Although statistical techniques like regression analysis and path analysis are widely used in the biomedical, behavioral and social sciences to make causal inferences there has been surprisingly little philosophical discussion of the details of such techniques and of the conceptions of causation and explanation implicit in them. There also has been relatively little attempt to compare such techniques with various probabilistic models of causation and explanation in the philosophical literature.In this paper I explore, for reasons of space in a very (...) sketchy and schematic way, some issues in philosophy of science raised by regression analysis. One general conclusion I reach is that it is considerably less obvious than one might suppose that the philosophical theories alluded to above are plausibly viewed as reconstructions of regression techniques. (shrink)

This paper explores the interpretation and use of polygenic risk scores (PRSs). We argue that PRSs generally do not directly embody causal information. Nonetheless, they can assist us in tracking other causal relationships concerning genetic effects. Although their purely predictive/correlational use is important, it is this tracking feature that contributes to their potential usefulness in other applications, such as genetic dissection, and their use as controls, which allow us, indirectly, to "see" more clearly the role of environmental variables.

This paper is an assessment of an attempt, by James Greeno, to measure the explanatory power of statistical theories by means of the notion of transmitted information (It). It is argued that It has certain features that are inappropriate in a measure of explanatory power. In particular, given a statistical theory T with explanans variables St and explanandum variables Mj, it is argued that no plausible measure of explanatory power should depend on the probability P(Si) of occurrence of initial conditions (...) in the systems to which T applies or the magnitudes of the conditional probabilities P(Mj/Si), in the manner in which Ir does. (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)

This essay advocates a “functional” approach to causation and causal reasoning: these are to be understood in terms of the goals and purposes of causal thinking. This approach is distinguished from accounts based on metaphysical considerations or on reconstruction of “intuitions.”.

Analytic Philosophy, Volume 62, Issue 1, Page 33-56, March 2021.

There is a systematic and suggestive analogy between grounding and causation. In my view, this analogy is no coincidence. Grounding and causation are alike because grounding is a type of causation: metaphysical causation. In this paper I defend the identification of grounding with metaphysical causation, drawing on the causation literature to explore systematic connections between grounding and metaphysical dependence counterfactuals, and I outline a non-reductive counterfactual theory of grounding along interventionist lines.

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)

The failure to recognize a correlation as spurious can lead people to adopt strategies to bring about a specific outcome that manipulate something other than a cause of the outcome. However, in a 2008 paper appearing in the journal Analysis, Bert Leuridan, Erik Weber and Maarten Van Dyck suggest that knowledge of spurious correlations can, at least sometimes, justify adopting a strategy aiming at bringing about some change. This claim is surprising and, if true, throws into question the claim of (...) Nancy Cartwright and others that knowledge of laws of association is insufficient for distinguishing effective and ineffective strategies. This paper examines the nature of spurious correlations and their value in crafting strategies for change. The conclusion of the paper is that while knowledge of a spurious correlation may have practical value, the value depends on either having knowledge of the causal structure underlying the correlation or it depends on the use of ‘causal criteria’. (shrink)

Recent articles published in this journal have highlighted the shortcomings of individualistic approaches to health promotion, and the potential contributions of relational analyses of autonomy to public health ethics. I argue that the latter helps to elucidate the former, by showing that an inadequate analysis of autonomy leads to misassignment of both forward-looking and backward-looking responsibility for health outcomes. Health promotion programmes predicated on such inadequate analyses are then ineffective, because they assign responsibility to agents whose social environment inhibits their (...) ability to act on such responsibilities; inequitable, because the social barriers to autonomous agency display a socio-economic gradient; and stigmatizing, because they license blaming of individuals for their own poor health without taking into account how reasonable it is to hold these individuals responsible, given the social barriers to autonomy they face. I further sketch how incorporating a relational understanding of autonomy could help to produce health promotion programmes that do not succumb to these difficulties, while avoiding coercive paternalism, exploring potential applications in ecological approaches to health promotion. (shrink)

