The traditional model and the contextual unanimity model are two probabilistic accounts of general causation subject to many well-known problems; e.g. cases of epiphenomena, causes raising their own probability, effects raising the probability of the cause, et cetera. After reviewing these problems and raising a new problem for the two models, I suggest the beginnings of an alternative probabilistic account. My suggestion avoids the problems encountered by earlier models, in large part, by an appeal to singular causation.

Philosophers of science, e.g. Cartwright (1979) and Skyrms (1980), have given accounts of general causation in probabilistic terms; not surprising since we often accept general causal sentences as true despite being aware of apparent counterinstances. Consider:(E1) Smoking is a cause of heart attacks.We accept (E1) as true though aware of smokers who never have a heart attack. Here I quickly review familiar problems in two existing probabilistic accounts, offer a new objection, and suggest the beginnings of an (...) alternative account.The traditional model of general causation maintains that causes, and only causes, raise the probability of the effect That is:(TM) F is a cause of G if and only if.Despite some intuitive appeal, the traditional model faces at least three basic objections. First, consider cases of epiphenomena in which there are properties F, G, and H such that F is a cause of G, F is a cause of H, but G is not a cause of H and H is not a cause of G. (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)

Hitchcock (2001a) argues that the distinction between singular and general causation conflates the two distinctions ‘actual causation vs. causal tendencies’ and ‘wide vs. narrow causation’. Based on a recent regularity account of causation I will show that Hitchcock’s introduction of the two distinctions is an unnecessary multiplication of causal concepts.

Consensus in the contemporary philosophical literature has it that conserved quantity theories of causation such as that of Dowe [2000]—according to which causation is to be analysed in terms of the exchange of conserved quantities (e.g., energy)—face damning problems when confronted with contemporary physics, where the notion of conservation becomes delicate. In particular, in general relativity it is often claimed that there simply are no conservation laws for (say) total-stress energy. If this claim is correct, it is (...) difficult to see how conserved quantity theories of causation could survive. In this article, we resist the above consensus and defend conserved quantity theories from this conclusion, at least when focusing on the apparent problems posed by general relativity. We argue that this approach to causation can continue to be defended in general relativity, once one appreciates (a) the availability of approximate symmetries in generic general relativistic spacetimes, and (b) the role of modelling and idealisation in that theory. Given these points, conserved quantity theories of causation must stand or fall on other grounds. (shrink)

The conservation of energy and momentum have been viewed as undermining Cartesian mental causation since the 1690s. Modern discussions of the topic tend to use mid-nineteenth century physics, neglecting both locality and Noether’s theorem and its converse. The relevance of General Relativity has rarely been considered. But a few authors have proposed that the non-localizability of gravitational energy and consequent lack of physically meaningful local conservation laws answers the conservation objection to mental causation: conservation already fails in (...) GR, so there is nothing for minds to violate. This paper is motivated by two ideas. First, one might take seriously the fact that GR formally has an infinity of rigid symmetries of the action and hence, by Noether’s first theorem, an infinity of conserved energies-momenta. Second, Sean Carroll has asked how one should modify the Dirac–Maxwell–Einstein equations to describe mental causation. This paper uses the generalized Bianchi identities to show that General Relativity tends to exclude, not facilitate, such Cartesian mental causation. In the simplest case, Cartesian mental influence must be spatio-temporally constant, and hence 0. The difficulty may diminish for more complicated models. Its persuasiveness is also affected by larger world-view considerations. The new general relativistic objection provides some support for realism about gravitational energy-momentum in GR. Such realism also might help to answer an objection to theories of causation involving conserved quantities, because energies-momenta would be conserved even in GR. (shrink)

This paper aims to discuss two realist conceptions about causation in the light of the general theory of relativity. I first consider the conserved quantity of causation, which explicitly relies on the energy conservation principle. Such principle is however problematic within GTR, mainly because of the dynamical nature of the spacetime structure itself. I then turn to the causal theory of properties, according to which properties are such that insofar as they are certain qualities, they are powers (...) to produce certain effects. In order to be compatible with GTR, such theory has to assume non-trivial global conditions on the spacetime structure; such assumptions seem to deprive the „singularist‟ non-Humean feature of this theory of causation. The question of the possible causal nature of spacetime properties is addressed in the conclusion. (shrink)

