An actual cause of some token effect is itself a token event that helped to bring about that effect. The notion of an actual cause is different from that of a potential cause – for example a pre-empted backup – which had the capacity to bring about the effect, but which wasn't in fact operative on the occasion in question. Sometimes actual causes are also distinguished from mere background conditions: as when we judge that the struck match was a cause (...) of the fire, while the presence of oxygen was merely part of the relevant background against which the struck match operated. Actual causation is also to be distinguished from type causation: actual causation holds between token events in a particular, concrete scenario; type causation, by contrast, holds between event kinds in scenario kinds. (shrink)

This paper explains what it is to believe something for a reason. My thesis is that you believe something for a reason just in case the reason non-deviantly causes your belief. In the course of arguing for my thesis, I present a new argument that reasons are causes, and offer an informative account of causal non-deviance.

Both biosemiotics and evolutionary epistemology are concerned with how knowledge evolves. (Applied) Evolutionary Epistemology thereby focuses on identifying the units, levels, and mechanisms or processes that underlie the evolutionary development of knowing and knowledge, while biosemiotics places emphasis on the study of how signs underlie the development of meaning. We compare the two schools of thought and analyze how in delineating their research program, biosemiotics runs into several problems that are overcome by evolutionary epistemologists. For one, by emphasizing signs, biosemiotics (...) needs to delineate a semiotic threshold, which is a problem not encountered by evolutionary epistemologists. Instead, the latter recognizes that all organisms are knowers that evolve knowledge, which they recognize to extend toward phenomena produced by organisms such as behavior, cognition, language, culture, science, and technology. Secondly, biosemiotics attempts at continuing adaptationist notions on how organisms relate to their environment, while especially Applied Evolutionary Epistemology comes to redefine the nature of the organism–environment relationship in such a way that it recognizes the spatiotemporal boundedness of existence, which in turn makes adaptationist accounts obsolete. (shrink)

This paper examines three views of what an omission or an instance of refraining is. The view advanced is that in many cases, an omission is simply an absence of an action of some type. However, generally one’s not doing a certain thing counts as an omission only if there is some norm, standard, or ideal that calls for one’s doing that thing.

We propose an account of dynamic predicates which draws on the notion of force, eliminating reference to events in the linguistic semantics. We treat dynamic predicates as predicates of forces, represented as functions from an initial situation to a final situation that occurs ceteris paribus, that is, if nothing external intervenes. The possibility that opposing forces might intervene to prevent the transition to a given final situation leads us to a novel analysis of non-culminating accomplishment predicates in a variety of (...) languages, including the English progressive. We then apply the force-theoretic framework to the composition of basic Vendlerian eventuality types within a lexical-decomposition syntax. The difference between predicates of forces and predicates of situations is argued to underlie the dynamic/stative contrast, and also to allow for a formal treatment of the difference between be and stay. Consequences for the relationship between language and cognition are discussed. (shrink)

According to the Simple Conditional Analysis of disposition ascriptions, disposition ascriptions are to be analyzed in terms of counterfactual conditionals. The Simple Conditional Analysis is notoriously vulnerable to counterexamples. In this paper, I introduce a new sort of counterexample to the Simple Conditional Analysis of disposition ascriptions, which I call ‘tricks’. I then explore a number of possible strategies to modify the Simple Conditional Analysis so as to avoid tricks and conclude that, in order to avoid tricks, the associated counterfactual (...) should be evaluated at the closest possible world at which the manifestation of the disposition does not obtain. (shrink)

I argue, contrary to standard claims, that accomplice liability need not be a causal relation. One can be an accomplice to another’s crime without causally contributing to the criminal act of the principal. This is because the acts of aid and encouragement that constitute the basis for accomplice liability typically occur in contexts of under- and over-determination, where causal analysis is confounded. While causation is relevant to justifying accomplice liability in general, only potential causation is necessary in particular cases. I (...) develop this argument through the example of the role of U.S. legal officials in abetting the acts of unlawful interrogation that have taken place since 2001. I also suggest that there may be a limited justification for ex post ratificatory accomplice liability. (shrink)

