How do we make causal judgments? Many studies have demonstrated that people are capable causal reasoners, achieving success on tasks from reasoning to categorization to interventions. However, less is known about the mental processes used to achieve such sophisticated judgments. We propose a new process model—the mutation sampler—that models causal judgments as based on a sample of possible states of the causal system generated using the Metropolis–Hastings sampling algorithm. Across a diverse array of tasks and conditions encompassing over 1,700 participants, (...) we found that our model provided a consistently closer fit to participant judgments than standard causal graphical models. In particular, we found that the biases introduced by mutation sampling accounted for people's consistent, predictable errors that the normative model by definition could not. Moreover, using a novel experimental methodology, we found that those biases appeared in the samples that participants explicitly judged to be representative of a causal system. We conclude by advocating sampling methods as plausible process‐level accounts of the computations specified by the causal graphical model framework and highlight opportunities for future research to identify not just what reasoners compute when drawing causal inferences, but also how they compute it. (shrink)

This paper takes up Huw Price׳s challenge to develop a retrocausal toy model of the Bell-EPR experiment. I develop three such models which show that a consistent, local, hidden-variables interpretation of the EPR experiment is indeed possible, and which give a feel for the kind of retrocausation involved. The first of the models also makes clear a problematic feature of retrocausation: it seems that we cannot interpret the hidden elements of reality in a retrocausal model as possessing determinate dispositions to (...) affect the outcome of experiments. This is a feature which Price has embraced, but Gordon Belot has argued that this feature renders retrocausal interpretations “unsuitable for formal development”, and the lack of such determinate dispositions threatens to undermine the motivation for hidden-variables interpretations in the first place. But Price and Belot are both too quick in their assessment. I show that determinate dispositions are indeed consistent with retrocausation. What is more, I show that the ontological economy allowed by retrocausation holds out the promise of a classical understanding of spin and polarization. (shrink)

The theory-theory of human uniqueness posits that the capacity to theorize, in a way strongly analogous to theorizing in scientific practice, was a key innovation in the hominid lineage and was responsible for many of our unique cognitive traits. One of the central arguments that its proponents have used to support the claim that animals are not theorists, the logical problem, bears strong similarities to Hempel's theoretician's dilemma, which purports to show that theories are unnecessary. This similarity threatens to undermine (...) both the claim that theorizing serves a unique, adaptive role in human cognition and our ability to test for the presence of theories. I examine two historical responses to the theoretician's dilemma and argue that they open up strategies for experimentally testing for theoretical ability in other animals. (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)

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)

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)

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)

Recently, it has been argued that the use of Big Data transforms the sciences, making data-driven research possible and studying causality redundant. In this paper, I focus on the claim on causal knowledge by examining the Big Data project EXPOsOMICS, whose research is funded by the European Commission and considered capable of improving our understanding of the relation between exposure and disease. While EXPOsOMICS may seem the perfect exemplification of the data-driven view, I show how causal knowledge is necessary for (...) the project, both as a source for handling complexity and as an output for meeting the project’s goals. Consequently, I argue that data-driven claims about causality are fundamentally flawed and causal knowledge should be considered a necessary aspect of Big Data science. In addition, I present the consequences of this result on other data-driven claims, concerning the role of theoretical considerations. I argue that the importance of causal knowledge and other kinds of theoretical engagement in EXPOsOMICS undermine theory-free accounts and suggest alternative ways of framing science based on Big Data. (shrink)

The purpose of this article is to examine two important issues concerning the agency theory of causality: the charge of anthropomorphism and the relation of simultaneous causation. After a brief outline of the agency theory, sections 2–4 contain the refutation of the three main forms in which the charge of anthropomorphism is to be found in the literature. It will appear that it is necessary to distinguish between the subjective and the objective aspect of the concept of causation. This will (...) lead, in section 5, to contrast two kinds of anthropomorphism, one which has been rightly rejected by modern science and one which is fully compatible with the objective reality of the causal processes. Finally, section 6 will apply the preceding considerations to simultaneous causation. On the one hand, in a basic sense, there can be no simultaneous causal relations. On the other hand, simultaneous causation arises when we consider the natural change by abstracting from the agent and from her/his projects of interven.. (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)

