Which country, politician, or policy is more of a cause of the Covid-19 pandemic death toll? Which of the two factories causally contributed more to the pollution of the nearby river? A wide-ranging portion of our everyday thought and talk, and attitudes rely on a graded notion of causation. However, it is sometimes highlighted that on most contemporary accounts, causation is on-off. Some philosophers further question the legitimacy of talk of degrees of causation and suggest that we (...) avoid it. Some hold that the notion of degrees of causation is an illusion. In this paper, I’ll argue that causation does come in degrees. (shrink)

There have recently been a number of strong claims that normative considerations, broadly construed, influence many philosophically important folk concepts and perhaps are even a constitutive component of various cognitive processes. Many such claims have been made about the influence of such factors on our folk notion of causation. In this paper, we argue that the strong claims found in the recent literature on causal cognition are overstated, as they are based on one narrow type of data about a (...) particular type of causal cognition; the extant data do not warrant any wide-ranging conclusions about the pervasiveness of normative considerations in causal cognition. Of course, almost all empirical investigations involve some manner of ampliative inference, and so we provide novel empirical results demonstrating that there are types of causal cognition that do not seem to be influenced by moral considerations. (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)

Causation is one of philosophy's most venerable and thoroughly-analyzed concepts. However, the study of how ordinary people make causal judgments is a much more recent addition to the philosophical arsenal. One of the most prominent views of causal explanation, especially in the realm of harmful or potentially harmful behavior, is that unusual or counternormative events are accorded privileged status in ordinary causal explanations. This is a fundamental assumption in psychological theories of counterfactual reasoning, and has been transported to philosophy (...) by Hitchcock and Knobe (2009). A different view--the basis of the culpable control model of blame (CCM)--is that primary causal status is accorded to behaviors that arouse negative evaluative reactions, including behaviors that stem from nefarious motives, negligence or recklessness, a faulty character, or behaviors that lead to harmful or potentially harmful consequences. This paper describes four empirical studies that show consistent support for the CCM. (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)

This paper presents a puzzle or antinomy about the role of properties in causation. In theories of properties, a distinction is often made between determinable properties, like red, and their determinates, like scarlet (see Armstrong 1978, volume II). Sometimes determinable properties are cited in causal explanations, as when we say that someone stopped at the traffic light because it was red. If we accept that properties can be among the relata of causation, then it can be argued that (...) there are good reasons for allowing that some of these are determinable properties. On the other hand, there are strong arguments in the metaphysics of properties to treat properties as sparse in David Lewis’s (1983) sense. But then it seems that we only need to believe in the most determinate properties: particular shades of colour, specific masses, lengths and so on. And if we also agree with Lewis that sparse properties are ‘the ones relevant to causal powers’ (1983: 13) it seems we must conclude that if properties are relevant to causation at all, then all of these are determinate properties. I call this ‘the antinomy of determinable causation’. On the one hand, we have a good argument for the claim that determinable properties can be causes, if any properties are. I call this the Thesis. But on the other hand, we have a good argument for the claim that only the most determinate properties can be causes, if any properties are. I call this the Antithesis. Clearly, we need to reject either the Thesis or the.. (shrink)

The Problems of Mental Causation. Functionalism in the philosophy of mind identifies mental states with their dispositional connections with other mental states, perceptions and actions. Many theories of the mind have sailed under the Functionalist flag. But what I take to be essential to Functionalism is that mental states are individuated causally: the reality of mental states depends essentially on their causal efficacy.

I propose a new formalist account of legal (/proximate) causation – one that holds legal causation to be a matter of amoral, descriptive fact. The account starts with a metaphysical relation, akin to but distinct from common-sense causation, and it argues that legal causation aligns exactly with that relation; it is unified and principled.