Schaffer proposes a new account of probabilistic causation that synthesizes the probability-raising and process-linkage views on causation. The driving idea of Schaffer's account is that, although an effect does not invariably depend on its cause, a process linked to the effect does. In this paper, however, I will advance counterexamples to Schaffer's account and then demonstrate that Schaffer's possible responses to them do not work. Finally, I will argue that my counterexamples suggest that the driving idea of Schaffer's account is (...) misdirected. (shrink)

Experimental philosophers have empirically challenged the connection between intuition and philosophical expertise. This paper reviews these challenges alongside other research findings in cognitive science on expert performance and argues for three claims. First, evidence taken to challenge philosophical expertise may also be explained by the well-researched failures and limitations of genuine expertise. Second, studying the failures and limitations of experts across many fields provides a promising research program upon which to base a new model of philosophical expertise. Third, a model (...) of philosophical expertise based on the limitations of genuine experts may suggest a series of constraints on the reliability of professional philosophical intuition. Even when the experts all agree, they may well be mistaken. — Bertrand Russell, On the Value of Scepticism. (shrink)

The counterfactual and regularity theories are universal accounts of causation. I argue that these should be generalized to produce local accounts of causation. A hallmark of universal accounts of causation is the assumption that apparent variation in causation between locations must be explained by differences in background causal conditions, by features of the causal-nexus or causing-complex. The local account of causation presented here rejects this assumption, allowing for genuine variation in causation to be explained by differences in location. I argue (...) that local accounts of causation are plausible, and have pragmatic, empirical and theoretical advantages over universal accounts. I then report on the use of presheaves as models of local causation. The use of presheaves as models of local variation has precedents in algebraic geometry, category theory and physics; they are here used as models of local causal variation. The paper presents this idea as stemming from an approach using presheaves as models of local truth. Finally, I argue that a proper balance between universal and local causation can be assuaged by moving from presheaves to fully-fledged sheaf models. (shrink)

The counterfactual analysis of causation has focused on one particular counterfactual conditional, taking as its starting-point the suggestion that C causes E iff (C E). In this paper, some consequences are explored of reversing this counterfactual, and developing an account starting with the idea that C causes E iff (E C). This suggestion is discussed in relation to the problem of pre-emption. It is found that the 'reversed' counterfactual analysis can handle even the most difficult cases of pre-emption with only (...) minimal complications. The paper closes with a discussion of the wider philosophical implications of developing a reversed counterfactual analysis, especially concerning the differentiation of causes from causal conditions, causation by absences, and the extent to which causes suffice for their effects. (shrink)

When is a cause of a cause of an effect also a cause of that effect? The right answer is either Sometimes or Always . In favour of Always , transitivity is considered by some to be necessary for distinguishing causes from redundant non-causal events. Moreover transitivity may be motivated by an interest in an unselective notion of causation, untroubled by principles of invidious discrimination. And causal relations appear to add up like transitive relations, so that the obtaining of the (...) overarching relation is not independent of the obtaining of the intermediaries. On the other hand, in favour of Sometimes , often we seem not to treat events that are very spatiotemporally remote from an effect as its causes, even when connected to the effect in question by a chain of counterfactual or chance-raising dependence. Moreover cases of double prevention provide counterexamples to causal transitivity even over short chains. According to the argument of this paper, causation is non-transitive. Transitizing causation provides no viable account of causal redundancy. An unselective approach to causation may motivate resisting the distance counterexamples to transitivity, but it does not help with double prevention, and even makes it more intractable. The strongest point in favour of transitivity is the adding up of causal relations, and this is the point that extant non-transitizing analyses have not adequately addressed. I propose a necessary condition on causation that explains the adding up phenomenon. In doing so it also provides a unifying explanation of distance and double prevention counterexamples to transitivity. (shrink)