In evolutionary biology changes in population structure are explained by citing trait fitness distribution. I distinguish three interpretations of fitness explanations—the Two‐Factor Model, the Single‐Factor Model, and the Statistical Interpretation—and argue for the last of these. These interpretations differ in their degrees of causal commitment. The first two hold that trait fitness distribution causes population change. Trait fitness explanations, according to these interpretations, are causal explanations. The last maintains that trait fitness distribution correlates with population change but does not cause (...) it. My defense of the Statistical Interpretation relies on a distinctive feature of causation. Causes conform to the Sure Thing Principle. Trait fitness distributions, I argue, do not. *Received July 2009; revised October 2009. †To contact the author, please write to: Department of Philosophy/Institute for the History, Philosophy of Science and Technology, University of Toronto, Victoria College, 91 Charles Street West, Toronto, ON M5S 1K7, Canada; e‐mail: [email protected]. (shrink)

Psychiatry is a discipline that deals with both the physical and the mental lives of individuals and though it is true that, largely because of this characteristic, different models are used for different disorders, there is still a remnant tendency towards reductionist views in the field. In this paper I argue that the available empirical evidence from psychiatry gives us reasons to question biological reductionism and that in its place we should adopt a pluralistic explanatory model that is more suited (...) to the needs of the discipline and to the needs of the patients it is meant to help. This will allow us to retain psychiatry as an autonomous science that can productively co-exist with neuroscience while also giving patients the kind of attention they need. I further argue that this same evidence supports a view of the mind that is anti-reductive and that allows that causation can be both bottom-up and top-down and that such a view is available in emergentism coupled with an interventionist model of causation. (shrink)

Causal eliminativists maintain that all causal talk is false. The prospects for such a view seem to be stymied by an indispensability argument, charging that any agent must distinguish between effective and ineffective strategies, and that such a distinction must commit that agent to causal notions. However, this argument has been under-explored. The contributions of this paper are twofold: first, I provide a thorough explication of the indispensability argument and the various ways it might be defended. Second, I point to (...) an important limitation in the argument and suggest that it does not give us sufficient reason to reject eliminativism. In support of this last claim, I show that the distinction between effective and ineffective strategies could perfectly well be grounded in a counterfactual rather than a causal decision theory and argue that there are fully adequate explanations of how we could come to make the requisite counterfactual judgments that need not invoke causal concepts. (shrink)

In the philosophy of causation, manipulationist literature is broadly divided into agency and interventionist accounts. The division between these accounts is partially due to a dispute regarding the meaning of “manipulation”, which specifically questions, “Must one analyse manipulation by appealing to human agency?” This paper attempts to clarify the notion of manipulation and defends the thesis that agency theorists and interventionists analyse manipulation by appealing to human agency. However, following Collingwood's work, I argue that there are two ways to interpret (...) “human agency”. With an extended notion of agency in place, I reveal a pathway towards a consensus between the agency and interventionist accounts. Further, I highlight the alleged discrepancies between agency and interventionist accounts, including the issues of scope and objectivity, and suggest additional pathways towards a consensus. (shrink)

The investigation of probabilistic causality has been plagued by a variety of misconceptions and misunderstandings. One has been the thought that the aim of the probabilistic account of causality is the reduction of causal claims to probabilistic claims. Nancy Cartwright (1979) has clearly rebutted that idea. Another ill-conceived idea continues to haunt the debate, namely the idea that contextual unanimity can do the work of objective homogeneity. It cannot. We argue that only objective homogeneity in combination with a causal interpretation (...) of Bayesian networks can provide the desired criterion of probabilistic causality. (shrink)

In a recent essay, Deery and Nahmias :1255–1276, 2017) utilize interventionism about causation to develop an account of causal sourcehood in order to defend compatibilism about free will and moral responsibility from manipulation arguments. In this paper, we criticize Deery and Nahmias’s analysis of sourcehood by drawing a distinction between two forms of causal invariance that can come into conflict on their account. We conclude that any attempt to resolve this conflict will either result in counterintuitive attributions of moral responsibility (...) or will undermine their response to manipulation arguments. (shrink)

