Randomized controlled trials (RCTs) are widely taken as the gold standard for establishing causal conclusions. Ideally conducted they ensure that the treatment ‘causes’ the outcome—in the experiment. But where else? This is the venerable question of external validity. I point out that the question comes in two importantly different forms: Is the specific causal conclusion warranted by the experiment true in a target situation? What will be the result of implementing the treatment there? This paper explains how the probabilistic theory (...) of causality implies that RCTs can establish causal conclusions and thereby provides an account of what exactly that causal conclusion is. Clarifying the exact form of the conclusion shows just what is necessary for it to hold in a new setting and also how much more is needed to see what the actual outcome would be there were the treatment implemented. (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)

Do component forces exist in conjoined circumstances? Cartwright (1980) says no; Creary (1981) says yes. I'm inclined towards Cartwright's side in this matter, but find several problems with her argumentation. My primary aim here is to present a better, distinctly causal, argument against component forces: very roughly, I argue that the joint posit of component and resultant forces in conjoined circumstances gives rise to a threat of causal overdetermination, avoidance of which best proceeds via eliminativism about component forces. A secondary (...) aim is to show that rejecting component forces does not require, pace Cartwright, rejecting certain attractive theses about what laws of nature express and the role such laws play in scientific explanations. (shrink)

I put forward several desiderata that a philosophical theory of causality should satisfy: it should account for the objectivity of causality, it should underpin formalisms for causal reasoning, it should admit a viable epistemology, it should be able to cope with the great variety of causal claims that are made, and it should be ontologically parsimonious. I argue that Nancy Cartwright’s dispositional account of causality goes part way towards meeting these criteria but is lacking in important respects. I go on (...) to argue that my epistemic account, which ties causal relationships to an agent’s knowledge and ignorance, performs well in the light of the desiderata. Such an account, I claim, is all we require from a theory of causality. (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)

In a recent article in this journal, Federica Russo and Jon Williamson argue that an analysis of causality in terms of probabilistic relationships does not do justice to the use of mechanistic evidence to support causal claims. I will present Ronald Giere's theory of probabilistic causation, and show that it can account for the use of mechanistic evidence (both in the health sciences—on which Russo and Williamson focus—and elsewhere). I also review some other probabilistic theories of causation (of Suppes, Eells, (...) and Humphreys) and show that they cannot account for the use of mechanistic evidence. I argue that these theories are also inferior to Giere's theory in other respects. (shrink)

Darwinians are realists about the force of selection, but there has been surprisingly little discussion about what form this realism should take. Arguments about the units of selection in general and genic selectionism in particular reveal two realist assumptions: (1) for any selection process, there is a uniquely correct identification of the operative selective forces and the level at which each impinges; and (2) selective forces must satisfy the Pareto-style requirement of probabilistic causation. I argue that both assumptions are false; (...) we must temper realism about the force of selection and revise the way we think about probabilistic causation. (shrink)

Why do people get sick? I argue that a disease explanation is best thought of as causal network instantiation, where a causal network describes the interrelations among multiple factors, and instantiation consists of observational or hypothetical assignment of factors to the patient whose disease is being explained. This paper first discusses inference from correlation to causation, integrating recent psychological discussions of causal reasoning with epidemiological approaches to understanding disease causation, particularly concerning ulcers and lung cancer. It then shows how causal (...) mechanisms represented by causal networks can contribute to reasoning involving correlation and causation. The understanding of causation and causal mechanisms provides the basis for a presentation of the causal network instantiation model of medical explanation. (shrink)

Data from medical research are typically summarized with various types of outcome measures. We present three arguments in favor of absolute over relative outcome measures. The first argument is from cognitive bias: relative measures promote the reference class fallacy and the overestimation of treatment effectiveness. The second argument is decision-theoretic: absolute measures are superior to relative measures for making a decision between interventions. The third argument is causal: interpreted as measures of causal strength, absolute measures satisfy a set of desirable (...) properties, but relative measures do not. Absolute outcome measures outperform relative measures on all counts. (shrink)