There are two no-change objections that can be raised against the B-theory of time. One stems from the observation that in a B-theoretic scenario changes of determinations can only be represented by propositions which have eternal truth values. The other derives from the principle that nothing can vary over a period of time if it doesn’t instantiate a state of change at all the instants of time which compose it. Here I argue that both objections apply to all comparative conceptions (...) of change, regardless of whether they take tense seriously or not. It follows that, contrary to what is widely believed, A-theoretic accounts of time are not immune to no-change objections, just in virtue of being realist about tense. A-theorists must either accept the conclusion that time, according to their account, does not flow, or put forward an account of flow that is not comparative. A number of difficulties with both of these options are discussed. (shrink)

The existence of non-local correlations between outcomes of measurements in quantum entangled systems strongly suggests that we are dealing with some form of causation here. An assessment of this conjecture in the context of the collapse interpretation of quantum mechanics is the primary goal of this paper. Following the counterfactual approach to causation, I argue that the details of the underlying causal mechanism which could explain the non-local correlations in entangled states strongly depend on the adopted semantics for counterfactuals. Several (...) relativistically-invariant interpretations of spatiotemporal counterfactual conditionals are discussed, and the corresponding causal stories describing interactions between parts of an entangled system are evaluated. It is observed that the most controversial feature of the postulated causal connections is not so much their non-local character as a peculiar type of circularity that affects them. (shrink)

David Lewis’s latest theory of causation defines the causal link in terms of the relation of influence between events. It turns out, however, that one event’s influencing another is neither a necessary nor sufficient condition for its being a cause of that event. In the article one particular case of causality without influence is presented and developed. This case not only serves as a counterexample to Lewis’s influence theory, but also threatens earlier counterfactual analyses of causation by admitting a particularly (...) troublesome type of preemption. The conclusion of the article is that Lewis’s influence method of solving the preemption problem fails, and that we need a new and fresh approach to the cases of redundant causation if we want to hold on to the counterfactual analysis of causation. (shrink)

Omissions – any events, actions, or things that do not occur – are central to numerous debates in causation and ethics. This article surveys views on what omissions are, whether they are causally efficacious, and how they ground moral responsibility.

Philosophical works on actual causation make wide use of thought experiments. The principal aim of this paper is to show how thought experiments are used in the contemporary debate over actual causation and to discuss their role in relation to formal approaches in terms of causal models. I claim that a recourse to thought experiments is not something old fashioned or superseded by abstract models, but it is useful to interpret abstract models themselves and to use our intuitions to judge (...) the results of the model. Recent research on actual causation has stressed the importance of integrating formal models with some notion of normality; I suggest that thought experiments can be useful in eliciting intuitions where normality is not intended in a statistical sense. The first expository part gives a short presentation of the notion of actual causation, summarising some typical problems of counterfactual approaches and how they are treated in causal and structural models. The second part focuses on the problems of model isomorphism and criticises some radical ideas opposing the role of thought experiments, claiming that they may also be of use in evaluating formal models. (shrink)

Philosophical works on actual causation make wide use of thought experiments. The principal aim of this paper is to show how thought experiments are used in the contemporary debate over actual causation and to discuss their role in relation to formal approaches in terms of causal models. I claim that a recourse to thought experiments is not something old fashioned or superseded by abstract models, but it is useful to interpret abstract models themselves and to use our intuitions to judge (...) the results of the model. Recent research on actual causation has stressed the importance of integrating formal models with some notion of normality; I suggest that thought experiments can be useful in eliciting intuitions where normality is not intended in a statistical sense. The first expository part gives a short presentation of the notion of actual causation, summarising some typical problems of counterfactual approaches and how they are treated in causal and structural models. The second part focuses on the problems of model isomorphism and criticises some radical ideas opposing the role of thought experiments, claiming that they may also be of use in evaluating formal models. (shrink)