The reduction of grounding to causation, or each to a more general relation of which they are species, has sometimes been justified by the impressive inferential capacity of structural equation modelling, causal Bayes nets, and interventionist causal modelling. Many criticisms of this assimilation focus on how causation is inadequate for grounding. Here, I examine the other direction: how treating grounding in the image of causation makes the resulting view worse for causation. The distinctive features of (...) causal modelling that make this connection appealing are distorted beyond use by forcing them to fit onto grounding. The very inferential strength that makes causation attractive is only possible because of a narrow construal of what counts as a causal relation; as soon as that broadens, the inferential capacity markedly diminishes. Making causation suitable for application to grounding spoils what was appealing about causation for this task in the first place. However, grounding need not appeal to causation: causal modelling does not have exclusive claim to structural equation modeling or other formal techniques of modelling structure. I offer a case in favour of a different kind of metaphysical frugality, which tend towards narrow, more restrictive construals of relations like causation or grounding, because then each relation behaves more homogenously. This more homogenous behavior delivers stronger inferential power per relation even though there may be more relations to which one is committed. (shrink)

The dominant assumption about the causal architecture of the mind is, that it is composed of a stable set of components that contribute independently to relevant observables that are employed to measure cognitive activity. This view has been called component-dominant dynamics. An alternative has been proposed, according to which the different components are not independent, but fundamentally interdependent, and are not stable basic properties of the mind, but rather an emergent feature of the mind given a particular task context. This (...) view has been called interaction-dominant dynamics. In this paper, we review evidence for interaction-dominant dynamics as the causal architecture of the mind. We point out, that such an architecture is consistent with problems of convergence in research on the level of results and theorizing. Moreover, we point out that if interaction-dominant dynamics as the causal architecture of the mind were to be true, this would naturally lead to problems with generalization and replicability in sciences of the mind and brain, and would probably warrant changes in the scientific practice with regard to study-design and data analysis. (shrink)

In this paper, I argue that causal theories of memory are typically committed to two independent, non-mutually entailing theses. The first thesis pertains to the necessity of appropriate causation in memory, specifying a condition token memories need to satisfy. The second pertains to the explanation of memory reliability in causal terms and it concerns memory as a type of mental state. Post-causal theories of memory can reject only the first (weak post-causalism) or both (strong post-causalism) theses. Upon this backdrop, (...) I examine Werning’s (2020) causalist argument from probabilistic correlation. I argue that it doesn’t establish the necessity of appropriate causation and thus it can only target strong post-causalist theories. I end up by presenting some general considerations, suggesting that memories may not always be causally linked to past experiences. (shrink)

Jaegwon Kim; XIV*—Does the Problem of Mental Causation Generalize?, Proceedings of the Aristotelian Society, Volume 97, Issue 1, 1 June 1997, Pages 281–298, htt.

In many people, caffeine causes slight muscle tremors, particularly in their hands. In general, the Caffeine → Muscle Tremors causal connection is a noisy one: someone can drink coffee and experience no hand shaking, and there are many other factors that can lead to muscle tremors. Now suppose that Jane drinks several cups of coffee and then notices that her hands are trembling; an obvious question is: did this instance of coffee drinking cause this instance of hand-trembling? Structurally similar (...) questions arise throughout everyday life: Did this pressing of the ‘k’ key cause this change in the pixels on the computer monitor? Did these episodes of smoking cause this lung cancer? Did this studying cause this test score? And so on. These questions all ask about singular causation in a particular situation, in contrast with general causation across multiple cases. They are thus particularly salient in situations in which we care about that specific case, as in many legal contexts, social interactions, physical explanations of anomalous events, and more. (shrink)

Jaegwon Kim; XIV*—Does the Problem of Mental Causation Generalize?, Proceedings of the Aristotelian Society, Volume 97, Issue 1, 1 June 1997, Pages 281–298, htt.