It is widely thought that there is an important argument to be made that starts with premises taken from the science of physics and ends with the conclusion of physicalism. The standard view is that this argument takes the form of a causal argument for physicalism. Roughly, physics tells us that the physical realm is causally complete, and so minds (among other entities) must be physical if they are to interact with the world as we think they do. In what (...) follows, I raise problems for this view. After an initial review of the causal argument, I begin my case by showing that the totality of physical truths do not deductively entail the causal completeness of the physical realm, using a double-prevention scenario and causation by omission to show that nonphysical causes of physical effects would not need to violate physical conservation laws. I then move on to raise problems for an inductive argument for causal completeness by drawing on the neo-Russellian view that there is no causation in fundamental physics, and so causation must itself be a realized or derived entity. I conclude by suggesting that the underlying problem is that the causal argument has fallen out of touch with the sophisticated understanding that philosophers have developed of the role of causation within physics. (shrink)

Explanatory realism is the position that all explanations give information about whatever metaphysically determines the explanandum. This view is popular and plays a central role in metaphysics, but in this paper I argue that explanatory realism is false. In Sect. 1 I introduce explanatory realism in its weak and strong versions, and discuss the argumentative work that explanatory realism is used for in contemporary metaphysics. In Sect. 2 I present a series of problem cases for explanatory realism, including explanation by (...) analogy, explanations involving rules, reduction ad absurdum explanations and certain statistical explanations. In Sect. 3 I consider and reject two modified versions of explanatory realism: the position that explanatory realism is true only of explanation in metaphysics, and the position that determinative explanation is the most complete form of explanation. In conclusion I consider explanatory antirealism and explanatory pluralism as alternatives to explanatory realism. (shrink)

Kerry et al. criticize our discussion of causal knowledge in evidence-based medicine (EBM) and our assessment of the relevance of their dispositionalist ontology for EBM. Three issues need to be addressed in response: (1) problems concerning transfer of causal knowledge across heterogeneous contexts; (2) how predictions about the effects of individual treatments based on population-level evidence from RCTs are fallible; and (3) the relevance of ontological theories like dispositionalism for EBM.

In her ‘Causality and Determination’, Anscombe argues for the strong thesis that despite centuries of philosophical assumption to the contrary, the supposition that causality and necessity have something essential to do with one another is baseless. In this paper, I assess Anscombe’s arguments and endorse her conclusion. I then attempt to argue that her arguments remain highly relevant today, despite the fact that most popular general views of causation today are firmly probabilistic in orientation and thus show no trace of (...) the assumptions Anscombe hoped to undermine. My suggestion is that Anscombe's interests in causality are distinct from those which mostly animate the modern debate about the general nature of causality and that in those specialized areas of philosophy in which those concerns still dominate, one can still see the effects of the fallacies and confusions to which she alerts us. I conclude by offering two possible complementary explanations of the tendency to suppose that causation is a variety of necessitation. (shrink)

Reasons transmit. If one has a reason to attain an end, then one has a reason to effect means for that end: reasons are transmitted from end to means. I argue that the likelihood ratio (LR) is a compelling measure of reason transmission from ends to means. The LR measure is superior to other measures, can be used to construct a condition specifying precisely when reasons transmit, and satisfies intuitions regarding end-means reason transmission in a broad array of cases.

I defend a radical interpretation of biological populations—what I call population pluralism—which holds that there are many ways that a particular grouping of individuals can be related such that the grouping satisfies the conditions necessary for those individuals to evolve together. More constraining accounts of biological populations face empirical counter-examples and conceptual difficulties. One of the most intuitive and frequently employed conditions, causal connectivity—itself beset with numerous difficulties—is best construed by considering the relevant causal relations as ‘thick’ causal concepts. I (...) argue that the fine-grained causal relations that could constitute membership in a biological population are huge in number and many are manifested by degree, and thus we can construe population membership as being defined by massively multidimensional constructs, the differences between which are largely arbitrary. I end by showing that positions in two recent debates in theoretical biology depend on a view of biological populations at odds with the pluralism defended here. (shrink)

