministic, probabilistic, and other causal concepts. Theorists like Lewis, Salmon, and Suppes have attempted to broaden our causal perspective by reductively analysing causal notions in other terms. By contrast, the present theory rests in the first place on a non-reductive analysis of traditional causal concepts — into formal or structural components, on the one hand, and a physical or metaphysical (...) component, on the other. The analyzans is then generalised. The theory also affords a more general propensity notion than is standard, one that helps solve major problems facing propensity interpretations of probability. (shrink)

Germund Hesslow has argued recently [2] that a probabilistic theory of causality as advocated by Patrick Suppes [4] has two problems that a deterministic theory avoids. In this paper, I argue that Suppes' probabilistic causal calculus is free of each of these problems and, moreover, that several broader issues raised by Hesslow's discussion tend to support a probabilistic conception of causes.

This paper examines Patrick Suppes’ probabilistic theory of causality understood as a theory of causal inference, and draws some lessons for empirical economics and contemporary debates in the foundations of econometrics. It argues that a standard method of empirical economics, multiple regression, is inadequate for most but the simplest applications, that the Bayes’ nets approach, which can be understood as a generalisation of Suppes’ theory, constitutes a considerable improvement but is still subject to important limitations, and that the currently fashionable (...) ‘design-based approach’ suffers from the same flaws Suppes anticipated a long time ago. It then sketches an alternative in response, one that differs drastically from the formalisms Suppes endorsed but is consistent with his pragmatic general take on science. (shrink)

According to Nancy Cartwright, a causal law holds just when a certain probabilistic condition obtains in all test situations which in turn satisfy a set of background conditions. These background conditions are shown to be inconsistent and, on separate account, logically incoherent. I offer a corrective reformulation which also incorporates a strategy for problems like Hesslow's thrombosis case. I also show that Cartwright's recent argument for modifying the condition to appeal to singular causes fails.Proposed modifications of the theory's probabilistic condition (...) to handle effects with extreme probabilities (0 or 1) are found unsatisfactory. I propose a unified solution which also handles extreme causes. Undefined conditional probabilities give rise to three good, but non-equivalent, ways of formulating the theory. Various formulations appear in the literature. I give arguments to eliminate all but one candidate. Finally, I argue for a crucial new condition clause, and show how to extend the results beyond a simple probabilistic framework. (shrink)

The issue of downward causation (and mental causation in particular), and the exclusion problem is discussed by taking into account some recent advances in the philosophy of science. The problem is viewed from the perspective of the new interventionist theory of causation developed by Woodward. It is argued that from this viewpoint, a higher-level (e.g., mental) state can sometimes truly be causally relevant, and moreover, that the underlying physical state which realizes it may fail to be such.

Despite the miraculous progress of science—it’s practitioners continue to run into mistakes, either discrediting research unduly or making leaps of causal inference where none are warranted. In this we isolate two of the reasons for such behavior involving the misplaced understanding of the role of mechanisms and mechanistic knowledge in the establishment of cause-effect relationships. We differentiate causal knowledge into causes, effects, mechanisms, cause-effect relationships, and causal stories. Failing to understand the role of mechanisms in this picture, including their absence (...) of knowledge or incorrect specification, leads to errors of wrongly excluding cause-effect relationships or wrongly inferring their existence. We highlight the primary of causality over mechanistic knowledge and causal stories in scientific reasoning. (shrink)

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)

This paper discusses Simpson's paradox and the problem of positive relevance in probabilistic causality. It is argued that Cartwright's solution to Simpson's paradox fails because it ignores one crucial form of the paradox. After clarifying different forms of the paradox, it is shown that any adequate solution to the paradox must allow a cause to be both a negative cause and a positive cause of..

There have been two principal paradigms for the formulation of the causal relation--logical implication and functional relationship. In this paper, I present a case for preferring the functional relationship formulation and then discuss how the functional relationship formulation may be implemented in the probabilistic case in a manner analogous to the way others have implemented the logical implication formulation in the probabilistic case. I show how the "local independence" assumption found in many models used in the behavioral and social sciences (...) is a consequence of the functional relation concept of probabilistic causality. I also discuss why causal relations are underdetermined in experience and are to be dealt with pragmatically in a hypothesis-testing framework. (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)

As a discipline of its own, the philosophy of science can be traced back to the founding of its academic journals, some of which go back to the first half of the twentieth century. While the discipline has been the object of many historical studies, notably focusing on specific schools or major figures of the field, little work has focused on the journals themselves. Here, we investigate contemporary philosophy of science by means of computational text-mining approaches: we apply topic-modeling algorithms (...) to eight major philosophy of science journals, from the 1930s up until 2017. Based on the full-text content of some 15,897 articles, we identified 25 research themes and 8 thematic clusters that show how the research agenda of the philosophy of science has changed in its content over the course of the last eight decades, up to the philosophy of science we now know. We also show how each one of the journals contributed in its own way to this thematic evolution. (shrink)