This paper develops axiomatic foundations for a probabilistic-interventionist theory of causal strength. Transferring methods from Bayesian confirmation theory, I proceed in three steps: I develop a framework for defining and comparing measures of causal strength; I argue that no single measure can satisfy all natural constraints; I prove two representation theorems for popular measures of causal strength: Pearl's causal effect measure and Eells' difference measure. In other words, I demonstrate these two measures can be derived from a set of plausible (...) adequacy conditions. The paper concludes by sketching future research avenues. (shrink)

The paper builds on the basically Humean idea that A is a cause of B iff A and B both occur, A precedes B, and A raises the metaphysical or epistemic status of B given the obtaining circumstances. It argues that in pursuit of a theory of deterministic causation this ‘status raising’ is best explicated not in regularity or counterfactual terms, but in terms of ranking functions. On this basis, it constructs a rigorous theory of deterministic causation that successfully deals (...) with cases of overdetermination and pre-emption. It finally indicates how the account's profound epistemic relativization induced by ranking theory can be undone. Introduction Variables, propositions, time Induction first Causation Redundant causation Objectivization. (shrink)

Michael Moore’s Causation and Responsibility offers an integrated conception of the law, morality, and metaphysics, centered on the notion of causation, grounded in a detailed knowledge of case law, and supported on every point by cogent argument. This is outstanding work. It is a worthy successor to Harte and Honoré’s classic Causation in the Law, and I expect that it will guide discussion for many years to come.

Two key ideas of scientific explanation−explanation as causal information and explanation as unification-have frequently been set into mutual opposition. This paper proposes a “dialectical solution” to this conflict, by arguing that causal explanations are preferable to non-causal ones, because they lead to a higherdegree of unification at the level of explaining statistical regularities. The core axioms of the theory of causal nets (TC) are justified because they offer the best if not the only unifying explanation of two statistical phenomena: screening (...) off and linking up. Alternative explanations of the two phenomena are discussed and it isshown why they don’t work. It is demonstrated that although the core axioms of TC are empirically vacuous, extended versions of TC have empirical content by means of which they can generate independently testable predictions.Con frecuencia se han planteado como contrapuestas dos ideas clave en la explicacion cientifica (explicacion como informacion causal y explicacion como unificacion). El presente articulo propone una “solucion dialectica” argumentando que las explicaciones causales son preferibles a las no-causales porque aquellas comportan un mayor grado de unificacion en la explicacion de regularidades estadisticas. Los axiomas centrales de la teoria de redes causales (TC) estan justificados porque ofrecen la mejor, si no la unica, explicacion unificada de dos fenomenos estadisticos: neutralizacion (screening off) y vinculacion (linking up). Se discuten las explicaciones alternativas de estos dos fenomenos y se razona por que no funcionan. Se demuestra ademas que aunque los axiomas centrales de TC son empiricamente vacuos, las versiones extendidas de TC tienen un contenido empirico gracias al cual pueden generar predicciones independientemente contrastables. (shrink)

The paper examines definitions of ‘cause’ in the epidemiological literature. Those definitions all describe causes as factors that make a difference to the distribution of disease or to individual health status. In the philosophical jargon, causes in epidemiology are difference-makers. Two claims are defended. First, it is argued that those definitions underpin an epistemology and a methodology that hinge upon the notion of variation, contra the dominant Humean paradigm according to which we infer causality from regularity. Second, despite the fact (...) that causes be defined in terms of ‘difference-making’, this cannot fixes the causal metaphysics. Causality in epidemiology ought to be interpreted according to the epistemic theory. In this approach relations are deemed causal depending on the evidence and on the available methods. Indeed, evidence to establish causal claims requires difference-making considerations; furthermore, those definitions of cause reflect the ‘variational’ epistemology and methodology of epidemiology. (shrink)