My primary aim is to defend a nonreductive solution to the problem of action. I argue that when you are performing an overt bodily action, you are playing an irreducible causal role in bringing about, sustaining, and controlling the movements of your body, a causal role best understood as an instance of agent causation. Thus, the solution that I defend employs a notion of agent causation, though emphatically not in defence of an account of free will, as most (...) theories of agent causation are. Rather, I argue that the notion of agent causation introduced here best explains how it is that you are making your body move during an action, thereby providing a satisfactory solution to the problem of action. (shrink)

What would it be for a process to happen backwards in time? Would such a process involve different causal relations? It is common to understand the time-reversal invariance of a physical theory in causal terms, such that whatever can happen forwards in time can also happen backwards in time. This has led many to hold that time-reversal symmetry is incompatible with the asymmetry of cause and effect. This article critiques the causal reading of time reversal. First, I argue that the (...) causal reading requires time-reversal-related models to be understood as representing distinct possible worlds and, on such a reading, causal relations are compatible with time-reversal symmetry. Second, I argue that the former approach does, however, raise serious sceptical problems regarding the causal relations of paradigm causal processes and as a consequence there are overwhelming reasons to prefer a non-causal reading of time reversal, whereby time reversal leaves causal relations invariant. On the non-causal reading, time-reversal symmetry poses no significant conceptual nor epistemological problems for causation. _1_ Introduction _1.1_ The directionality argument _1.2_ Time reversal _2_ What Does Time Reversal Reverse? _2.1_ The B- and C-theory of time _2.2_ Time reversal on the C-theory _2.3_ Answers _3_ Does Time Reversal Reverse Causal Relations? _3.1_ Causation, billiards, and snooker _3.2_ The epistemology of causal direction _3.3_ Answers _4_ Is Time-Reversal Symmetry Compatible with Causation? _4.1_ Incompatibilism _4.2_ Compatibilism _4.3_ Answers _5_ Outlook. (shrink)

Many philosophical theories of causation are egalitarian, rejecting a distinction between causes and mere causal conditions. We sought to determine the extent to which people's causal judgments discriminate, selecting as causes counternormal events—those that violate norms of some kind—while rejecting non-violators. We found significant selectivity of this sort. Moreover, priming that encouraged more egalitarian judgments had little effect on subjects. We also found that omissions are as likely as actions to be judged as causes, and that counternormative selectivity appears (...) to apply equally to actions and omissions. (shrink)

Theories of graded causation attract growing attention in the philosophical debate on causation. An important field of application is the controversial relationship between causation and moral responsibility. However, it is still unclear how exactly the notion of graded causation should be understood in the context of moral responsibility. One question is whether we should endorse a proportionality principle, according to which the degree of an agent’s moral responsibility is proportionate to their degree of causal contribution. A (...) second question is whether a theory of graded causation should measure closeness to necessity or closeness to sufficiency. In this paper, we argue that we should indeed endorse a proportionality principle and that this principle supports a notion of graded causation relying on closeness to sufficiency rather than closeness to necessity. Furthermore, we argue that this insight helps to provide a plausible analysis of the so-called ‘Moral Difference Puzzle’ recently described by Bernstein. (shrink)

The standard objection to dualist theories of mind is that they seemingly cannot account for the obvious fact that mental phenomena cause our behaviour. On the plausible assumption that all our behaviour is physically necessitated by entirely physical phenomena, there appears to be no room for dualist mental causation. Some argue that dualists can address this problem by making minimal adjustments in their ontology. I argue that no such adjustments are required. Given recent developments in philosophy of causation, (...) it is plausible that mental phenomena cause behaviour in standard dualist ontologies. (shrink)

Disputes about the causal structure of natural selection have implications for teleosemantics. Etiological, mainstream teleosemantics is based on a causalist view of natural selection. The core of its solution to Brentano’s Problem lies in the solution to Kant’s Puzzle provided by the Modern Synthesis concerning populational causation. In this paper, I suggest that if we adopt an alternative, statisticalist view on natural selection, the door is open for two reflections. First, it allows for setting different challenges to etiological teleosemantics (...) that arise if a statisticalist reading of natural selection is right. Second, by providing a different solution to Kant’s Puzzle based on individual causes of evolution, statisticalism promotes a different answer to Brentano’s Problem, what I label as Agential Teleosemantics. (shrink)