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)

This paper offers a new way to evaluate counterfactual conditionals on the supposition that actually, there is no time. We then parlay this method of evaluation into a way of evaluating causal claims. Our primary aim is to preserve, at a minimum, the assertibility of certain counterfactual and causal claims once time has been excised from reality. This is an important first step in a more general reconstruction project that has two important components. First, recovering our ordinary language claims (...) involving notions such as persistence, change and agency and, second, recovering enough observational evidence so that any timeless metaphysics is not empirically self-refuting. However, the project of investigating causation in a timeless setting has a greater relevance than its application to timeless physical theory alone. For, as we show, it can be used to model the assertibility conditions of causal claims more generally. (shrink)

Causation is widely assumed to be a binary relation: c causes e. I will argue that causation is a quaternary, contrastive relation: c rather than C* causes e rather than E*, where C* and E* are nonempty sets of contrast events. Or at least, I will argue that treating causation as contrastive helps resolve some paradoxes.

Causation is important. It is, as Hume said, the cement of the universe, and lies at the heart of our conceptual structure. Causation is one of the most fundamental tools we have for organizing our apprehension of the external world and ourselves. But philosophers' disagreement about the correct interpretation of causation is as limitless as their agreement about its importance. The history of attempts to elucidate the nature of this concept and to situate it with respect to (...) other fundamental concepts is almost as long as the history of philosophy itself. In this first English translation of Causalite; et lois de la nature Max Kistler seeks to reconstruct a unified concept of causation that is general enough to adequately deal with both elementary physical processes and the macroscopic level of phenomena we encounter in everyday life. It will be of great interest to philosophers of science and metaphysics; and also to students and scholars of philosophy of mind where concepts of causation and law play a prominent role. (shrink)

Fundamental Causation addresses issues in the metaphysics of deterministic singular causation, the metaphysics of events, property instances, facts, preventions, and omissions, as well as the debate between causal reductionists and causal anti-reductionists. The book also pays special attention to causation and causal structure in physics. Weaver argues that causation is a multigrade obtaining relation that is transitive, irreflexive, and asymmetric. When causation is singular, deterministic and such that it relates purely contingent events, the relation is (...) also universal, intrinsic, and well-founded. He shows that proper causal relata are events understood as states of substances at ontological indices. He then proves that causation cannot be reduced to some non-causal base, and that the best account of that relation should be unashamedly primitivist about the dependence relation that underwrites its very nature. The book demonstrates a distinctive realist and anti-reductionist account of causation by detailing precisely how the account outperforms reductionist and competing anti-reductionist accounts in that it handles all of the difficult cases while overcoming all of the general objections to anti-reductionism upon which other anti-reductionist accounts falter. This book offers an original and interesting view of causation and will appeal to scholars and advanced students in the areas of metaphysics, philosophy of science, and philosophy of physics. (shrink)

I provide a comprehensive metaphysics of causation based on the idea that fundamentally things are governed by the laws of physics, and that derivatively difference-making can be assessed in terms of what fundamental laws of physics imply for hypothesized events. Highlights include a general philosophical methodology, the fundamental/derivative distinction, and my mature account of causal asymmetry.

In many toxic-tort cases - notably in Oxendine v. Merrell Dow Pharmaceuticals, Inc, and in Joiner v. G.E., - plaintiffs argue that the expert testimony they wish to present, though no part of it is sufficient by itself to establish causation "by a preponderance of the evidence," is jointly sufficient to meet this standard of proof; and defendants sometimes argue in response that it is a mistake to imagine that a collection of pieces of weak evidence can be any (...) stronger than its individual components. This article draws on the epistemological theory I first presented in 1993 in Evidence and Inquiry, and then amplified and refined in 2003 in Defending Science - Within Reason. This theory of evidence shows that, under certain conditions, a combination of pieces of evidence none of which is sufficient by itself really can warrant a casual conclusion to a higher degree than any of its components alone. When my account is applied to the very complex congeries of evidence typically proffered to prove general causation in these toxic-tort cases, it improves on the influential "Bradford Hill criteria" for assessing causation; and it suggests answers to questions frequently raised in such cases: e.g., whether epidemiological evidence is essential for proof of causation, and whether such evidence should be excluded if it is not statistically significant. Moreover, the argument of this paper reveals that by obliging courts to screen each item of expert testimony individually for reliability, the atomism implicit in Daubert will sometimes stand in the way of an accurate assessment of the worth of complex causation evidence. (shrink)

