Where E is the proposition that [If H and O were true, H would explain O], William Roche and Elliot Sober have argued that P(H|O&E) = P(H|O). In this paper I argue that not only is this equality not generally true, it is false in the very kinds of cases that Roche and Sober focus on, involving frequency data. In fact, in such cases O raises the probability of H only given that there is an explanatory connection between them.

"Correlation is not causation" is one of the mantras of the sciences—a cautionary warning especially to fields like epidemiology and pharmacology where the seduction of compelling correlations naturally leads to causal hypotheses. The standard view from the epistemology of causation is that to tell whether one correlated variable is causing the other, one needs to intervene on the system—the best sort of intervention being a trial that is both randomized and controlled. In this paper, we argue that some purely correlational (...) data contains information that allows us to draw causal inferences: statistical noise. Methods for extracting causal knowledge from noise provide us with an alternative to randomized controlled trials that allows us to reach causal conclusions from purely correlational data. (shrink)

In earlier work ( Cleland [2001] , [2002]), I sketched an account of the structure and justification of ‘prototypical’ historical natural science that distinguishes it from ‘classical’ experimental science. This article expands upon this work, focusing upon the close connection between explanation and justification in the historical natural sciences. I argue that confirmation and disconfirmation in these fields depends primarily upon the explanatory (versus predictive or retrodictive) success or failure of hypotheses vis-à-vis empirical evidence. The account of historical explanation that (...) I develop is a version of common cause explanation. Common cause explanation has long been vindicated by appealing to the principle of the common cause. Many philosophers of science (e.g., Sober and Tucker) find this principle problematic, however, because they believe that it is either purely methodological or strictly metaphysical. I defend a third possibility: the principle of the common cause derives its justification from a physically pervasive time asymmetry of causation (a.k.a. the asymmetry of overdetermination). I argue that explicating the principle of the common cause in terms of the asymmetry of overdetermination illuminates some otherwise puzzling features of the practices of historical natural scientists. (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 this paper, I critically evaluate several related, provocative claims made by proponents of data-intensive science and “Big Data” which bear on scientific methodology, especially the claim that scientists will soon no longer have any use for familiar concepts like causation and explanation. After introducing the issue, in Section 2, I elaborate on the alleged changes to scientific method that feature prominently in discussions of Big Data. In Section 3, I argue that these methodological claims are in tension with a (...) prominent account of scientific method, often called “Inference to the Best Explanation”. Later on, in Section 3, I consider an argument against IBE that will be congenial to proponents of Big Data, namely, the argument due to Roche and Sober Analysis, 73:659–668, that “explanatoriness is evidentially irrelevant.” This argument is based on Bayesianism, one of the most prominent general accounts of theory-confirmation. In Section 4, I consider some extant responses to this argument, especially that of Climenhaga Philosophy of Science, 84:359–368,. In Section 5, I argue that Roche and Sober’s argument does not show that explanatory reasoning is dispensable. In Section 6, I argue that there is good reason to think explanatory reasoning will continue to prove indispensable in scientific practice. Drawing on Cicero’s oft-neglected De Divinatione, I formulate what I call the “Ciceronian Causal-nomological Requirement”, which states, roughly, that causal-nomological knowledge is essential for relying on correlations in predictive inference. I defend a version of the CCR by appealing to the challenge of “spurious correlations,” chance correlations which we should not rely upon for predictive inference. In Section 7, I offer some concluding remarks. (shrink)

In this paper, I examine Cicero’s oft-neglected De Divinatione, a dialogue investigating the legitimacy of the practice of divination. First, I offer a novel analysis of the main arguments for divination given by Quintus, highlighting the fact that he employs two logically distinct argument forms. Next, I turn to the first of the main arguments against divination given by Marcus. Here I show, with the help of modern probabilistic tools, that Marcus’ skeptical response is far from the decisive, proto-naturalistic assault (...) on superstition that it is sometimes portrayed to be. Then, I offer an extended analysis of the second of the main arguments against divination given by Marcus. Inspired by Marcus’ second main argument, I formulate, explicate, and defend a substantive principle of scientific methodology that I call the “Ciceronian Causal-Nomological Requirement” (CCR). Roughly, this principle states that causal knowledge is essential for relying on correlations in predictive inference. Although I go on to argue that Marcus’ application of the CCR in his debate with Quintus is dialectically inadequate, I conclude that De Divinatione deserves its place in Cicero’s philosophical corpus, and that ultimately, its significance for the history and philosophy of science ought to be recognized. (shrink)