The issue of downward causation (and mental causation in particular), and the exclusion problem is discussed by taking into account some recent advances in the philosophy of science. The problem is viewed from the perspective of the new interventionist theory of causation developed by Woodward. It is argued that from this viewpoint, a higher-level (e.g., mental) state can sometimes truly be causally relevant, and moreover, that the underlying physical state which realizes it may fail to be such.

This paper explores the prospects of employing a functional approach in order to improve our concept of actual causation. Claims of actual causation play an important role for a variety of purposes. In particular, they are relevant for identifying suitable targets for intervention, and they are relevant for our practices of ascribing responsibility. I argue that this gives rise to the challenge of purpose. The challenge of purpose arises when different goals demand adjustments of the concept that pull (...) in opposing directions. More specifically, I argue that a common distinction between certain kinds of preempted and preempting factors is difficult to motivate from an interventionist viewpoint. This indicates that an appropriately revised concept of actual causation would not distinguish between these two kinds of factors. From the viewpoint of retributivist responsibility, however, the distinction between preempted and preempting factors sometimes is important, which indicates that the distinction should be retained. (shrink)

The problem of mental causation is discussed by taking into account some recent developments in the philosophy of science. The problem is viewed from the perspective of the new interventionist theory of causation developed by Woodward. The import of the idea that causal claims involve contrastive classes in mental causation is also discussed. It is argued that mental causation is much less a problem than it has appeared to be.

We propose that all actual causes are simultaneous with their direct effects, as illustrated by both everyday examples and the laws of physics. We contrast this view with the sequential conception of causation, according to which causes must occur prior to their effects. The key difference between the two views of causation lies in differing assumptions about the mathematical structure of time.

This paper takes a critical stance on Tallis’s separation of causation and agency. While his critique of the causal theory of action and the assumptions about causation underlying different versions of determinism, including the one based on neuroscience is right, his rejection of causation (of all sorts) has implausible consequences. Denying the link between action and causation amounts to overlooking the role action plays in causal inference and in the origin of causal concepts. I suggest that (...) a weaker version of Tallis’ claim, compatible with causation understood as agency, would work better. (shrink)

In many spheres, the law takes the legal concept of causation to correspond to the folk concept (the correspondence assumption). Courts, including the US Supreme Court, tend to insist on the "common understanding" and that which is "natural to say" (Burrage v. United States) when it comes to expressions relating to causation, and frequently refuse to clarify the expression to juries. As recent work in psychology and experimental philosophy has uncovered, lay attributions of causation are susceptible to (...) a great number of unexpected factors, some of which seem rather peripheral to causation. One of those is the norm effect (Knobe & Fraser, 2008): Agents who, in acting as they do, break a salient norm, are more likely to be considered as having caused a certain consequence than when they do not violate a norm. According to some (e.g., Alicke, 1992) this constitutes a bias. According to others (e.g., Sytsma, 2020), the folk concept of causation is sensitive to normative factors, and there’s nothing wrong with that. In this paper, we explore the question whether the norm effect should be considered a bias from the legal perspective on the one hand, and from the psychological perspective on the other. To do this, we test whether norms which are nonpertinent to the consequences or outright silly also impact causation judgements. The data from two preregistered experiments (total N=593) clearly show they do. This, we argue, makes the bias interpretation plausible from the psychological perspective, and both plausible and problematic from the legal perspective. It also shows that the law should abstain from unreflectively assuming conceptual correspondence between legal and ordinary language concepts. (shrink)