I defend a radical interpretation of biological populations—what I call population pluralism—which holds that there are many ways that a particular grouping of individuals can be related such that the grouping satisfies the conditions necessary for those individuals to evolve together. More constraining accounts of biological populations face empirical counter-examples and conceptual difficulties. One of the most intuitive and frequently employed conditions, causal connectivity—itself beset with numerous difficulties—is best construed by considering the relevant causal relations as ‘thick’ causal concepts. I (...) argue that the fine-grained causal relations that could constitute membership in a biological population are huge in number and many are manifested by degree, and thus we can construe population membership as being defined by massively multidimensional constructs, the differences between which are largely arbitrary. I end by showing that positions in two recent debates in theoretical biology depend on a view of biological populations at odds with the pluralism defended here. 1 Introduction2 Biological Population, Broad and Narrow3 Difficulties with Narrow Biological Population Conditions3.1 Against the genealogical condition3.2 Against the conspecificity condition3.3 Against the proximity condition3.4 Against the typology condition4 Causal Connectivity5 Massively Multidimensional Population Constructs6 Population Uniqueness and Natural Selection6.1 Statisticalism and its discontents6.2 Price at what price?7 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.

Evidence hierarchies are widely used to assess evidence in systematic reviews of medical studies. I give several arguments against the use of evidence hierarchies. The problems with evidence hierarchies are numerous, and include methodological shortcomings, philosophical problems, and formal constraints. I argue that medical science should not employ evidence hierarchies, including even the latest and most-sophisticated of such hierarchies.

I apply James Woodward’s interventionist theory of causation to organic chemistry, modelling three different ways that chemists are able to manipulate the reaction conditions in order to control the outcome of a reaction. These consist in manipulations to the reaction kinetics, thermodynamics, and whether the kinetics or thermodynamics predominates. It is possible to construct interventionist causal models of all of these kinds of manipulation, and therefore to account for them using Woodward’s theory. However, I show that there is an alternate, (...) more illuminating way of thinking about the third kind of reaction control, according to which chemists are thought of as manipulating which causal system is instantiated. I show that our ability to manipulate which system is instantiated is an important part of our ability to control the world, as is therefore especially relevant to interventionism. Thus, considering examples from organic chemistry leads to the identification of an important extension to Woodward’s theory. Finally, this investigation into reaction control in organic chemistry also has a more general implication: it suggests that interventionism results in a version of pragmatism about causation. (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)

This is one of a pair of discussion notes comparing some features of the account of causation in Wolfgang Spohn’s Laws of Belief with the “interventionist” account in James Woodward’s Making Things Happen. This note locates the core difference of the accounts in the fact that Woodward’s account follows an epistemological order, while Spohn’s follows a conceptual order. This unfolds in five further differences: type- versus token-level causation, reference to time, actual/counterfactual intervention versus epistemic/suppositional wiggling, a circular versus a circle-free (...) conception of the circumstances of a direct causal relation, and absolute versus model-relative causation. (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)

In this paper I want to clarify what biologists are talking about when they talk about the evolution of altruism. I'll begin by saying something about the common sense concept. This familiar idea I'll call 'vernacular altruism.' One point of doing this is to make it devastatingly obvious that the common sense concept is very different from the concept as it's used in evolutionary theory. After that preliminary, I'll describe some features of the evolutionary concept. Then I'll conclude by briefly (...) considering what explanatory relation might obtain between vernacular altruism and evolutionary altruism. (shrink)

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

In this paper I want to clarify what biologists are talking about when they talk about the evolution of altruism. I’ll begin by saying something about the common sense concept. This familiar idea I’ll call ‘vernacular altruism.’ One point of doing this is to make it devastatingly obvious that the common sense concept is very different from the concept as it’s used in evolutionary theory. After that preliminary, I’ll describe some features of the evolutionary concept. Then I’ll conclude by briefly (...) considering what explanatory relation might obtain between vernacular altruism and evolutionary altruism. Although the points I’ll make are rather elementary ones, their interest is not restricted to those who have never heard of the evolutionary problem. The reason for this is that there is some amount of confusion about evolutionary altruism among evolutionary biologists themselves. (shrink)

Russell (1948), Reichenbach (1956), and Salmon (1975, 1979) have argued that a fundamental principle of science and common sense is that "matching" events should not be chalked up to coincidence, but should be explained by postulating a common cause. Reichenbach and Salmon provided this intuitive idea with a probabilistic formulation, which Salmon used to argue for a version of scientific realism. Van Fraassen (1980, 1982) showed that the principle, so construed, runs afoul of certain results in quantum mechanics. In this (...) paper a new formulation of the principle is offered that emerges from its use in evolutionary theory. This characterization identifies fairly general conditions in which postulating common causes will be more explanatory than postulating separate causes. (shrink)