In this paper, I consider the relationship between Inference to the Best Explanation and Bayesianism, both of which are well-known accounts of the nature of scientific inference. In Sect. 2, I give a brief overview of Bayesianism and IBE. In Sect. 3, I argue that IBE in its most prominently defended forms is difficult to reconcile with Bayesianism because not all of the items that feature on popular lists of “explanatory virtues”—by means of which IBE ranks competing explanations—have confirmational import. (...) Rather, some of the items that feature on these lists are “informational virtues”—properties that do not make a hypothesis \ more probable than some competitor \ given evidence E, but that, roughly-speaking, give that hypothesis greater informative content. In Sect. 4, I consider as a response to my argument a recent version of compatibilism which argues that IBE can provide further normative constraints on the objectively correct probability function. I argue that this response does not succeed, owing to the difficulty of defending with any generality such further normative constraints. Lastly, in Sect. 5, I propose that IBE should be regarded, not as a theory of scientific inference, but rather as a theory of when we ought to “accept” H, where the acceptability of H is fixed by the goals of science and concerns whether H is worthy of commitment as research program. In this way, IBE and Bayesianism, as I will show, can be made compatible, and thus the Bayesian and the proponent of IBE can be friends. (shrink)

What Do the Data Tell Us? Justification of scientific theories is a three-place relation between data, theories, and background knowledge. Though this should be a commonplace, many methodologies in science neglect it. The article will elucidate the significance and function of our background knowledge in epistemic justification and their consequences for different scientific methodologies. It is argued that there is no simple and at the same time acceptable statistical algorithm that justifies a given theory merely on the basis of certain (...) data. And even if we think to know the probability of a theory, that does not decide whether we should accept it or not. (shrink)

We offer a review of some of the most influential views on the status of Reichenbach’s Principle of the Common Cause (RPCC) for genuinely indeterministic systems. We first argue that the RPCC is properly a conjunction of two distinct claims, one metaphysical and another methodological. Both claims can and have been contested in the literature, but here we simply assume that the metaphysical claim is correct, in order to focus our analysis on the status of the methodological claim. We briefly (...) review the most entrenched or classical positions, including Salmon’s ‘interactive forks’, van Fraassen’s scepticism, and Cartwright’s generalisation of the fork criterion. We then go on to review the results of the ‘Budapest school’ on the existence of formally defined screening­ off events for any correlation —by means of the ideas of probability space extensibility and (Reichenbachian common cause) completability. We distinguish the Budapest doctrine clearly from any of the classical conceptions, and thus present an overall framework for discussions of causal inference in quantum mechanics. We argue that this review is preliminary essential work for a thorough assessment of the conditions under which RCCP may be a reliable tool for causal inference in a genuinely probabilistic (indeterministic) context. (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)

Quantum mechanics portrays the universe as involving non-local influences that are difficult to reconcile with relativity theory. By postulating backward causation, retro-causal interpretations of quantum mechanics could circumvent these influences and accordingly reconcile quantum mechanics with relativity. The postulation of backward causation poses various challenges for the retro-causal interpretations of quantum mechanics and for the existing conceptual frameworks for analyzing counterfactual dependence, causation and causal explanation. In this chapter, we analyze the nature of time, causation and explanation in a local, (...) deterministic retro-causal interpretation of quantum mechanics that is inspired by Bohmian mechanics. This interpretation of quantum mechanics offers a deterministic, local ‘hidden-variables’ model of the Einstein-Podolsky-Rosen experiment that poses a new challenge for Reichenbach’s principle of the common cause. In this model, the common cause – the state of particles at the emission from the source – screens off the correlation between its effects – the distant measurement outcomes – but nevertheless fails to explain the correlation between the effects. (shrink)