Using Jim Woodward's Counterfactual Dependency account as an example, I argue that causal claims about indeterministic systems cannot be satisfactorily analysed as including counterfactual conditionals among their truth conditions because the counterfactuals such accounts must appeal to need not have truth values. Where this happens, counterfactual analyses transform true causal claims into expressions which are not true.

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)

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)

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)

While ideal interventions are acknowledged by many as valuable tools for the analysis of causation, recent discussions have shown that, since there are no ideal interventions on upper-level phenomena that non-reductively supervene on their underlying mechanisms, interventions cannot—contrary to a popular opinion—ground an informative analysis of constitution. This has led some to abandon the project of analyzing constitution in interventionist terms. By contrast, this paper defines the notion of a horizontally surgical intervention, and argues that, when combined with some innocuous (...) metaphysical principles about the relation between upper and lower levels of mechanisms, that notion delivers a sufficient condition for constitution. This, in turn, strengthens the case for an interventionist analysis of constitution. (shrink)

While ideal interventions are acknowledged by many as valuable tools for the analysis of causation, recent discussions have shown that, since there are no ideal interventions on upper-level phenomena that non-reductively supervene on their underlying mechanisms, interventions cannot—contrary to a popular opinion—ground an informative analysis of constitution. This has led some to abandon the project of analyzing constitution in interventionist terms. By contrast, this paper defines the notion of a horizontally surgical intervention, and argues that, when combined with some innocuous (...) metaphysical principles about the relation between upper and lower levels of mechanisms, that notion delivers a sufficient condition for constitution. This, in turn, strengthens the case for an interventionist analysis of constitution. (shrink)

The transference theory reduces causation to the transmission of physical conserved quantities, like energy or momenta. Although this theory aims at applying to all felds of physics, we claim that it fails to account for a quantum electrodynamic effect, viz. the Aharonov-Bohm effect. After having argued that the Aharonov-Bohm effect is a genuine counter-example for the transference theory, we offer a new physicalist approach of causation, ontic and modal, in which this effect is embedded.

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)

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)

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)

Building on self-professed perspectival approaches to both scientific knowledge and causation, I explore the potentially radical suggestion that perspectivalism can be extended to account for a type of objectivity in science. Motivated by recent claims from quantum foundations that quantum mechanics must admit the possibility of observer-dependent facts, I develop the notion of ‘perspectival objectivity’, and suggest that an easier pill to swallow, philosophically speaking, than observer-dependency is perspective-dependency, allowing for a notion of observer-independence indexed to an agent perspective. Working (...) through the case studies of colour perception and causal perspectivalism, I identify two places within which I claim perspectival objectivity is already employed, and make the connection to quantum mechanics through Bohr’s philosophy of quantum theory. I contend that perspectival objectivity can ensure, despite the possibility of perspective-dependent scientific facts, the objectivity of scientific inquiry. (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)

In the causal inference framework of Spirtes, Glymour, and Scheines, inferences about causal relationships are made from samples from probability distributions and a number of assumptions relating causal relations to probability distributions. The most controversial of these assumptions is the Causal Faithfulness Assumption, which roughly states that if a conditional independence statement is true of a probability distribution generated by a causal structure, it is entailed by the causal structure and not just for particular parameter values. In this paper we (...) show that the addition of the Causal Faithfulness Assumption plays three quite different roles in the SGS framework: it reduces the degree of underdetermination of causal structure by probability distribution; computationally, it justifies reliable causal inference algorithms that would otherwise have to be slower in order to be reliable; and statistically, it implies that those algorithms reliably obtain the correct answer at smaller sample sizes than would otherwise be the case. We also consider a number of variations on the Causal Faithfulness Assumption, and show how they affect each of these three roles. (shrink)