I have two main aims. The first is general, and more philosophical. The second is specific, and more closely related to physics. The first aim is to state my general views about laws and causation at different ”levels’. The main task is to understand how the higher levels sustain notions of law and causation that ”ride free’ of reductions to the lower level or levels. I endeavour to relate my views to those of other symposiasts. The (...) second aim is to give a framework for describing dynamics at different levels, emphasizing how the various levels’ dynamics can mesh or fail to mesh. This framework is essentially that of elementary dynamical systems theory. The main idea will be, for simplicity, to work with just two levels, dubbed ”micro’ and ”macro’, which are related by coarse-graining. I use this framework to describe, in part, the first four of Ellis’ five types of top-down causation. (shrink)

Three general accounts of causation stand out in early modern philosophy: Cartesian interactionism, occasionalism, and Leibniz's preestablished harmony. The contributors to this volume examine these theories in their philosophical and historical context. They address them both as a means for answering specific questions regarding causal relations and in their relation to one another, in particular, comparing occasionalism and the preestablished harmony as responses to Descartes's metaphysics and physics and the Cartesian account of causation. Philosophers discussed include Descartes, (...) Gassendi, Malebranche, Arnauld, Leibniz, Bayle, La Forge, and other, less well-known figures. (shrink)

In this book, Reiss argues in favor of a tight fit between evidence, concept and purpose in our causal investigations in the sciences. There is no doubt that the sciences employ a vast array of techniques to address causal questions such as controlled experiments, randomized trials, statistical and econometric tools, causal modeling and thought experiments. But how do these different methods relate to each other and to the causal inquiry at hand? Reiss argues that there is no "gold standard" in (...) settling causal issues against which other methods can be measured. Rather, the various methods of inference tend to be good only relative to certain interpretations of the word "cause", and each interpretation, in turn, helps to address some salient purpose but not others. The main objective of this book is to explore the metaphysical and methodological consequences of this view in the context of numerous cases studies from the natural and social sciences. (shrink)

In this paper, I offer one example of conceptual change. Specifically, I contend that the discovery that viruses could cause cancer represents an excellent example of branch jumping, one of Thagard’s nine forms of conceptual change. Prior to about 1960, cancer was generally regarded as a degenerative, chronic, non-infectious disease. Cancer causation was therefore usually held to be a gradual process of accumulating cellular damage, caused by relatively non-specific component causes, acting over long periods of time. Viral infections, on (...) the other hand, were generally understood to be acute processes, whereby single, specific and necessary causal agents acted alone to produce disease. However, during the 1960s and 1970s, a number of cancers were discovered to have an infectious aetiology. Of particular note were two—Burkitt’s lymphoma and cervical cancer—which I will discuss in detail later in this piece. Together, these discoveries led, in the short term, to a tentative aetiological reclassification of some types of cancer as infectious diseases and, in the longer term, to a full-blown reclassification of cancer as an aetiological disease branch in its own right. This process of reclassification forms the empirical basis for my concluding remarks on the influence of classification upon causation in medicine. Through this, I aim to demonstrate that conceptual change, far from being a purely abstract concern of the philosopher of science, is of substantial import to scientific practitioners. (shrink)

I survey recent work on mental causation. The discussion is conducted under the twin presumptions that mental states, including especially what subjects believe and desire, causally explain what subjects do, and that the physical sciences can in principle give a complete explanation for each and every bodily movement. I start with sceptical discussions of various views that hold that, in some strong sense, the causal explanations offered by psychology are autonomous with respect to those offered by the physical sciences. (...) I then proceed to views that see the problem of mental causation as that of identifying where in the physical story about us and our world lie the parts that in effect tell us abut mental causation - the kind of position that is pretty much standard in the cognitive science community - and consider issues raised by various forms of functionalism and externalism. The general thrust of my discussion is sympathetic to the story about mental causation suggested by those type-type versions of the mind-brain identity theory that allow for the possiblity of multiple realisability. I include a brief discussion of how a map-system account of belief, by contrast with a language of thought one, should understand explanations of behaviour in terms of what a subject believes. (shrink)