We argue that the health sciences make causal claims on the basis of evidence both of physical mechanisms, and of probabilistic dependencies. Consequently, an analysis of causality solely in terms of physical mechanisms or solely in terms of probabilistic relationships, does not do justice to the causal claims of these sciences. Yet there seems to be a single relation of cause in these sciences - pluralism about causality will not do either. Instead, we maintain, the health sciences require a theory (...) of causality that unifies its mechanistic and probabilistic aspects. We argue that the epistemic theory of causality provides the required unification. (shrink)

The aim of this paper is to elaborate a notion of explanation which is applicable to stochastic processes such as quantum processes. The model-theoretic approach was adopted in order to delimit appropriate classes, by defining set-theoretical predicates, of different kinds of physical transformations that quantum systems suffer, either of transitions or of transmutations, by interaction or in a spontaneous manner. To explain a singular quantum process consists in showing that it is feasible to model it as an indeterministic process of (...) certain specified kind. (shrink)

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)

This paper examines the relationship between physical theories of causation and theories of difference-making. It is plausible to think that such theories are compatible with one another as they are aimed at different targets: the former, an empirical account of actual causal relations; the latter, an account that will capture the truth of most of our ordinary causal claims. The question then becomes: what is the relationship between physical causation and difference-making? Is one kind of causal fact more fundamental than (...) the other? This paper defends causal foundationalism: the view that facts about difference-making are dependent on the obtaining of facts about physical causation. However, the paper's main goal is to clarify the structure of the debate. At the end of the paper, it is shown how settling the issue about the relationship between physical theories of causation and theories of difference-making has more than mere intrinsic interest in unifying the very different pursuits that have been undertaken in the philosophy of causation. It can help to break a stalemate that has arisen in the current debate about mental causation. (shrink)

This essay is concerned with concentrations of entities, which play an important—albeit often overlooked—role in scientific explanation. First, I discuss an example from molecular biology to show that concentrations can play an irreducible causal role. Second, I provide a preliminary philosophical analysis of this causal role, suggesting some implications for extant theories of causation. I conclude by introducing the concept of causation by concentration, a form of statistical causation whose widespread presence throughout the sciences has been unduly neglected and which (...) deserves to be studied in more depth. 1 Introduction2 Solving Lillie's Paradox: Lysogenic Induction in Phage λ3 Repressor Concentration and the Tuning of the Switch4 Concentration and Causality5 Preemption in Concentrations: Analysis and Implications6 Causation by Concentration: General Definition, Refinements, and Further Applications. (shrink)

Causal analysis in the social sciences takes advantage of a variety of methods and of a multi-fold source of information and evidence. This pluralistic methodology and source of information raises the question of whether we should accordingly have a pluralistic metaphysics and epistemology. This paper focuses on epistemology and argues that a pluralistic methodology and evidence don’t entail a pluralistic epistemology. It will be shown that causal models employ a single rationale of testing, based on the notion of variation. Further, (...) I shall argue that this monistic epistemology is also involved in alternative philosophical theories of causation. (shrink)

In this paper we defend the view that the ordinary notions of cause and effect have a direct and essential connection with our ability to intervene in the world as agents.1 This is a well known but rather unpopular philosophical approach to causation, often called the manipulability theory. In the interests of brevity and accuracy, we prefer to call it the agency theory.2 Thus the central thesis of an agency account of causation is something like this: an event A is (...) a cause of a distinct event B just in case bringing about the occurrence of A would be an effective means by which a free agent could bring about the occurrence of B. In our view the unpopularity of the agency approach to causation may be traced to two factors. The first is a failure to appreciate certain distinctive advantages that this approach has over its various rivals. We have drawn attention to some of these advantages elsewhere, and we summarize below. However, the second and more important factor is the influence of a number of stock objections, objections that seem to have persuaded many philosophers that agency accounts face insuperable obstacles. In this paper we want to show that these objections have been vastly overrated. There are four main objections. (shrink)

In his recent paper in the Journal of Economic Methodology, Tobias Henschen puts forth a manipulationist definition of macroeconomic causality that strives for adequacy. As the notion of ‘adequacy’...