We argue against some of Reichenbach's claims about causal forks are incorrect. We do not see why the Second Law of Thermodynamics rules out the existence of conjunctive forks open to the past. In addition, we argue that a common effect rarely forms a conjunctive fork with its joint causes, but it sometimes does. Nevertheless, we think there is something to be said for Reichenbach's idea that forks of various kinds are relevant to explaining why we know more about the (...) past than about the future. And entropy turns out to play a role in the explanation, though not the determining role that Reichenbach envisions. (shrink)

The papers collected here are, with three exceptions, those presented at a conference on probability and causation held at the University of California at Irvine on July 15-19, 1985. The exceptions are that David Freedman and Abner Shimony were not able to contribute the papers that they presented to this volume, and that Clark Glymour who was not able to attend the conference did contribute a paper. We would like to thank the National Science Foundation and the School of Humanities (...) of the University of California at Irvine for generous support. WILLIAM HARPER University of Western Ontario BRIAN SKYRMS University of California at Irvine VII INTRODUCTION TO CAUSATION, CHANCE, AND CREDENCE The search for causes is so central to science that it has sometimes been taken as the defining attribute of the scientific enterprise. Yet even after twenty-five centuries of philosophical analysis the meaning of "cause" is still a matter of controversy, among scientists as well as philosophers. Part of the problem is that the servicable concepts of causation built out of Necessity, Sufficiency, Locality, and Temporal Precedence were constructed for a deterministic world-view which has been obsolete since the advent of quantum theory. A physically credible theory of causation must be, at basis, statistical. And statistical analyses of caus­ ation may be of interest even when an underlying deterministic theory is assumed, as in classical statistical mechanics. (shrink)

Price’s :157–176, 1991; 44:187–203, 1993 ; 2007, 2017) agency theory of causation has takes itself to provide a use-theory of our causal discourse. The theory’s aim is to describe the rules implicit to our linguistic behaviour when we describe things in causal terms. According to this theory, the rules governing our use of the concept of causation are based on our perspective as agents and our associated experiences of manipulating events. I argue that the observed relation between agency and our (...) concept of causation cannot exhaustively describe the conditions under which we enter into causal discourse. In particular, I demonstrate that the agency theory faces familiar problems with accounting for causal ascriptions to token cases. (shrink)

Humean Supervenience is a metaphysical model of the world according to which all truths hold in virtue of nothing but the total spatiotemporal distribution of perfectly natural, intrinsic properties. David Lewis and others have worked out many aspects of HS in great detail. A larger motivational question, however, remains unanswered: As Lewis admits, there is strong evidence from fundamental physics that HS is false. What then is the purpose of defending HS? In this paper, we argue that the philosophical merit (...) of HS is largely independent of whether it correctly represents the world’s fundamental structure. In particular, we show that insofar as HS is an apt model of the world’s higher-level structure, it thereby provides a powerful argument for reductive physicalism and explains otherwise opaque inferential relations. Recent criticism of HS on the grounds that it misrepresents fundamental physical reality is, therefore, beside the point. (shrink)

Costa and Shrapnel have recently proposed an interventionist theory of quantum causation. The formalism generalizes the classical methods of Pearl and allows for the discovery of quantum causal structure via localized interventions. Classical causal structure is presented as a special case of this more general framework. I introduce the account and consider whether this formalism provides a causal explanation for the Bell correlations.

This paper describes the development of theories of scientific explanation since Hempel's earliest models in the 1940ies. It focuses on deductive and probabilistic whyexplanations and their main problems: lawlikeness, explanation-prediction asymmetries, causality, deductive and probabilistic relevance, maximal specifity and homogenity, the height of the probability value. For all of these topic the paper explains the most important approaches as well as their criticism, including the author's own accounts. Three main theses of this paper are: (1) Both deductive and probabilistic explanations (...) are important in science, not reducible to each other. (2) One must distinguish between (cause giving) explanations and (reason giving) justifications and predictions. (3) The adequacy of deductive as well as probabilistic explanations is relative to a pragmatically given background knowledge-which does not exclude, however, the possibility of purely semantic models. (shrink)

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