I defend the thesis that, if there are substances, substance causation (i.e., causation by substances) is the only sort of causation in the universe – or the only fundamental sort. Subsequently, I develop an account of substance causation that is partly grounded on a peculiar interpretation of absolute change (i.e., of entities' coming and ceasing to be) and qualitative change, on some ontological assumptions about modes (i.e., individual properties that ontologically depend on their bearers) and powers. (...) Finally, I reply to some objections against substance causation in general (e.g., C. D. Broad's objection against causes' being non-essentially-dated entities) and to some possible objections against my own account and I briefly explore three advantages given by the acceptance of the latter. (shrink)

This is the first English translation of _Causalite´ et Lois de La Nature,_ and is an important contribution to the theory of causation_._ Max Kistler reconstructs a unified concept of causation that is general enough to adequately deal with both elementary physical processes, and the macroscopic level of phenomena we encounter in everyday life. This book will be of great interest to philosophers of science and metaphysics, and also to students and scholars of philosophy of mind where concepts (...) of causation and law play a prominent role. (shrink)

A cause has traditionally been thought of as that which produces an effect, and in terms of which this effect can be explained or accounted for. However spontaneously we turn to the idea of a cause in daily life, and however inevitable in jurisprudence, in modern science it is generally considered a relic of the past, and in philosophy it remains a topic of inexhaustible controversy. For almost twenty‐five centuries philosophers have been debating the nature of a cause, claiming that (...) it is an object producing an effect by virtue of its power, or arguing that it is an explanation accounting for some effect. Which of all the conditions contributing to an event is to be selected as its cause? Do causes exist in reality or are they read into our experience with the force of our expectations, or produced by the a priori categories of our minds as they structure reality in causal relations? To widen the horizon of this discussion and trace the concept of causation in non‐Western philosophical traditions – such as the ancient Chinese – might enrich this ongoing controversy and allow unfamiliar authors to contribute their views. (shrink)

I deny that the world is fundamentally causal, deriving the skepticism on non-Humean grounds from our enduring failures to find a contingent, universal principle of causality that holds true of our science. I explain the prevalence and fertility of causal notions in science by arguing that a causal character for many sciences can be recovered, when they are restricted to appropriately hospitable domains. There they conform to loose and varying collections of causal notions that form folk sciences of causation. (...) This recovery of causation exploits the same generative power of reduction relations that allows us to recover gravity as a force from Einstein's general relativity and heat as a conserved fluid, the caloric, from modern thermal physics, when each theory is restricted to appropriate domains. Causes are real in science to the same degree as caloric and gravitational forces. (shrink)

I deny that the world is fundamentally causal, deriving the skepticism on non-Humean grounds from our enduring failures to find a contingent, universal principle of causality that holds true of our science. I explain the prevalence and fertility of causal notions in science by arguing that a causal character for many sciences can be recovered, when they are restricted to appropriately hospitable domains. There they conform to a loose collection of causal notions that form a folk science of causation. (...) This recovery of causation exploits the same generative power of reduction relations that allows us to recover gravity as a force from Einstein's general relativity and heat as a conserved fluid, the caloric, from modern thermal physics, when each theory is restricted to appropriate domains. Causes are real in science to the same degree as caloric and gravitational forces. (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)

Explanations are very important to us in many contexts: in science, mathematics, philosophy, and also in everyday and juridical contexts. But what is an explanation? In the philosophical study of explanation, there is long-standing, influential tradition that links explanation intimately to causation: we often explain by providing accurate information about the causes of the phenomenon to be explained. Such causal accounts have been the received view of the nature of explanation, particularly in philosophy of science, since the 1980s. However, (...) philosophers have recently begun to break with this causal tradition by shifting their focus to kinds of explanation that do not turn on causal information. The increasing recognition of the importance of such non-causal explanations in the sciences and elsewhere raises pressing questions for philosophers of explanation. What is the nature of non-causal explanations – and which theory best captures it? How do non-causal explanations relate to causal ones? How are non-causal explanations in the sciences related to those in mathematics and metaphysics? This volume of new essays explores answers to these and other questions at the heart of contemporary philosophy of explanation. The essays address these questions from a variety of perspectives, including general accounts of non-causal and causal explanations, as well as a wide range of detailed case studies of non-causal explanations from the sciences, mathematics and metaphysics. (shrink)