The principle of the common cause claims that if an improbable coincidence has occurred, there must exist a common cause. This is generally taken to mean that positive correlations between non-causally related events should disappear when conditioning on the action of some underlying common cause. The extended interpretation of the principle, by contrast, urges that common causes should be called for in order to explain positive deviations between the estimated correlation of two events and the expected value of their correlation. (...) The aim of this paper is to provide the extended reading of the principle with a general probabilistic model, capturing the simultaneous action of a system of multiple common causes. To this end, two distinct models are elaborated, and the necessary and sufficient conditions for their existence are determined. (shrink)

In this paper, using a multilevel approach, we defend the positive role of natural selection in the generation of organismal form. Despite the currently widespread opinion that natural selection only plays a negative role in the evolution of form, we argue, in contrast, that the Darwinian factor is a crucial (but not exclusive) factor in morphological organization. Analyzing some classic arguments, we propose incorporating the notion of ‘downward causation’ into the concept of ‘natural selection.’ In our opinion, this kind of (...) causation is fundamental to the operation of selection as a creative evolutionary process. (shrink)

Philosophical discussions on causal inference in medicine are stuck in dyadic camps, each defending one kind of evidence or method rather than another as best support for causal hypotheses. Whereas Evidence Based Medicine advocates the use of Randomised Controlled Trials and systematic reviews of RCTs as gold standard, philosophers of science emphasise the importance of mechanisms and their distinctive informational contribution to causal inference and assessment. Some have suggested the adoption of a pluralistic approach to causal inference, and an inductive (...) rather than hypothetico-deductive inferential paradigm. However, these proposals deliver no clear guidelines about how such plurality of evidence sources should jointly justify hypotheses of causal associations. We here develop such guidelines by first giving a philosophical analysis of the underpinnings of Hill’s viewpoints on causality. We then put forward an evidence-amalgamation framework adopting a Bayesian net approach to model causal inference in pharmacology for the assessment of harms. Our framework accommodates a number of intuitions already expressed in the literature concerning the EBM vs. pluralist debate on causal inference, evidence hierarchies, causal holism, relevance, and reliability. (shrink)

Backtracking influence is influence that zigzags in time. For example, backtracking influence exists when an event E_1 makes an event E_2 more likely by way of a nomic connection that goes from E_1 back in time to an event C and then forward in time to E_2. I contend that in our local region of spacetime, at least, backtracking influence is redundant in the sense that any existing backtracking influence exerted by E_1 on E_2 is equivalent to E_1's temporally direct (...) influence on E_2. I prove the redundancy of backtracking influence using several plausible physical principles without assuming any fundamental temporal or causal asymmetry. This explanation can play a prominent role in an account of why causation appears to be objectively asymmetric regardless of whether the fundamental laws are symmetric. (shrink)

Changing weather conditions and barometer changes usually coincide. Accordingly, the propositions that my barometer falls and that the weather conditions deteriorate are quite coherent—especially under the assumption that there is a drop in atmospheric pressure. Nevertheless, scenarios like these involving common causes turn out to be highly problematic for a prominent class of probabilistic coherence measures, namely, those explicating coherence based on the idea of relevance-sensitivity. In this article, we show that none of these measures accords with the intuition that (...) in the light of a common cause, two propositions referring to the cause’s effects should turn out to be coherent. This result casts doubts on the view that these measures can be considered proper explications of the concept of coherence. 1Introduction2Relevance-Sensitive Coherence Measures3Common Causes, Screening-off, and Coherence4Discussion 4.1Multiple explications of coherence4.2Conditionalization versus set expansion5Conclusion. (shrink)