Causal discovery becomes especially challenging when the possibility of latent confounding and/or selection bias is not assumed away. For this task, ancestral graph models are particularly useful in that they can represent the presence of latent confounding and selection effect, without explicitly invoking unobserved variables. Based on the machinery of ancestral graphs, there is a provably sound causal discovery algorithm, known as the FCI algorithm, that allows the possibility of latent confounders and selection bias. However, the orientation rules used in (...) the algorithm are not complete. In this paper, we provide additional orientation rules, augmented by which the FCI algorithm is shown to be complete, in the sense that it can, under standard assumptions, discover all aspects of the causal structure that are uniquely determined by facts of probabilistic dependence and independence. The result is useful for developing any causal discovery and reasoning system based on ancestral graph models. (shrink)

A main message from the causal modelling literature in the last several decades is that under some plausible assumptions, there can be statistically consistent procedures for inferring (features of) the causal structure of a set of random variables from observational data. But whether we can control the error probabilities with a finite sample size depends on the kind of consistency the procedures can achieve. It has been shown that in general, under the standard causal Markov and Faithfulness assumptions, the procedures (...) can only be pointwise but not uniformly consistent without substantial background knowledge. This implies the impossibility of choosing a finite sample size to control the worst case error probabilities. In this paper, I consider the simpler task of inferring causal directions when the skeleton of the causal structure is known, and establish a similarly negative result concerning the possibility of controlling error probabilities. Although the result is negative in form, it has an interesting positive implication for causal discovery methods. (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)

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)

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)

This is a wonderful book; indeed, it is easily one of the most important and creative books I have ever read on the subject of causation and causal inference. Causality is impressive on many levels and should be of great interest to many different audiences. Philosophers will find of particular interest Pearl's defense of what might be described as a broadly manipulationist or interventionist treatment of causation: Causal claims have to do with what would happen under ideal, suitably surgical experimental (...) manipulations . But Pearl moves far beyond philosophical generalities on this theme: He makes the case for the approach that he favors by developing a formal apparatus for talking about interventions and how they relate to causation and information about probabilities that is at once both intuitively compelling and genuinely useful for purposes of calculation and estimation. He also actively engages the philosophical literature on causation at many points – for example, there are illuminating discussions of evidential decision theory, of probabilistic theories of causation of the sort favored by Eells and Cartwright, of Lewisian counterfactual theories of causation, and of the relationship between so-called type and token causal claims, as well as a quite novel treatment of the latter. (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)

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)

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)

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)

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)

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)

The goal of research in social epidemiology is not simply conceptual clarification or theoretical understanding, but more importantly it is to contribute to, and enhance the health of populations (and so, too, the people who constitute those populations). Undoubtedly, understanding how various individual risk factors such as smoking and obesity affect the health of people does contribute to this goal. However, what is distinctive of much on-going work in social epidemiology is the view that analyses making use of individual-level variables (...) is not enough. In the spirit of Durkheim and Weber, S. Leonard Syme makes this point by writing that just “as bad water and food may be harmful to our health, unhealthful forces in our society may be detrimental to our capacity to make choices and to form opinions” conducive to health and well-being. Advocates of upstream (distal) causes of adverse health outcomes propose to identify the most important of these “unhealthful forces” as the fundamental causes of adverse health outcomes. However, without a clear, theoretically precise and well-grounded understanding of the characteristics of fundamental causes, there is little hope in applying the statistical tools of the health sciences to hypotheses about fundamental causes, their outcomes, and policies intended to enhance the health of populations. This paper begins the process of characterizing the social epidemiological concept of fundamental cause in a theoretically respectable and robust way. (shrink)