The problem of mental causation in contemporary philosophy of mind concerns the possibility of holding two different views that are in apparent tension. The first is physicalism, the view that there is nothing more to the world than the physical. The second is that the mental has genuine causal efficacy in a way that does not reduce to pure physical particle-bumping. This article provides a historical background to this question, with focus on Davidson’s anomalous monism and Kim’s causal exclusion (...) problem. Responses to causal exclusion are categorized in terms of six different argumentative strategies. In conclusion, caution is advised regarding the inclination to reduce the mental to the physical and sketch a positive direction for substantively characterizing mental causation by recourse to well-confirmed accounts of causation coupled with empirical research. (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 a recent paper I argued that agent causation theorists should be compatibilists. In this paper, I argue that compatibilists should be agent causation theorists. I consider six of the main problems facing compatibilism: (i) the powerful intuition that one can't be responsible for actions that were somehow determined before one was born; (ii) Peter van Inwagen's modal argument, involving the inference rule (β); (iii) the objection to compatibilism that is based on claiming that the ability to do (...) otherwise is a necessary condition for freedom; (iv) "manipulation arguments," involving cases in which an agent is manipulated by some powerful being into doing something that he or she would not normally do, but in such a way that the compatibilist's favorite conditions for a free action are satisfied; (v) the problem of constitutive luck; and (vi) the claim that it is not fair to blame someone for an action if that person was determined by forces outside of his or her control to perform that action. And in the case of each of these problems, I argue that the compatibilist has a much more plausible response to that problem if she endorses the theory of agent causation than she does otherwise. (shrink)

Suppose that, for every event, whether mental or physical, there is some physical event causally sufficient for it. Suppose, moreover, that physical reductionism in its various forms fails—that mental properties cannot be reduced to physical properties and mental events cannot be reduced to physical events. In this case, how could there be mental causation? More specifically, how could mental events cause other mental events, physical events, and intentional actions? The primary goal of this paper is to answer this question.

The problem of downward causation is that an intuitive response to an intuitive picture leads to counterintuitive results. Suppose a mental event, m1, causes another mental event, m2. Unless the mental and the physical are completely independent, there will be a physical event in your brain or your body or the physical world as a whole that underlies this event. The mental event occurs at least partly in virtue of the physical event’s occurring. And the same goes for m2 (...) [2] and p2. Let’s not worry about what exactly “underlying” or “in virtue of” means here. Here’s the picture. m1 -----> m2 | | p1 -----> p2 The horizontal arrows represent causation, and the vertical lines represent underlying, whatever that may be. There’s some reason to think that the only way m1 can bring about m2 is by bringing about p2. You can’t convince someone of something through mental telepathy. You need to interact with the physical world, perhaps by saying something and so making some noise, or by pointing and getting them to turn their head and see. What goes for the case of two people goes for the case of one person as well. Superstition aside, there is no purely mental energy that floats free of the merely physical workings of the brain. If m1 brings about m2 by bringing about p2, then m1 brings about p2. This is downward causation. But wait. Doesn’t p1 bring about p2? Isn’t that what the bottom arrow represents? Maybe m1 and p1 work together to bring about p2. There are little holes in the physical causal structure that need to be filled by mental events. You don’t need a sweeping metaphysical thesis about the causal closure of the physical to find this implausible. Maybe p2 is overdetermined. (shrink)

What is offered here is an interpretation of Hume’s views on causation. While it might not be literally Hume’s view, it is certainly consistent with Hume, and is probably what Hume should say on causation, in light of recent developments in science and logic. As a way in, it is argued that the considerations that Hume brings against rationalist theories of causation can be applied to counterfactual theories of causation. Since, counterfactuals, possible worlds and modality were (...) not ideas that would have been overly familiar to Hume, some supplementation of Hume’s arguments will be necessary. (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)