It is surely obvious that medicine, like any other rational activity, must be based on evidence. The interest is in the details: how exactly are the general principles of the logic of evidence to be applied in medicine? Focussing on the development, and current claims of the ‘Evidence-Based Medicine’ movement, this article raises a number of difficulties with the rationales that have been supplied in particular for the ‘evidence hierarchy’ and for the very special role within that hierarchy of randomized (...) controlled trials (and meta-analyses of the results of randomized controlled trials). The point is not at all to question the application of a scientific approach to evidence in medicine, but, on the contrary, to indicate a number of areas where philosophers of science can contribute to a proper implementation of exactly that scientific-evidential approach. (shrink)

We argued that explanatoriness is evidentially irrelevant in the following sense: Let H be a hypothesis, O an observation, and E the proposition that H would explain O if H and O were true. Then our claim is that Pr = Pr. We defended this screening-off thesis by discussing an example concerning smoking and cancer. Climenhaga argues that SOT is mistaken because it delivers the wrong verdict about a slightly different smoking-and-cancer case. He also considers a variant of SOT, called (...) “SOT*”, and contends that it too gives the wrong result. We here reply to Climenhaga’s arguments and suggest that SOT provides a criticism of the widely held theory of inference called “inference to the best explanation”. (shrink)

In a recent article, Elliot Sober responds to challenges to a counter-example that he posed some years earlier to the Principle of the Common Cause (PCC). I agree that Sober has indeed produced a genuine counter-example to the PCC, but argue against the methodological moral that Sober wishes to draw from it. Contrary to Sober, I argue that the possibility of exceptions to the PCC does not undermine its status as a central assumption for methods that endeavor to draw causal (...) conclusions from statistical data. 1 The PCC and the counter-example 2 Making non-stationary time series stand still 3 Sober's alternative. (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)

In this paper two accounts of Reichenbachian common cause systems are compared. Examples are provided which show that Hofer-Szabó and Rédei account and Hofer-Szabó et al. account is compatible, with but not equivalent, to Mazzola’s. Moreover, the difference of the two accounts with respect to their explanatory adequacy is discussed, in the light of Salmon’s statistical-relevance approach to statistical explanation.

We begin by considering two principles, each having the form causal completeness ergo screening-off. The first concerns a common cause of two or more effects; the second describes an intermediate link in a causal chain. They are logically independent of each other, each is independent of Reichenbach's principle of the common cause, and each is a consequence of the causal Markov condition. Simple examples show that causal incompleteness means that screening-off may fail to obtain. We derive a stronger result: in (...) a rather general setting, if the composite cause C1 & C2 & … & Cn screens-off one event from another, then each of the n component causes C1, C2, …, Cn must fail to screen-off. The idea that a cause may be ordinally invariant in its impact on different effects is defined; it plays an important role in establishing this no-go theorem. Along the way, we describe how composite and component causes can all screen-off when ordinal invariance fails. We argue that this theorem is relevant to assessing the plausibility of the two screening-off principles. The discovery of incomplete causes that screen-off is not evidence that causal completeness must engender screening-off. Formal and epistemic analogies between screening-off and determinism are discussed. (shrink)

This paper is a sympathetic critique of the argument that Reichenbach develops in Chap. 2 of Experience and Prediction for the thesis that sense experience justifies belief in the existence of an external world. After discussing his attack on the positivist theory of meaning, I describe the probability ideas that Reichenbach presents. I argue that Reichenbach begins with an argument grounded in the Law of Likelihood but that he then endorses a different argument that involves prior probabilities. I try to (...) show how this second step in Reichenbach's approach can be strengthened by using ideas that have been developed recently for understanding causation in terms of the idea of intervention. (shrink)

This paper is a sympathetic critique of the argument that Reichenbach develops in Chap. 2 of Experience and Prediction for the thesis that sense experience justifies belief in the existence of an external world. After discussing his attack on the positivist theory of meaning, I describe the probability ideas that Reichenbach presents. I argue that Reichenbach begins with an argument grounded in the Law of Likelihood but that he then endorses a different argument that involves prior probabilities. I try to (...) show how this second step in Reichenbach’s approach can be strengthened by using ideas that have been developed recently for understanding causation in terms of the idea of intervention. (shrink)