We argue that any account of mental disorders that meets the desideratum of assigning causal efficacy to mental disorders faces the so-called “causal exclusion problem”. We argue that fully reductive accounts solve this problem but run into the problem of multiple realizability. Recently advocated symptom-network approaches avoid the problem of multiple realizability, but they also run into the causal exclusion problem. Based on a critical analysis of these accounts, we will present our own account according to which mental disorders are (...) dispositional properties that are token-identical to physical properties. More specifically, they are analyzed as dispositions to cause the specific set of symptoms. We argue that our account is not only able to account for multiple realizability without running into the causal exclusion problem, but that it also allows for the integration of very different factors into the description and explanation of mental disorders, such as neurological and neurochemical factors on the one side and social and cultural factors on the other. It thereby gives the psychiatric level of causal explanation autonomy while securing the causal efficacy of mental disorders in a causally closed physical world. (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)

This article examines methodological individualism in terms of the theory that invariance under intervention is the signal feature of generalizations that serve as a basis for causal explanation. This theory supports the holist contention that macro-level generalizations can explain, but it also suggests a defense of methodological individualism on the grounds that greater range of invariance under intervention entails deeper explanation. Although this individualist position is not threatened by multiple-realizability, an argument for it based on rational choice theory is called (...) into question by experimental results concerning preference reversals. Key Words: methodological individualism • mechanisms • explanation • invariance • preference reversal. (shrink)

Jim Joyce has argued that David Lewis’s formulation of causal decision theory is inadequate because it fails to apply to the “small world” decisions that people face in real life. Meanwhile, several authors have argued that causal decision theory should be developed such that it integrates the interventionist approach to causal modeling because of the expressive power afforded by the language of causal models, but, as of now, there has been little work towards this end. In this paper, I propose (...) a variant of Lewis’s causal decision theory that is intended to meet both of these demands. Specifically, I argue that Lewis’s causal decision theory can be rendered applicable to small world decisions if one analyzes his dependency hypotheses as causal hypotheses that depend on the interventionist causal modeling framework for their semantics. I then argue that this interventionist variant of Lewis’s causal decision theory is preferable to interventionist causal decision theories that purportedly generalize Lewis’s through the use of conditional probabilities. This is because Lewisian interventionist decision theory captures the causal decision theorist’s conviction that any correlation between what the agent does and cannot cause should be irrelevant to the agent’s choice, while purported generalizations do not. (shrink)

The causal Markov condition (CMC) plays an important role in much recent work on the problem of causal inference from statistical data. It is commonly thought that the CMC is a more problematic assumption for genuinely indeterministic systems than for deterministic ones. In this essay, I critically examine this proposition. I show how the usual motivation for the CMC—that it is true of any acyclic, deterministic causal system in which the exogenous variables are independent—can be extended to the indeterministic case. (...) In light of this result, I consider several arguments for supposing indeterminism a particularly hostile environment for the CMC, but conclude that none are persuasive. Introduction Functional models and directed graphs The causal Markov theorem The causal Markov theorem and genuine indeterminism Are the exogenous variables independent? EPR Conclusion. (shrink)

Meek and Glymour use the graphical approach to causal modeling to argue that one and the same norm of rational choice can be used to deliver both causal-decision-theoretic verdicts and evidential-decision-theoretic verdicts. Specifically, they argue that if an agent maximizes conditional expected utility, then the agent will follow the causal decision theorist’s advice when she represents herself as intervening, and will follow the evidential decision theorist’s advice when she represents herself as not intervening. Since Meek and Glymour take no stand (...) on whether agents should represent themselves as intervening, they provide more general advice than standard causal decision theorists and evidential decision theorists. But I argue here that even Meek and Glymour’s advice is not sufficiently general. This is because their advice is not sensitive to the distinct ways in which agents can fail to intervene, and there are decision-making contexts in which agents can reasonably have non-extreme confidence that they are intervening. I then show that the most natural extension of Meek and Glymour’s framework fails, but offer a generalization of my “Interventionist Decision Theory” that does not suffer from the same problems. (shrink)