Downward causation is commonly held to create problems for ontologically emergent properties. In this paper I describe two novel examples of ontologically emergent properties and show how they avoid two main problems of downward causation, the causal exclusion problem and the causal closure problem. One example involves an object whose colour does not logically supervene on the colours of its atomic parts. The other example is inspired by quantum entanglement cases but avoids controversies regarding quantum mechanics. These examples (...) show that the causal exclusion problem can be avoided, in one case by showing how it is possible to interact with an object without interacting with its atomic parts. I accept that emergence cannot be reconciled with causal closure, but argue that violations of causal closure do not entail violations of the base-level laws. Only the latter would conflict with empirical science. (shrink)

In his influential book 'Making Things Happen' and in other places, Jim Woodward has noted some affinities between his own account of causation and that of Menzies and Price, but argued that the latter view is implausibly ‘subjective’. In this piece I discuss Woodward’s criticisms. I argue that the Menzies and Price view is not as different from Woodward’s own account as he believes, and that in so far as it is different, it has some advantages whose importance Woodward (...) misses; but also that the Menzies and Price view lacks some elements whose importance Woodward rightly stresses. When properly characterized, however, the ‘subjectivity’ survives unscathed. (shrink)

Our ordinary causal concept seems to fit poorly with how our best physics describes the world. We think of causation as a time-asymmetric dependence relation between relatively local events. Yet fundamental physics describes the world in terms of dynamical laws that are, possible small exceptions aside, time symmetric and that relate global time slices. My goal in this paper is to show why we are successful at using local, time-asymmetric models in causal explanations despite this apparent mismatch with fundamental (...) physics. In particular, I will argue that there is an important connection between time asymmetry and locality, namely: understanding the locality of our causal models is the key to understanding why the physical time asymmetries in our universe give rise to time asymmetry in causal explanation. My theory thus provides a unified account of why causation is local and time asymmetric and thereby enables a reply to Russell’s famous attack on causation. (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)

This paper examines a promising probabilistic theory of singular causation developed by David Lewis. I argue that Lewis' theory must be made more sophisticated to deal with certain counterexamples involving pre-emption. These counterexamples appear to show that in the usual case singular causation requires an unbroken causal process to link cause with effect. I propose a new probabilistic account of singular causation, within the framework developed by Lewis, which captures this intuition.

This paper articulates an account of causation as a collection of information-theoretic relationships between patterns instantiated in the causal nexus. I draw on Dennett’s account of real patterns to characterize potential causal relata as patterns with specific identification criteria and noise tolerance levels, and actual causal relata as those patterns instantiated at some spatiotemporal location in the rich causal nexus as originally developed by Salmon. I develop a representation framework using phase space to precisely characterize causal relata, including their (...) degree of counterfactual robustness, causal profiles, causal connectivity, and privileged grain size. By doing so, I show how the philosophical notion of causation can be rendered in a format that is amenable for direct application of mathematical techniques from information theory such that the resulting informational measures are causal informational measures. This account provides a metaphysics of causation that supports interventionist semantics and causal modeling and discovery techniques. (shrink)

Nonreductive physicalism states that actions have sufficient physical causes and distinct mental causes. Nonreductive physicalism has recently faced the exclusion problem, according to which the single sufficient physical cause excludes the mental causes from causal efficacy. Autonomists respond by stating that while mental-to-physical causation fails, mental-to-mental causation persists. Several recent philosophers establish this autonomy result via similar models of causation :1031–1049, 2016; Zhong, J Philos 111:341–360, 2014). In this paper I argue that both of these autonomist models (...) fail on account of the problem of Edwards’s Dictum. However, I appeal to foundational principles of action theory to resuscitate mental-to-mental causation in a manner that is consistent with the models of causation endorsed by these autonomists. (shrink)