This paper presents a symmetry condition for probabilistic measures of confirmation which is weaker than commutativity symmetry, disconfirmation commutativity symmetry but also antisymmetry. It is based on the idea that for any value a probabilistic measure of confirmation can assign there is a corresponding case where degrees of confirmation are symmetric. It is shown that a number of prominent confirmation measures such as Carnap’s difference function, Rescher’s measure of confirmation, Gaifman’s confirmation rate and Mortimer’s inverted difference function do not satisfy (...) this condition and instead exhibit a previously unnoticed and rather puzzling behavior in certain cases of disconfirmation. This behavior also carries over to probabilistic measures of information change, causal strength, explanatory power and coherence. (shrink)

Bayesian networks are computer programs which represent probabilitistic relationships graphically as directed acyclic graphs, and which can use those graphs to reason probabilistically , often at relatively low computational cost. Almost every expert system in the past tried to support probabilistic reasoning, but because of the computational difficulties they took approximating short-cuts, such as those afforded by MYCIN's certainty factors. That all changed with the publication of Judea Pearl's Probabilistic Reasoning in Intelligent Systems, in 1988, which synthesized a decade of (...) research making accurate graphical probabilistic reasoning computationally achievable.Bayesian network technology is now one of the fastest growing fields of research in artificial intelligence. That it has become a publication industry in its own right is shown by a search on Google scholar :This development, together with a parallel related growth in the use of causal discovery algorithms which automate the learning of Bayesian networks from sample data, has generated considerable interest, and controversy, within the philosophy-of-science community.Three central questions bringing together AI researchers and philosophers of science are: Are Bayesian networks Bayesian? What is the relation between probability and causality? Are the assumptions behind causal discovery of Bayesian networks realistic or fantastical?Jon Williamson, as a philosopher of science with a keen interest in the technology, asks and answers these questions in his new book. Although it is self-contained, his book is not very likely as an introduction to the technology , nor is it optimal even as an introduction to the philosophical problems in interpreting Bayesian networks . Rather Williamson's book is an attempt to move the debate forward by solving the central problems of the …. (shrink)

This paper argues against Papineau's claim that causal relations can be reduced to correlations and defends Cartwright's thesis that they can be nevertheless boot-strapped from them, given sufficiently rich causal background knowledge.

Existing research suggests that people's judgments of actual causation can be influenced by the degree to which they regard certain events as normal. We develop an explanation for this phenomenon that draws on standard tools from the literature on graphical causal models and, in particular, on the idea of probabilistic sampling. Using these tools, we propose a new measure of actual causal strength. This measure accurately captures three effects of normality on causal judgment that have been observed in existing studies. (...) More importantly, the measure predicts a new effect ("abnormal deflation"). Two studies show that people's judgments do, in fact, show this new effect. Taken together, the patterns of people's causal judgments thereby provide support for the proposed explanation. (shrink)

This paper shows that causation in the sense of Lewis is a special case of causation in the sense of Spohn.

It is shown that, given any finite set of pairs of random events in a Boolean algebra which are correlated with respect to a fixed probability measure on the algebra, the algebra can be extended in such a way that the extension contains events that can be regarded as common causes of the correlations in the sense of Reichenbach's definition of common cause. It is shown, further, that, given any quantum probability space and any set of commuting events in it (...) which are correlated with respect to a fixed quantum state, the quantum probability space can be extended in such a way that the extension contains common causes of all the selected correlations, where common cause is again taken in the sense of Reichenbach's definition. It is argued that these results very strongly restrict the possible ways of disproving Reichenbach's Common Cause Principle. (shrink)

Philosophers have used the probabilistic relation of ’screening-off‘ to explicate concepts in the theories of causation and explanation. Brandon has used screening-off relations in an attempt to reconstruct an argument of Mayr and Gould that natural selection acts at the level of the organism. I argue that Brandon‘s reconstruction is unsuccessful.