I discuss two versions of the doomsday argument. According to ``Gott's Line'',the fact that the human race has existed for 200,000 years licences the predictionthat it will last between 5100 and 7.8 million more years. According to ``Leslie'sWedge'', the fact that I currently exist is evidence that increases the plausibilityof the hypothesis that the human race will come to an end sooner rather than later.Both arguments rest on substantive assumptions about the sampling process thatunderlies our observations. These sampling assumptions have (...) testable consequences,and so the sampling assumptions themselves must be regarded as empirical claims.The result of testing some of these consequences is that both doomsday argumentsare empirically disconfirmed. (shrink)

Evidential Pluralism maintains that in order to establish a causal claim one normally needs to establish the existence of an appropriate conditional correlation and the existence of an appropriate mechanism complex, so when assessing a causal claim one ought to consider both association studies and mechanistic studies. Hitherto, Evidential Pluralism has been applied to medicine, leading to the EBM+ programme, which recommends that evidence-based medicine should systematically evaluate mechanistic studies alongside clinical studies. This paper argues that Evidential Pluralism can also (...) be fruitfully applied to the social sciences. In particular, Evidential Pluralism provides (i) a new approach to evidence-based policy; (ii) an account of the evidential relationships in more theoretical research; and (iii) new philosophical motivation for mixed methods research. The application of Evidential Pluralism to the social sciences is also defended against two objections. (shrink)

In this paper I assess the adequacy of no-conspiracy conditions employed in the usual derivations of the Bell inequality in the context of EPR correlations. First, I look at the EPR correlations from a purely phenomenological point of view and claim that common cause explanations of these cannot be ruled out. I argue that an appropriate common cause explanation requires that no-conspiracy conditions are re-interpreted as mere common cause-measurement independence conditions. In the right circumstances then, violations of measurement independence need (...) not entail any kind of conspiracy (nor backwards in time causation). To the contrary, if measurement operations in the EPR context are taken to be causally relevant in a specific way to the experiment outcomes, their explicit causal role provides the grounds for a common cause explanation of the corresponding correlations. (shrink)

Current Perspectives in Philosophy of Biology.

En un libro reciente McShea y Brandon defienden que la diversidad y la complejidad de la vida se explican, principalmente, por la acción de un principio que llaman “la ley evolutiva de fuerzas cero” o “ZFEL”. Tal principio actuaría de un modo implícito por detrás de muchas explicaciones de la biología, pero nunca habría sido explicitado. Asumiendo que esta idea es interesante, y que los autores en cuestión tienen razón, discutiremos el modo metateórico en que presentan dicho principio, como siendo (...) parte de la teoría de la probabilidad. Esto permite a los autores afirmar que la teoría de la probabilidad brindaría la base reductiva para toda la biología evolutiva (dado que consideran que otros principios, como el de selección natural, también serían parte de la teoría de la probabilidad). Defenderemos que, efectivamente, ZFEL no es propio de la biología únicamente, pero no por formar parte de la teoría de la probabilidad, sino por tratarse de una versión específica del principio de causa común. -/- In a recent book, McShea and Brandon argue that the observed diversity and complexity of life are explainable by a principle they call the “zero-force evolutionary law” or “ZFEL”. Although this principle would be implicit in many explanations given by biologists, it would have never been made explicit. Assuming that this idea is interesting, and that the authors are right, we will discuss the metatheoretical way in which they present said principle, as being a part of probability theory. This allows the authors to claim that probability theory provides the reductive basis for all evolutionary biology. We will defend, in accordance with them, that ZFEL is not a solely biological principle, but not because it is a part of probability theory, but rather because it is a specific version of the principle of common cause. (shrink)

All univocal analyses of causation face counterexamples. An attractive response to this situation is to become a pluralist about causal relationships. "Causal pluralism" is itself, however, a pluralistic notion. In this article, I argue in favor of pluralism about concepts of cause in the social sciences. The article will show that evidence for, inference from, and the purpose of causal claims are very closely linked. Key Words: causation • pluralism • evidence • methodology.