We further develop the mathematical theory of causal interventions, extending earlier results of Korb, Twardy, Handfield, & Oppy, (2005) and Spirtes, Glymour, Scheines (2000). Some of the skepticism surrounding causal discovery has concerned the fact that using only observational data can radically underdetermine the best explanatory causal model, with the true causal model appearing inferior to a simpler, faithful model (cf. Cartwright, (2001). Our results show that experimental data, together with some plausible assumptions, can reduce the space of viable explanatory (...) causal models to one. (shrink)

John Campbell has claimed that the interventionist account of causation must be amended if it is to be applied to causation in psychology. The problem, he argues, is that it follows from the so-called ‘surgical’ constraint that intervening on psychological states requires the suspension of the agent’s rational autonomy. In this paper, I argue that the problem Campbell identifies is in fact an instance of a wider problem for interventionism, extending beyond psychology, which I call the problem of ‘abrupt transitions’. (...) I then defend a solution to the problem, which replaces the surgical constraint with a weaker constraint on interventions that nevertheless does all the work the surgical constraint was designed to do. I conclude by exploring some interesting consequences of this weaker constraint for causation in psychology. (shrink)

Traditionally, mechanistic reasoning has been assigned a negligible role in standard EBM literature, although some recent authors have argued for an upgrade. Even so, the mechanistic reasoning that has received attention has almost exclusively been positive—both in an epistemic sense of claiming that there is a mechanistic chain and in a health-related sense of there being claimed benefits for the patient. Negative mechanistic reasoning has been neglected, both in the epistemic and in the health-related sense. I distinguish three main types (...) of negative mechanistic reasoning and subsume them under a new definition of mechanistic reasoning in the context of assessing medical interventions. This definition is wider than a previous suggestion in the literature. Each negative type corresponds to a range of evidential strengths, and it is argued that there are differences with respect to typical evidential strengths. The variety of negative mechanistic reasoning should be acknowledged in EBM, and it presents a serious challenge to proponents of so-called medical hierarchies of evidence. (shrink)

Philosophers of science have insisted that evidence of underlying mechanisms is required to support claims about the effects of medical interventions. Yet evidence about mechanisms does not feature on dominant evidence-based medicine “hierarchies.” After arguing that only inferences from mechanisms (“mechanistic reasoning”)—not mechanisms themselves—count as evidence, I argue for a middle ground. Mechanistic reasoning is not required to establish causation when we have high-quality controlled studies; moreover, mechanistic reasoning is more problematic than has been assumed. Yet where the problems can (...) be overcome, mechanistic reasoning can and should be used as evidence. (shrink)

In recent years, there has been a philosophical cottage industry producing arguments that our concept of causation is not univocal: that there are in fact two concepts of causation, corresponding to distinct species of causal relation. Papers written in this tradition have borne titles like “Two Concepts of Cause” and “Two Concepts of Causation”. With due apologies to Charles Dickens, I hereby make my own contribution to this genre.

Good explanations are not only true or probably true, but are also relevant to a causal question. Current models of causal explanation either only address the question of the truth of an explanation, or do not distinguish the probability of an explanation from its relevance. The tasks of scenario construction and conversational explanation are distinguished, which in turn shows how scenarios can interact with conversational principles to determine the truth and relevance of explanations. The proposed model distinguishes causal discounting from (...) causal backgrounding , and makes predictions concerning the differential effects of contextual information about alternative explanations on: (a) the kind of mental models constructed; (b) belief revision about probable cause; and (c) the perceived quality of a focal explanation. Four experiments are reported that test these predictions. The significance of the notion of explanatory relevance for research on causal explanation is then discussed. (shrink)

A previous paper of mine, that criticized Suppes' probabilistic theory of causality, was in turn criticized by Deborah Rosen. This paper is a development of my argument and an answer to Rosen. It is argued that the concept of causation is used in contemporary science in a way that presupposes determinism. It is shown that deterministic assumptions are necessary for inferences from generic to individual causal relations and for various kinds of eliminative arguments.

The analyses of explanation and causal beliefs are heavily dependent on using probability functions as models of epistemic states. There are, however, several aspects of beliefs that are not captured by such a representation and which affect the outcome of the analyses. One dimension that has been neglected in this article is the temporal aspect of the beliefs. The description of a single event naturally involves the time it occurred. Some analyses of causation postulate that the cause must not occur (...) later than the effect. If we want this kind of causality it is easy to add the appropriate clause to ( CAUS ). An alternative is not to rule out backwards causation or causal loops a priori , but expect that ( CAUS ), via the properties of the contraction P C - , will result in the desired temporal relation between C and E . One way of ensuring this is to postulate that when the probability function P is contracted to P C - , the probabilities of all events that occurred before C remain the same in P C - as in P . This means that all beliefs about the history of events up to C are left unaltered in the construction of the hypothetical state of belief P C - . In conclusion, I hope to have shown that, in spite of these limitations, ( EXP ) and ( CAUS ) provide viable analyses of explanation and causality between single events for the case when epistemic states can be described by probability functions. I have also shown that the two analyses can be used to explicate the close connections between the two notions. These analyses reduce the problems of explanation and causality, hopefully in a non-circular way, to the problem of identifying contractions of states of belief. (shrink)