For a long time, regularity accounts of causation have virtually vanished from the scene. Problems encountered within other theoretical frameworks have recently induced authors working on causation, laws of nature, or methodologies of causal reasoning – as e.g. May (Kausales Schliessen. Eine Untersuchung über kausale Erklärungen und Theorienbildung. Ph.D. thesis, Universität Hamburg, Hamburg, 1999), Ragin (Fuzzy-set social science. Chicago: University of Chicago Press, 2000), Graßhoff and May (Causal regularities. In W. Spohn, M. Ledwig, & M. Esfeld (Eds.), Current issues in (...) causation (pp. 85–114). Paderborn: Mentis, 2001), Swartz (The concept of physical law (2nd ed.). http://www.sfu.ca/philosophy/physical-law/, 2003), Halpin (Erkenntnis, 58, 137–168, 2003) – to direct their attention back to regularity theoretic analyses. In light of the latest proposals of regularity theories, the paper at hand therefore reassesses the criticism raised against regularity accounts since the INUS theory of causation of Mackie (The cement of the universe. A study of causation. Oxford: Clarendon Press, 1974). It is shown that most of these objections target strikingly over-simplified regularity theoretic sketches. By outlining ways to refute these objections it is argued that the prevalent conviction as to the overall failure of regularity theories has been hasty. (shrink)

The majority of the currently flourishing theories of actual causation are located in a broadly counterfactual framework that draws on structural equations. In order to account for cases of symmetric overdeterminiation and preemption, these theories resort to rather intricate analytical tools, most of all, to what Hitchcock has labeled explicitly nonforetracking counterfactuals. This paper introduces a regularity theoretic approach to actual causation that only employs material conditionals, standard Boolean minimization procedures, and a stability condition that regulates the behavior of causal (...) models under model expansions. Notwithstanding its lightweight analytical toolbox, this regularity theory performs at least as well as the structural equations accounts with their heavy appliances. (shrink)

According to orthodoxy, the most fundamental kind of causation involves one event causing another event. I argue against this event‐causal view. Instead, the most fundamental kind of causation is thing causation, which involves a thing causing a thing to do something. Event causation is reducible to thing causation, but thing causation is not reducible to event causation, because event causation cannot accommodate cases of fine‐grained causation. I defend my view from objections, including C. D. Broad's influential “timing” argument, and I (...) conclude with implications for agent‐causal theories of free will. (shrink)

Instances of negative causation—preventions, omissions, and the like—have long created philosophical worries. In this paper, I argue that concerns about negative causation can be addressed in the context of causal explanation generally, and mechanistic explanation specifically. The gravest concern about negative causation is that it exacerbates the problem of causal promiscuity—that is, the problem that arises when a particular account of causation identifies too many causes for a particular effect. In the explanatory context, the problem of promiscuity can be solved (...) by characterizing the phenomenon to be explained as a contrast between two or more events or non-events. This contrastive strategy also can solve other problems that negative causation presents for the leading accounts of mechanistic explanation. Along the way, I argue that to be effective, accounts of causal explanation must incorporate negative causation. I also develop a taxonomy of negative causation and incorporate each variety of negative causation into the leading accounts of mechanistic explanation. (shrink)

An important strategy in the discovery of biological mechanisms involves the piecing together of experimental results from interventions. However, if mechanisms are investigated by means of ideal interventions, as defined by James Woodward and others, then the kind of information revealed is insufficient to discriminate between modular and non-modular causal contributions. Ideal interventions suffice for constructing webs of causal dependencies that can be used to make some predictions about experimental outcomes, but tell us little about how causally relevant factors are (...) organized together and how they interact with each other in order to produce a phenomenon. I argue that lab research relies on more elaborated types of interventions targeting in a controlled fashion multiple variables at the same time in order to probe the temporal organization of causally-relevant factors along distinct causal pathways and to test for non-modular interaction effects, thus providing crucial spatial-temporal constraints guiding the formulation of more detailed mechanistic explanations. (shrink)