<b> </b>Abstract: It is generally accepted that the most serious threat to the possibility of mental causation is posed by the causal self-sufficiency of physical causal processes. I argue, however, that this feature of the world, which I articulate in principle I call Completeness, in fact poses no genuine threat to mental causation. Some find Completeness threatening to mental causation because they confuse it with a stronger principle, which I call Closure. Others do not simply conflate Completeness (...) and Closure, but hold that Completeness, together with certain plausible assumptions, _entails_ Closure. I refute the most fully worked-out version of such an argument. Finally, some find Completeness all by itself threatening to mental causation. I argue that one will only find Completeness threatening if one operates with a philosophically distorted conception of mental causation. I thereby defend what I call naïve realism about mental causation. (shrink)

Manipulablity theories of causation, according to which causes are to be regarded as handles or devices for manipulating effects, have considerable intuitive appeal and are popular among social scientists and statisticians. This article surveys several prominent versions of such theories advocated by philosophers, and the many difficulties they face. Philosophical statements of the manipulationist approach are generally reductionist in aspiration and assign a central role to human action. These contrast with recent discussions employing a broadly manipulationist framework for understanding (...) causation, such as those due to the computer scientist Judea Pearl and others, which are non-reductionist and rely instead on the notion of an intervention. This is simply an appropriately exogenous causal process; it has no essential connection with human action. This interventionist framework manages to avoid at least some of these difficulties faced by traditional philosophical versions of the manipulability theory and helps to clarify the content of causal claims. (shrink)

Mental causation occurs when mental entities cause other mental and physical entities: seeings causing believings, itches causing scratchings, headaches causing eye twitches, and so on. The term “mental causation” is most often used to refer to the problem of mental causation, which is really a collection of problems with each possessing its own character and tradition of debate. The problem of mental causation began in earnest with an objection to Cartesian dualism raised by Princess Elizabeth of (...) Bohemia (how can immaterial minds causally interact with material bodies?) and still persists via a series of different objections raised against various views including non-reductive physicalism, anomalous monism, and psychological externalism. What unites the different problems of mental causation is their attempt to address a question of this general form: is model x of the non-causal mental-physical relationship (e.g., non-reductive physicalism) consistent with there being mental causation? A negative answer is usually taken to constitute a fatal objection to model x, but not always. There have been two major avenues of inquiry since Elizabeth’s original objection began the debate: (a) what theories of causation can tell us about the consistency of model x with mental causation; or (b) what theories about the non-causal mental-physical relationship can tell us about the consistency of model x with mental causation. Nearly every contribution in the literature on the problem of mental causation can be understood as belonging in either category (a) or (b), or as containing distinguishable elements which so belong. The most important discussions about mental causation have taken place over the last few decades, hence this entry will focus largely on work conducted in that period. Mental causation is also discussed in other areas of philosophy, such as political philosophy or ethics, but this entry will be primarily concerned with the metaphysical and philosophy of mind literature. (shrink)

In this paper I show how the conserved quantity theory, or more generally the process theory of Wesley Salmon and myself, provides a sufficient condition in an analysis of causation. To do so I will show how it handles the problem of alleged 'misconnections'. I show what the conserved quantity theory says about such cases, and why intuitions are not to be taken as sacrosanct.