The starting point in the development of probabilistic analyses of token causation has usually been the naïve intuition that, in some relevant sense, a cause raises the probability of its effect. But there are well-known examples both of non-probability-raising causation and of probability-raising non-causation. Sophisticated extant probabilistic analyses treat many such cases correctly, but only at the cost of excluding the possibilities of direct non-probability-raising causation, failures of causal transitivity, action-at-a-distance, prevention, and causation by absence and omission. I show that (...) an examination of the structure of these problem cases suggests a different treatment, one which avoids the costs of extant probabilistic analyses. (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)

Recent approaches to causal modelling rely upon the causal Markov condition, which specifies which probability distributions are compatible with a directed acyclic graph. Further principles are required in order to choose among the large number of DAGs compatible with a given probability distribution. Here we present a principle that we call frugality. This principle tells one to choose the DAG with the fewest causal arrows. We argue that frugality has several desirable properties compared to the other principles that have been (...) suggested, including the well-known causal faithfulness condition. _1_ Introduction _2_ The Causal Markov Condition _3_ Faithfulness _4_ Frugality _4.1_ Basic independences and frugality _4.2_ General properties of directed acyclic graphs satisfying frugality _4.3_ Connection to minimality assumptions _5_ Frugality as a Parsimony Principle _6_ Conclusion Appendix. (shrink)

In their article 'Causes and Explanations: A Structural-Model Approach. Part I: Causes', Joseph Halpern and Judea Pearl draw upon structural equation models to develop an attractive analysis of 'actual cause'. Their analysis is designed for the case of deterministic causation. I show that their account can be naturally extended to provide an elegant treatment of probabilistic causation.

ABSTRACT Joseph Halpern and Judea Pearl draw upon structural equation models to develop an attractive analysis of ‘actual cause’. Their analysis is designed for the case of deterministic causation. I show that their account can be naturally extended to provide an elegant treatment of probabilistic causation. 1Introduction 2Preemption 3Structural Equation Models 4The Halpern and Pearl Definition of ‘Actual Cause’ 5Preemption Again 6The Probabilistic Case 7Probabilistic Causal Models 8A Proposed Probabilistic Extension of Halpern and Pearl’s Definition 9Twardy and Korb’s Account 10Probabilistic (...) Fizzling 11Conclusion. (shrink)

Wood and Spekkens argue that any causal model explaining the EPRB correlations and satisfying the no-signalling constraint must also violate the assumption that the model faithfully reproduces the statistical dependences and independences—a so-called ‘fine-tuning’ of the causal parameters. This includes, in particular, retrocausal explanations of the EPRB correlations. I consider this analysis with a view to enumerating the possible responses an advocate of retrocausal explanations might propose. I focus on the response of Näger, who argues that the central ideas of (...) causal explanations can be saved if one accepts the possibility of a stable fine-tuning of the causal parameters. I argue that in light of this view, a violation of faithfulness does not necessarily rule out retrocausal explanations of the EPRB correlations. However, when we consider a plausible retrocausal picture in some detail, it becomes clear that the causal modelling framework is not a natural arena for representing such an account of retrocausality. _1_ Causal Models, Quantum Mechanics, and Faithfulness _2_ Fine-Tuning _2.1_ Fine-tuning in a retrocausal model _3_ Possible Responses _4_ Quantum Causal Models and Retrocausality _4.1_ A more detailed retrocausal account _4.2_ A model of the EPRB probabilities _4.3_ Mapping to a causal model _5_ Conclusion. (shrink)

Schupbach and Sprenger introduce a novel probabilistic approach to measuring the explanatory power that a given explanans exerts over a corresponding explanandum. Though we are sympathetic to their general approach, we argue that it does not adequately capture the way in which the causal explanatory power that c exerts on e varies with background knowledge. We then amend their approach so that it does capture this variance. Though our account of explanatory power is less ambitious than Schupbach and Sprenger’s in (...) the sense that it is limited to causal explanatory power, it is also more ambitious because we do not limit its domain to cases where c genuinely explains e. Instead, we claim that c causally explains e if and only if our account says that c explains e with some positive amount of causal explanatory power. (shrink)

Schupbach and Sprenger introduce a novel probabilistic approach to measuring the explanatory power that a given explanans exerts over a corresponding explanandum. Though we are sympathetic to their general approach, we argue that it does not adequately capture the way in which the causal explanatory power that c exerts on e varies with background knowledge. We then amend their approach so that it does capture this variance. Though our account of explanatory power is less ambitious than Schupbach and Sprenger’s in (...) the sense that it is limited to causal explanatory power, it is also more ambitious because we do not limit its domain to cases where c genuinely explains e. Instead, we claim that c causally explains e if and only if our account says that c explains e with some positive amount of causal explanatory power. 1Introduction 2The Logic of Explanatory Power 3Subjective and Nomic Distributions 3.1Actual degrees of belief 3.2The causal distribution 4Background Knowledge 4.1Conditionalization and colliders 4.2A helpful intervention 5Causal Explanatory Power 5.1The applicability of explanatory power 5.2Statistical relevance ≠ causal explanatory power 5.3Interventionist explanatory power 5.4E illustrated 6Conclusion. (shrink)