Examples from the sciences showing that mechanisms do not always succeed in producing the phenomena for which they are responsible have led some authors to conclude that the regularity requirement can be eliminated from characterizations of mechanisms. In this article, I challenge this conclusion and argue that a minimal form of regularity is inextricably embedded in examples of elucidated mechanisms that have been shown to be causally responsible for phenomena. Examples of mechanistic explanations from the sciences involve mechanisms that have (...) been shown to produce phenomena with a reproducible rate of success. By contrast, if phenomena are infrequent to the point that they amount to irreproducible observations and experimental results, they are indistinguishable from the background noise of accidental happenings. The inability to detect or measure the phenomenon of interest against the background noise of accidental correlations makes it impossible to elucidate a mechanism by experimental means, to demonstrate that a proposed mechanism actually produces the phenomenon, and ultimately to justify why a hypothetical scenario involving an irregular mechanism should be preferred over attributing irreproducible happenings to chance. (shrink)

In his latest book Physicalism, or Something near Enough, Jaegwon Kim argues that his version of functional reductionism is the most promising way for saving mental causation. I argue, on the other hand, that there is an internal tension in his position: Functional reductionism does not save mental causation if Kim’s own supervenience argument is sound. My line of reasoning has the following steps: (1) I discuss the supervenience argument and I explain how it motivates Kim’s functional reductionism; (2) I (...) present what I call immense multiple realization, which says that macro-properties are immensely multiply realized in determinate micro-based properties; (3) on that background I argue that functional reductionism leads to a specified kind of irrealism for mental properties. Assuming that such irrealism is part of Kim’s view, which Kim himself seems to acknowledge, I argue that Kim’s position gets the counterfactual dependencies between macro-causal relata wrong. Consequently, his position does not give a conservative account of mental causation. I end the paper by discussing some alternative moves that Kim seems to find viable in his latest book. I argue on the assumption that the supervenience argument is sound, so the discussion provides further reasons to critically reevaluate that argument because it generalizes in deeply problematic ways. (shrink)

RESUMEN Trabajos recientes han propuesto un tratamiento de la fundación “a la imagen de la causalidad”. Hay importantes analogías entre la fundación y la causalidad: ambas parecen ser relaciones de ‘construcción’, ambas parecen ser órdenes estrictos y ambas parecen ser representables por modelos de ecuaciones estructurales. Pero también parece que hay importantes diferencias, porque la causalidad es usualmente considerada como una relación externa, mientras que la fundación es interna; hay casos de causalidad probabilística, pero no hay nada como una fundación (...) probabilística; la fundación se considera una relación ‘bien fundada’, pero no la causalidad; la fundación implica superveniencia ontológica, pero no la causalidad. Se argumenta aquí que la mayoría de estas supuestas diferencias están motivadas por una concepción humeana de la causalidad en la que no hay conexiones necesarias entre causa y efecto. Una perspectiva no humeana de la causalidad, sin embargo, hace que la unificación de la fundación y la causalidad sea mucho más razonable que cualquier tratamiento separado. ABSTRACT Recent works have proposed a treatment of grounding “in the image of causation”. There are important analogies between grounding and causation: both seem to be ‘building’ relations, both seem to be strict orders, and both seem amenable to representation by models of structural equations. But it seems also that there are important differences, because causation is usually considered as an external relation, while grounding is internal; there are cases of probabilistic causation, but there is nothing like probabilistic grounding; grounding is taken to be a well-founded relation, but not causation; grounding entails ontological supervenience, but not causation. It is argued here that most of those supposed differences are motivated by a Humean conception of causation in which there are no necessary connections between cause and effect. A non-Humean view of causation, though, makes the unification of grounding and causation much more reasonable that any separate treatment. (shrink)

The paper defends Humean approaches to autonomous mental causation against recent attacks in the literature. One important criticism launched at Humean approaches says that the truth-makers of the counterfactuals in question include laws of nature, and there are laws that support physical-to-physical counterfactuals, but no laws in the same sense that support mental-to-physical counterfactuals. This paper argues that special science causal laws and physical causal laws cannot be distinguished in terms of degrees of strictness. It follows that mental-to-physical counterfactuals are (...) supported—or not supported—by laws in just the same way as are physical-to-physical counterfactuals. (shrink)