It is often said that singular causal statements express a relationship between one event and another or between a fact and an event. This is a very strong view, which has the following simple corollary: singular causal statements whose cause-term purports to refer to an event and whose effect-term purports to refer to an event express a relationship between an event and an event.Thus, both Davidson and Kim would claim that the singular causal Statement Socrates’ drinking hemlock at dusk caused (...) his death expresses a relationship between two events, referred to, respectively, by the expressions “Socrates’ drinking hemlock at dusk” and “his death.” For Kim, but not for Davidson, an event is analyzable as a thing's having a property at or during a time. The event of Socrates’ drinking hemlock at dusk consists of Socrates’ at a certain time having the property of drinking hemlock at dusk. I shall not here try to choose between their respective theories of events but will only note that both theorists would say that expresses a relationship between events however the latter are to be construed. (shrink)

According to what I call the reductive standard-causal theory of agency, the exercise of an agent's power to act can be reduced to the causal efficacy of agent-involving mental states and events. According to a non-reductive agent-causal theory, an agent's power to act is irreducible and primitive. Agent-causal theories have been dismissed on the ground that they presuppose a very contentious notion of causation, namely substance-causation. In this paper I will assume, with the proponents of the agent-causal approach, (...) that substance-causation is possible, as I will argue against that theory on the ground that it fails as a theory of agency. I will argue that the non-reductive agent-causal theory fails to account for agency, because it fails to account for agential control: it cannot explain why the stipulated irreducible relation between the agent and an action constitutes the agent's exercise of control over the action. This objection, I will argue, applies to the agent-causal theory in particular, and to the non-reductive approach in general. (shrink)

For the framework of event causation—i.e. the framework according to which causation is a relation between events—absences or omissions pose a problem. Absences, it is generally agreed, are not events; so, under the framework of event causation, they cannot be causally related. But, as a matter of fact, absences are often taken to be causes or effects. The problem of absence causation is thus how to make sense of causation that apparently involves absences as causes (...) or effects. In an influential paper, Helen Beebee offers a partial solution to the problem by giving an account of causation by absence. I argue that Beebee's account can be extended to cover causation of absence as well. More importantly, I argue that the extended Beebeeian account calls for a major modification to David Lewis's theory of causal explanation, usually taken as standard. Compared to the standard theory, the.. (shrink)

In The Biopsychosocial Model of Health and Disease, Derek Bolton and Grant Gillett argue that a defensible updated version of the biopsychosocial model requires a metaphysically adequate account of disease causation that can accommodate biological, psychological, and social factors. This present paper offers a philosophical critique of their account of biopsychosocial causation. I argue that their account relies on claims about the normativity and the semantic content of biological information that are metaphysically contentious. Moreover, I suggest that these (...) claims are unnecessary for a defence of biopsychosocial causation, as the roles of multiple and diverse factors in disease causation can be readily accommodated by a more widely accepted and less metaphysically contentious account of causation. I then raise the more general concern that they are misdiagnosing the problem with the traditional version of the biopsychosocial model. The challenge when developing an explanatorily valuable version of the biopsychosocial model, I argue, is not so much providing an adequate account of biopsychosocial causation, but providing an adequate account of causal selection. Finally, I consider how this problem may be solved to arrive at a more explanatorily valuable and clinically useful version of the biopsychosocial model. (shrink)

One of the jobs of philosophers of the special sciences is to connect the local concerns of particular disciplines with those of philosophy in general. The two-way complexities of this task are well-illustrated by the case of causation. On the one hand—from the outside, as it were— philosophers interested in general issues about causation are prone to turn to the special sciences for real-life examples of the use of causal notions. On the other hand, from the (...) inside, the special disciplines themselves throw up philosophical puzzles in which the notion of causation plays a role. When does correlation indicate causation, for example? Physics and economics both generate hard cases of this kind. (shrink)

Non-reductive Physicalism together with environment-dependence of content has been thought to be incompatible with the claim that beliefs are efficacious partly in virtue of their possession of content, that is, in virtue of their intentional properties. I argue that this is not so. First, I provide a general account of property causation. Then, I explain how, even given the truth of Non-reductive Physicalism and the environment-dependence of content, intentional properties will be efficacious according to this account. I go (...) on to relate my discussion to that concerning whether Anomalous Monism is committed to epiphenomenalism. I close by considering how my proposal suggests we should conceive of different levels of causation in a layered world. (shrink)