Two approaches to evidential reasoning compete in the biomedical and social sciences: the experimental and the pragmatist. Whereas experimentalism has received considerable philosophical analysis and support since the times of Bacon and Mill, pragmatism about evidence has been neither articulated nor defended. The overall aim is to fill this gap and develop a theory that articulates the latter. The main ideas of the theory will be illustrated and supported by a case study on the smoking/lung cancer controversy in the 1950s.

Analogical reasoning addresses the question how evidence from various phenomena can be combined and made relevant for theory development and prediction. In the first part of my contribution, I review some influential accounts of analogical reasoning, both historical and contemporary, focusing in particular on Keynes, Carnap, Hesse, and more recently Bartha. In the second part, I sketch a general framework. To this purpose, a distinction between a predictive and a conceptual type of analogical reasoning is introduced. I then take up (...) a common intuition according to which analogical inferences hold if the differences between source and target concern only irrelevant circumstances. I attempt to make this idea more precise by addressing possible objections and in particular by specifying a notion of causal irrelevance based on difference making in homogeneous contexts. (shrink)

Philosophers of science have often favoured reductive approaches to how-possibly explanation. This article identifies three alternative conceptions making how-possibly explanation an interesting phenomenon in its own right. The first variety approaches “how possibly X?” by showing that X is not epistemically impossible. This can sometimes be achieved by removing misunderstandings concerning the implications of one’s current belief system but involves characteristically a modification of this belief system so that acceptance of X does not result in contradiction. The second variety offers (...) a potential how-explanation of X. It is usually followed by a range of further potential how-explanations of the same phenomenon. In recent literature the factual claims implied by the second variety have been downplayed whereas the heuristic role of mapping the space of conceptual possibilities has been emphasized. I will focus especially on this truth-bracketing sense of potentiality when looking closer at the second variety in the paper. The third variety has attracted less interest. It presents a partial how-explanation of X. Typically it aims to establish the existence of a mechanism by which X could be and was generated. The third conception stands out as the natural alternative for the advocate of ontic how-possibly explanations. This article transfers Salmon’s view that explanation-concepts can be broadly divided into epistemic, modal, and ontic to the context of how-possibly explanations. Moreover, it is argued that each of the three above-mentioned varieties of how-possibly explanation occurs in science. To recognize this may be especially relevant for philosophers. We are often misled by the promises of various why-explanation accounts, and seem to have forgotten nearly everything about the diversity of how-possibly explanations. (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 defends the thesis of learning from non-causal models: viz. that the study of some model can prompt justified changes in one’s confidence in empirical hypotheses about a real-world target in the absence of any known or predicted similarity between model and target with regards to their causal features. Recognizing that we can learn from non-causal models matters not only to our understanding of past scientific achievements, but also to contemporary debates in the philosophy of science. At one end (...) of the philosophical spectrum, my thesis undermines the views of those who, like Cartwright (Erkenntnis 70:45–58, 2009), follow Hesse (Models and Analogies in Science, Notre Dame, University of Notre Dame Press, 1963) in restricting the possibility of learning from models to only those situations where a model identifies some causal factors present in the target. At the other end of the spectrum, my thesis also helps undermine some extremely permissive positions, e.g., Grüne-Yanoff’s (Erkenntnis 70(1):81–99, 2009, Philos Sci 80(5): 850–861, 2013) claim that learning from a model is possible even in the absence of any similarity at all between model and target. The thesis that we can learn from non-causal models offers a cautious middle ground between these two extremes. (shrink)

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. Angrist et al. has argued that the principle is necessary for instrumental variables methods in econometrics, and Angrist Krueger builds a framework using it that he proposes as a means of resolving an important methodological dispute among econometricians. Through analysis of instrumental variables methods and the issue of multicollinearity, we aim to show 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)