This paper investigates the conception of causation required in order to make sense of natural selection as a causal explanation of changes in traits or allele frequencies. It claims that under a counterfactual account of causation, natural selection is constituted by the causal relevance of traits and alleles to the variation in traits and alleles frequencies. The “statisticalist” view of selection (Walsh, Matthen, Ariew, Lewens) has shown that natural selection is not a cause superadded to the causal interactions between individual (...) organisms. It also claimed that the only causation at work is those aggregated individual interactions, natural selection being only predictive and explanatory, but it is implicitly committed to a process-view of causation. I formulate a counterfactual construal of the causal statements underlying selectionist explanations, and show that they hold because of the reference they make to ecological reliable factors. Considering case studies, I argue that this counterfactual view of causal relevance proper to natural selection captures more salient features of evolutionary explanations than the statisticalist view, and especially makes sense of the difference between selection and drift. I eventually establish equivalence between causal relevance of traits and natural selection itself as a cause. (shrink)

This paper presents a line of thought against the possibility of causation without time. That possibility, insofar as it is supposedly rested upon a Lewisian counterfactual theory of causation, does not stand up to scrutiny. The key point is that, as a reflection on the trans-world identity of events reveals, (distinct) events deprived of times are—according to Lewis’s own semantics of counterfactuals—no longer eligible to stand in counterfactual dependence.

Defenders of pragmatic encroachment in epistemology (or what I call practicalism) need to address two main problems. First, the view seems to imply, absurdly, that knowledge can come and go quite easily—in particular, that it might come and go along with our variable practical interests. We can call this the stability problem. Second, there seems to be no fully satisfying way of explaining whose practical interests matter. We can call this the “whose stakes?” problem. I argue that both problems can (...) be addressed in roughly the same terms. More exactly, I argue that by first clarifying the whose stakes? problem an answer to the stability problem naturally falls out. (shrink)

When one takes an intersectional perspective on patterns of oppression and domination, it becomes clear that familiar forms of systemic injustice, such as misogyny and anti-Black racism, are inseparable. Some feminist theorists conclude, from this, that the systems behind these injustices cannot be individuated—for example, that there isn’t patriarchy and white supremacy, but instead only white supremacist patriarchy. This chapter offers a different perspective. Philosophers have long observed that a statue and a lump of clay can be individuated although inseparable, (...) and that statues and lumps of clay do different explanatory and predictive work for the same causal outcomes. This chapter suggests that the same is true of systems such as patriarchy and white supremacy. These systems, like the injustices they produce, are inseparable. But they can be individuated, and when they are individuated, they do different explanatory and predictive work. (shrink)

Accounts of ontic explanation have often been devised so as to provide an understanding of mechanism and of causation. Ontic accounts differ quite radically in their ontologies, and one of the latest additions to this tradition proposed by Peter Machamer, Lindley Darden and Carl Craver reintroduces the concept of activity. In this paper I ask whether this influential and activity-based account of mechanisms is viable as an ontic account. I focus on polygenic scenarios—scenarios in which the causal truths depend on (...) more than one cause. The importance of polygenic causation was noticed early on by Mill (1893). It has since been shown to be a problem for both causal-law approaches to causation (Cartwright 1983) and accounts of causation cast in terms of capacities (Dupré 1993; Glennan 1997, pp. 605-626). However, whereas mechanistic accounts seem to be attractive precisely because they promise to handle complicated causal scenarios, polygenic causation needs to be examined more thoroughly in the emerging literature on activity-based mechanisms. The activity-based account proposed in Machamer et al. (2000, pp. 1-25) is problematic as an ontic account, I will argue. It seems necessary to ask, of any ontic account, how well it performs in causal situations where—at the explanandum level of mechanism—no activity occurs. In addition, it should be asked how well the activity-based account performs in situations where there are too few activities around to match the polygenic causal origin of the explanandum. The first situation presents an explanandum-problem and the second situation presents an explanans-problem—I will argue—both of which threaten activity-based frameworks. (shrink)