I advance a new theory of causal relevance, according to which causal claims convey information about conditional probability functions. This theory is motivated by the problem of disjunctive factors, which haunts existing probabilistic theories of causation. After some introductory remarks, I present in Section 3 a sketch of Eells's (1991) probabilistic theory of causation, which provides the framework for much of the discussion. Section 4 explains how the problem of disjunctive factors arises within this framework. After rejecting three proposed solutions, (...) I offer in Section 6 a new approach to causation that avoids the problem. Decision-theoretic considerations also support the new approach. Section 8 develops the consequences of the new theory for causal explanation. The resulting theory of causal explanation incorporates the new insights while respecting important work on scientific explanation by Salmon (1971), Railton (1981), and Humphreys (1989). My conclusions are enumerated in Section 9. (shrink)

This paper discusses two challenges for a Boolean method for establishing constitutive regularity statements which, according to the regularity theory of mechanistic constitution, form the core of any mechanistic explanation in neuroscience. After presenting the regularity definition for the constitution relation and a methodology for constitutive inference, the paper discusses the problem of full variation of tested mechanistic factors and the problem of informational redundancy. A solution is offered for each problem. The first requires some adjustments to the original theory (...) by introducing the technical notion of a set of types satisfying independent instantiability. The second one is resolved by demonstrating that the problem of informational redundancy is based on a confusion that fails to challenge the theory. It is concluded that the methodology of constitutive inference is consistent and plausible with respect to actual practice in neuroscience. (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)

This paper outlines a theory and computer implementation of causal meanings and reasoning. The meanings depend on possibilities, and there are four weak causal relations: A causes B, A prevents B, A allows B, and A allows not‐B, and two stronger relations of cause and prevention. Thus, A causes B corresponds to three possibilities: A and B, not‐A and B, and not‐A and not‐B, with the temporal constraint that B does not precede A; and the stronger relation conveys only the (...) first and last of these possibilities. Individuals represent these relations in mental models of what is true in the various possibilities. The theory predicts a number of phenomena, and, contrary to many accounts, it implies that the meaning of causation is not probabilistic, differs from the meaning of enabling conditions, and does not depend on causal powers or mechanisms. The theory also implies that causal deductions do not depend on schemas or rules. (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)

I argue that there are non-trivial objective chances (that is, objective chances other than 0 and 1) even in deterministic worlds. The argument is straightforward. I observe that there are probabilistic special scientific laws even in deterministic worlds. These laws project non-trivial probabilities for the events that they concern. And these probabilities play the chance role and so should be regarded as chances as opposed, for example, to epistemic probabilities or credences. The supposition of non-trivial deterministic chances might seem to (...) land us in contradiction. The fundamental laws of deterministic worlds project trivial probabilities for the very same events that are assigned non-trivial probabilities by the special scientific laws. I argue that any appearance of tension is dissolved by recognition of the level-relativity of chances. There is therefore no obstacle to accepting non-trivial chance-role-playing deterministic probabilities as genuine chances. (shrink)

Several philosophers have embraced the view that high-level events—events like Zimbabwe's monetary policy and its hyper-inflation—are causally related if their corresponding low-level, fundamental physical events are causally related. I dub the view which denies this without denying that high-level events are ever causally related causal emergentism. Several extant philosophical theories of causality entail causal emergentism, while others are inconsistent with the thesis. I illustrate this with David Lewis's two theories of causation, one of which entails causal emergentism, the other of (...) which entails its negation. I then argue for causal emergentism on the grounds that it provides the only adequate means of squaring the apparent plenitude of causal relations between low-level events with the apparent scarcity of causal relations between high-level events. This tension between the apparent abundance of low-level causation and the apparent scarcity of high-level causation has been noted before. However, it has been thought that various theses about the semantics or the pragmatics of causal claims could be used to ameliorate the tension without going in for causal emergentism. I argue that none of the suggested semantic or pragmatic strategies meet with success, and recommend emergentist theories of causality in their stead. As Lewis's 1973 account illustrates, causal emergentism is consistent with the thesis that all facts reduce to microphysical facts. (shrink)