Social research, from economics to demography and epidemiology, makes extensive use of statistical models in order to establish causal relations. The question arises as to what guarantees the causal interpretation of such models. In this paper we focus on econometrics and advance the view that causal models are ‘augmented’ statistical models that incorporate important causal information which contributes to their causal interpretation. The primary objective of this paper is to argue that causal claims are established on the basis of a (...) plurality of evidence. We discuss the consequences of ‘evidential pluralism’ in the context of econometric modelling. (shrink)

The existing philosophical views on what is the meaning of causality adequate to medicine are vastly divided. We approach this question and offer two arguments in favor of pluralism regarding concepts of causality. First, we analyze the three main types of research designs (randomized-controlled trials, observational epidemiology and laboratory research). We argue, using examples, that they allow for making causal conclusions that are best understood differently in each case (in agreement with a version of manipulationist, probabilistic and mechanistic definitions, respectively). (...) Second, we analyze clinical practice and argue that these manipulationist, probabilistic and mechanistic causal claims can be used as evidence for different therapeutic decisions. We differentiate among ‘predicting’ that does not change the relata of causal claims, (mechanistic) ‘interferences’, and ‘interventions’ in the strict sense that act on causes to change effects. The central conclusion is that causal claims agreeing with diverse concepts of causality can deliver evidence for different types of therapeutic decisions. (shrink)

We give a few results concerning the notions of causal completability and causal closedness of classical probability spaces . We prove that any classical probability space has a causally closed extension; any finite classical probability space with positive rational probabilities on the atoms of the event algebra can be extended to a causally up-to-three-closed finite space; and any classical probability space can be extended to a space in which all correlations between events that are logically independent modulo measure zero event (...) have a countably infinite common-cause system. Collectively, these results show that it is surprisingly easy to find Reichenbach-style ‘explanations' for correlations, underlining doubts as to whether this approach can yield a philosophically relevant account of causality. 1 Introduction2 Basic Definitions and Results in the Literature3 Causal Completability the Easy Way: ‘Splitting the Atom’4 Causal Completability of Classical Probability Spaces: The General Case5 Infinite Statistical Common-Cause Systems for Arbitrary Pairs6 ConclusionAppendix A. (shrink)

We prove new results on common cause closedness of quantum probability spaces, where by a quantum probability space is meant the projection lattice of a non-commutative von Neumann algebra together with a countably additive probability measure on the lattice. Common cause closedness is the feature that for every correlation between a pair of commuting projections there exists in the lattice a third projection commuting with both of the correlated projections and which is a Reichenbachian common cause of the correlation. The (...) main result we prove is that a quantum probability space is common cause closed if and only if it has at most one measure theoretic atom. This result improves earlier ones published in [1]. The result is discussed from the perspective of status of the Common Cause Principle. Open problems on common cause closedness of general probability spaces (L, ϕ) are formulated, where L is an orthomodular bounded lattice and ϕ is a probability measure on L. (shrink)

Modern empirical macroeconomic models, known as structural autoregressions (SVARs) are dynamic models that typically claim to represent a causal order among contemporaneously valued variables and to merely represent non-structural (reduced-form) co-occurence between lagged variables and contemporaneous variables. The strategy is held to meet the minimal requirements for identifying the residual errors in particular equations in the model with independent, though otherwise not directly observable, exogenous causes (“shocks”) that ultimately account for change in the model. In nonstationary models, such shocks accumulate (...) so that variables have discernible trends. Econometricians have conceived of variables that trend in sympathy with each other (so-called “cointegrated variables”) as sharing one or more of these unobserved trends as a common cause. It is possible for estimates of the values of both the otherwise unobservable individual shocks and the otherwise unobservable common trends to be backed-out of cointegrated systems of equations. The issue addressed in this paper is whether and in what circumstances these values can be regarded as observations of real entities rather than merely artifacts of the representation of variables in the model. The issue is related, on the one hand, to practical methodological problems in the use of SVARs for policy analysis—e.g., does it make sense to estimate of shocks or trends in one model and then use them as measures of variables in a conceptually distinct model? The issue is also related to debates in the philosophical analysis of causation—particularly, whether we are entitled, as assumed by the developers of Bayes-net approaches, to rely on the causal Markov condition (a generalization of Reichenbach’s common-cause condition) or whether cointegration generates a practical example of Nancy Cartwright’s “byproducts” objection to the causal Markov condition. (shrink)