Does A cause B simply if A prevents what would have prevented B? Such a case is known as double prevention: where we have the prevention of a prevention. One theory of causation is that A causes B when B counterfactually depends on A and, as there is such a dependence, proponents of the view must rule that double prevention is causation.<br><br>However, if double prevention is causation, it means that causation can be an extrinsic matter, that the cause and effect (...) need not be connected by a continuous chain of events, that there can be causation by absence, and that there can be causation at a distance. All of these implications jar with strong intuitions we have about the nature of causation. There is, on the other hand, a theory of causation based on an ontology of real dispositions, where causation involves the passing around of powers. This theory in contrast entails that double prevention is not causation and, on this issue, it can claim a victory over the counterfactual dependence account. (shrink)

Part I of this paper introduced a range of mechanistic theories of causality, including process theories and the complex-systems theories, and some of the problems they face. Part II argues that while there is a decisive case against a purely mechanistic analysis, a viable theory of causality must incorporate mechanisms as an ingredient, and describes one way of providing an analysis of causality which reaps the rewards of the mechanistic approach without succumbing to its pitfalls.

Part I of this paper introduces a range of mechanistic theories of causality, including process theories and the complex-systems theories, and some of the problems they face. Part II argues that while there is a decisive case against a purely mechanistic analysis, a viable theory of causality must incorporate mechanisms as an ingredient, and describes one way of providing an analysis of causality which reaps the rewards of the mechanistic approach without succumbing to its pitfalls.

This paper addresses questions about how the levels of causality (generic and single-case causality) are related. One question is epistemological: can relationships at one level be evidence for relationships at the other level? We present three kinds of answer to this question, categorised according to whether inference is top-down, bottom-up, or the levels are independent. A second question is metaphysical: can relationships at one level be reduced to relationships at the other level? We present three kinds of answer to this (...) second question, categorised according to whether single-case relations are reduced to generic, generic relations are reduced to single-case, or the levels are independent. We then explore causal inference in autopsy. This is an interesting case study, we argue, because it refutes all three epistemologies and all three metaphysics. We close by sketching an account of causality that survives autopsy—the epistemic theory. (shrink)

It is tempting to analyse causality in terms of just one of the indicators of causal relationships, e.g., mechanisms, probabilistic dependencies or independencies, counterfactual conditionals or agency considerations. While such an analysis will surely shed light on some aspect of our concept of cause, it will fail to capture the whole, rather multifarious, notion. So one might instead plump for pluralism: a different analysis for a different occasion. But we do not seem to have lots of different concepts of cause (...) – just one eclectic notion. The resolution of this conundrum, I think, requires us to accept that our causal beliefs are generated by a wide variety of indicators, but to deny that this variety of indicators yields a variety of concepts of cause. This focus on the relation between evidence and causal beliefs leads to what I call epistemic causality. Under this view, certain causal beliefs are appropriate or rational on the basis of observed evidence; our notion of cause can be understood purely in terms of these rational beliefs. Causality, then, is a feature of our epistemic representation of the world, rather than of the world itself. This yields one, multifaceted notion of cause. (shrink)

This paper examines the relationship between causality and intrinsicality. Construed in one way, that relationship can be defended against some proposed counterexamples. However, I argue that trumping cases pose a more serious, if not fatal, problem. I then examine an alternative way of thinking about the relationship, but suggest that this too meets the same fate.