Nineteenth-century medical advances were entwined with a conceptual innovation: the idea that many cases of disease which were previously thought to have diverse causes could be explained by the action of a single kind of cause, for example a certain bacterial or parasitic infestation. The focus of modern epidemiology, however, is on chronic non-communicable diseases, which frequently do not seem to be attributable to any single causal factor. This paper is an effort to resolve the resulting tension. The paper criticises (...) the monocausal model of disease, so successful in the nineteenth century. It also argues that a multifactorial model of disease can only be satisfactory if it amounts to more than a mere rejection of the monocausal model. A third alternative, the contrastive model, is proposed and defended on the grounds that it links the notions of disease and of general explanation, while avoiding the philosophical naiveties and practical difficulties of the monocausal model. (shrink)

Donald Davidson has two central aims in his celebrated paper ‘Mental Events.’ First, he argues for the impossibility of ‘strict … laws on the basis of which mental events can be predicted and explained’. I shall call the resulting view ‘mental anomalism.’ Second, he argues, based partially on this impossibility, for a version of monism which holds that every mental event is token-identical with some physical event. This second aim puts constraints on how the argument for mental anomalism can plausibly (...) proceed. That argument cannot assume anything that presupposes monism or adversely affects the argument for it. When elaborated, this constraint by itself rules out otherwise attractive conceptions of how the argument for mental anomalism works. More generally, in order to be compelling, the overall argument for anomalous monism ought not to incorporate excessively controversial presuppositions even if they do not themselves beg any questions about monism. The argument needs to be built upon relatively intuitive premises. (shrink)

In this article, I begin by giving a brief history of melanoma causation. I then discuss the current manner in which malignant melanoma is classified. In general, these systems of classification do not take account of the manner of tumour causation. Instead, they are based on phenomenological features of the tumour, such as size, spread, and morphology. I go on to suggest that misclassification of melanoma is a major problem in clinical practice. I therefore outline an alternative (...) means of classifying these tumours based on causal factors. By analogy with similar systems that have recently emerged for other cancers, I suggest that this causal classification is likely to be both workable and helpful, even in the absence of a full causal-mechanistic understanding of the aetiology of the tumour. (shrink)

While it is generally agreed that the concept of homology refers to individuated traits that have been inherited from common ancestry, we still lack an adequate account of trait individuation or inheritance. Here I propose that we utilize a counterfactual criterion of causation to link each trait with a developmental-causal (DC) gene. A DC gene is made up of the genetic information (which might or might not be physically contiguous in the genome) that is needed for the production of (...) the organismic attributes that comprise the trait. I argue that individuated traits—phenes—correspond to organismic features that are caused by DC genes. Using such an approach, we can define a DC map, which shows the relations between each pair of phenes and provides a succinct summary of genotype-phenotype relationships and phenotypic complexity. Phenes in parents and offspring are judged to be homologous if their DC genes are composed of orthologous genetic factors. When comparing more distantly related organisms, traits are homologous when linked by a chain of parent-offspring homologs along the path of ancestry that links the two organisms. There are three possible ways to deal with the potential for multiple equivalent DC genes: maximal, minimal, and consensus homology. Whereas maximal homology has limited utility, the other two approaches have value and can help to guide research at the intersection of evolution and development. (shrink)

Appraisal theories of emotion generally presuppose that emotions are “directed at” various items. They also hold that emotions have motivational properties. However, although it coheres well with their views, they have yet to seriously develop the idea that the function of emotional direction is to guide those properties. I argue that this “guidance hypothesis” can open up a promising new field of research in emotion theory. But I also argue that before appraisal theorists can take full advantage of it, they (...) must drop their further assumption that to determine an emotion's direction, one need only retrace the process that caused it. Contrary to this “retracing view,” I argue for an “independence thesis”: directed emotions are produced by two functionally independent sub-processes. The first, “affect-causation,” functions in part to produce a state with certain motivational properties given certain representations. The second, “affect-direction,” has the function of optimally guiding those motivational properties by associating them with representations that may properly be quite dissimilar from the causal ones. By provisionally adopting the independence thesis and empirically testing the guidance hypothesis, I argue that appraisal theorists stand a good chance of significantly increasing the explanatory power of their theories. (shrink)