Elliot Sober ([2001]) forcefully restates his well-known counterexample to Reichenbach's principle of the common cause: bread prices in Britain and sea levels in Venice both rise over time and are, therefore, correlated; yet they are ex hypothesi not causally connected, which violates the principle of the common cause. The counterexample employs nonstationary data—i.e., data with time-dependent population moments. Common measures of statistical association do not generally reflect probabilistic dependence among nonstationary data. I demonstrate the inadequacy of the counterexample and of (...) some previous responses to it, as well as illustrating more appropriate measures of probabilistic dependence in the nonstationary case. A challenge to the principle of the common causeSober's argument and the attempts to rescue the principleProbabilistic dependenceNonstationary time seriesProbabilistic dependence in nonstationary time seriesDo Venetian sea levels and British bread prices violate the principle of the common cause? (shrink)

ABSTRACT Causes must be distinct from their effects. If the temperature in a room is 15°F, this can cause water pipes to freeze. However, the temperature’s being 15°F is not a cause of the temperature’s being below the freezing point. In general, conceptual, logical, mathematical, and other non-causal dependence relations should not be misclassified as causal. In this paper, I discuss how interventionist theories of causation can meet the challenge of distinguishing between (direct or indirect) causal relations and dependence relations (...) that are due to non-causal factors. I survey several approaches to solving this problem, and propose a novel criterion based on the notion of supervenience. According to this criterion, variables are sufficiently distinct to qualify as the relata of a causal relation iff they do not have overlapping minimal supervenience bases. (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)

The notion of common cause closedness of a classical, Kolmogorovian probability space with respect to a causal independence relation between the random events is defined, and propositions are presented that characterize common cause closedness for specific probability spaces. It is proved in particular that no probability space with a finite number of random events can contain common causes of all the correlations it predicts; however, it is demonstrated that probability spaces even with a finite number of random events can be (...) common cause closed with respect to a causal independence relation that is stronger than logical independence. Furthermore it is shown that infinite, atomless probability spaces are always common cause closed in the strongest possible sense. Open problems concerning common cause closedness are formulated and the results are interpreted from the perspective of Reichenbach's Common Cause Principle. (shrink)

The role of measure theoretic atomicity in common cause closedness of general probability theories with non-distributive event structures is raised and investigated. It is shown that if a general probability space is non-atomic then it is common cause closed. Conditions are found that entail that a general probability space containing two atoms is not common cause closed but it is common cause closed if it contains only one atom. The results are discussed from the perspective of the Common Cause Principle.

A probability space is common cause closed if it contains a Reichenbachian common cause of every correlation in it and common cause incomplete otherwise. It is shown that a probability space is common cause incomplete if and only if it contains more than one atom and that every space is common cause completable. The implications of these results for Reichenbach's Common Cause Principle are discussed, and it is argued that the principle is only falsifiable if conditions on the common cause (...) are imposed that go beyond the requirements formulated by Reichenbach in the definition of common cause. (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)

According to a widespread view, which can be traced back to Russell’s famous attack on the notion of cause, causal notions have no legitimate role to play in how mature physical theories represent the world. In this paper I first critically examine a number of arguments for this view that center on the asymmetry of the causal relation and argue that none of them succeed. I then argue that embedding the dynamical models of a theory into richer causal structures can (...) allow us to decide between models in cases where our observational data severely underdetermine our choice of dynamical models. (shrink)

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

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

The causal Bayes net framework specifies a set of axioms for causal discovery. This article explores the set of causal variables that function as relata in these axioms. Spirtes showed how a causal system can be equivalently described by two different sets of variables that stand in a non-trivial translation-relation to each other, suggesting that there is no “correct” set of causal variables. I extend Spirtes’ result to the general framework of linear structural equation models and then explore to what (...) extent the possibility to intervene or a preference for simpler causal systems may help in selecting among sets of causal variables. (shrink)

To clarify and illuminate the place of probability in science Ellery Eells and James H. Fetzer have brought together some of the most distinguished philosophers ...