If counterfactual dependence is sufficient for causation and if omissions can be causes, then all events have many more causes than common sense tends to recognize. This problem is standardly addressed by appeal to pragmatics. However, Carolina Sartorio [2010] has recently raised what I shall argue is a more interesting problem concerning omissions for counterfactual theories of causation—more interesting because it demands a more subtle pragmatic solution. I discuss the relationship between the idea that causes are proportional to their effects, (...) the idea that causation is contrastive, and the question of the dimensions along which causal explanations should be evaluated with respect to one another. (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)

Humeanism is “the thesis that the whole truth about a world like ours supervenes on the spatiotemporal distribution of local qualities.” (Lewis, 1994, 473) Since the whole truth about our world contains truths about causation, causation must be located in the mosaic of local qualities that the Humean says constitute the whole truth about the world. The most natural ways to do this involve causation being in some sense extrinsic. To take the simplest possible Humean analysis, we might say that (...) c causes e iff throughout the mosaic events of the same type as c are usually followed by events of type e. For short, the causal relation is the constant conjunction relation. Whether this obtains is determined by the mosaic, so this is a Humean theory, but it isn’t determined just by c and e themselves, so whether c causes e is extrinsic to the pair. Now this is obviously a bad theory of causation, but the fact that causation is extrinsic is retained even by good Humean theories of causation. John Hawthorne (2004) objects to this feature of Humeanism. I’m going to argue that his arguments don’t work, but first we need to clear up three preliminaries about causation and intrinsicness. (shrink)

The most compelling extant accounts of explanation casts all explanations as causal. Yet there are sciences, theoretical population biology in particular, that explain their phenomena by appeal to statistical, non-causal properties of ensembles. I develop a generalised account of explanation. An explanation serves two functions: metaphysical and cognitive. The metaphysical function is discharged by identifying a counterfactually robust invariance relation between explanans event and explanandum. The cognitive function is discharged by providing an appropriate description of this relation. I offer examples (...) of explanations from portfolio theory and population genetics that meet this characterisation. In each case the invariance relation holds between a statistical property of an ensemble and a change in structure of the ensemble. In neither case, however, does the statistical property cause the outcome it explains. There are genuine statistical, non-causal scientific explanations. (shrink)

Causal selection and priority are at the heart of discussions of the causal parity thesis, which says that all causes of a given effect are on a par, and that any justified priority assigned to a given cause results from causal explanatory interests. In theories of causation that provide necessary and sufficient conditions for the truth of causal claims, status as cause is an either/or issue: either a given cause satisfies the conditions or it does not. Consequently, assessments of causal (...) parity and priority require more resources, which can either be additional or part of the causal analysis itself. While adding resources in terms of a theory of causal explanation has been standard, here we develop a unified conceptual analysis that includes a range of different precise causal concepts that allows for assessments of causal priority in terms of different kinds of causal relevance. (shrink)

Hall has recently argued that there are two concepts of causality, picking out two different kinds of causal relation. McGrath, and Hitchcock and Knobe, have recently argued that the facts about causality depend on what counts as a “default” or “normal” state, or even on the moral facts. In the light of these claims you might be tempted to agree with Skyrms that causal relations constitute, metaphysically speaking, an “amiable jumble”, or with Cartwright that ‘causation’, though a single word, encompasses (...) many different kinds of things. This paper argues, drawing on the author’s recent work on explanation, that the evidence adduced in support of causal pluralism can be accommodated easily by a unified theory of causality—a theory according to which all singular causal claims concern the same fundamental causal network. (shrink)

Conditionals somehow express conditional beliefs. However, conditional belief is a bi-propositional attitude that is generally not truth-evaluable, in contrast to unconditional belief. Therefore, this article opts for an expressivistic semantics for conditionals, grounds this semantics in the arguably most adequate account of conditional belief, that is, ranking theory, and dismisses probability theory for that purpose, because probabilities cannot represent belief. Various expressive options are then explained in terms of ranking theory, with the intention to set out a general interpretive scheme (...) that is able to account for the most variegated usage of conditionals. The Ramsey test is only the first option. Relevance is another, familiar, but little understood item, which comes in several versions. This article adds a further family of expressive options, which is able to subsume also counterfactuals and causal conditionals, and indicates at the end how this family allows for partial recovery of truth conditions for conditionals. (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)