Whereas many philosophers take backwards causation to be impossible, the few who maintain its possibility either take it to be absent from the actual world or else confined to theoretical physics. Here, however, I argue that backwards causation is not only actual, but common, though occurring in the context of our social institutions. After juxtaposing my cases with a few others in the literature and arguing that we should take seriously the reality of causal cases in these contexts, (...) I consider several objections. These objections involve whether the cases should be reinterpreted, whether they are properly within the institution, whether they involve necessitation or else Cambridge changes, whether and how they involve changing the past, and whether this should call us to question institutional reality. I end by suggesting that it is a virtue of our institutions that they allow backwards causation, that this is a kind of technology that they are often built to incorporate. (shrink)

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)

Several philosophers claim that the phenomenology of one’s own agency conflicts with standard causal theories of action, couched in terms of causation by mental events or states. Others say that the phenomenology is prima facie incompatible with such a theory, even if in the end a reconciliation can be worked out. Here it is argued that the type of action theory in question is consistent with what can plausibly be said to be presented to us in our experience of (...) our agency. Several routes to a claim that there is nevertheless a prima facie incompatibility are examined, and all are found wanting. The phenomenology of agency, it is argued, is no threat to a standard causal theory of action. (shrink)

On the dominant interpretation, Ockham is an externalist about mental content. This reading is founded principally on his theory of intuitive cognition. Intuitive cognition plays a foundational role in Ockham’s account of concept formation and judgment, and Ockham insists that the content of intuitive states is determined by the causal relations such states bear to their objects. The aim of this paper is to challenge the externalist interpretation by situating Ockham’s account of intuitive cognition vis-à-vis his broader account of efficient (...) causation. While there can be no doubt that intuitive states are causally individuated, I argue that, given Ockham’s broader theory of efficient causation (on which causation turns out to be an internal relation), this very fact entails that the content of such states is determined by factors internal (rather than external) to the states themselves. (shrink)

This chapter explores the idea that causal inference is warranted if and only if the mechanism underlying the inferred causal association is identified. This mechanistic stance is discernible in the epidemiological literature, and in the strategies adopted by epidemiologists seeking to establish causal hypotheses. But the exact opposite methodology is also discernible, the black box stance, which asserts that epidemiologists can and should make causal inferences on the basis of their evidence, without worrying about the mechanisms that might underlie their (...) hypotheses. I argue that the mechanistic stance is indeed a bad methodology for causal inference. However, I detach and defend a mechanistic interpretation of causal generalisations in epidemiology as existence claims about underlying mechanisms. (shrink)

Much of the modern philosophy of causation has been governed by two ideas: (i) causes make their effects inevitable; (ii) a cause is something that makes a difference to whether its effect occurs. I focus on explaining the origin of idea (ii) and its connection to (i). On my view, the frequent attempts to turn (ii) into an analysis of causation are wrongheaded. Patterns of difference-making aren't what makes causal claims true. They merely provide a useful test for (...) causal claims. Moreover, what justifies us in using them as a test is idea (i). That's how (i) and (ii) are connected. (shrink)

Sometimes you make a choice. Whether or not you made it was up to you. The choice was free. But how can this be? A scientific view of the world may leave no room for free choice. Free will literature continually explodes. Yet experts still focus on control or on a power to do otherwise. Sadly, they neglect another intuitive feature of free will: being an underived source or ultimate originator. When acting freely, one is a self-determined, self-directed, sole author (...) of change. Surprisingly, though the literature is replete with this pre-theoretic feature of free will, virtually no one makes rigorous use of it when constructing arguments. Equipped with fresh research, this book contends that agent-causation—currently an unpopular theory—deserves serious reconsideration. Only agent-causation accounts for ultimate origination, and popular objections fail under rigorous scrutiny. This book is tightly argued. It challenges and deepens recent advances in free will scholarship made by Peter van Inwagen, Robert Kane, Carl Ginet, Randy Clarke, Stewart Goetz, Tim O’Connor, and others. (shrink)

This paper is about a puzzle which lies at the heart of contemporary physicalist theories of mind. On the one hand, the original motivation for physicalism was the need to explain the place of mental causation in the physical world. On the other hand, physicalists have recently come to see the explanation of mental causation as one of their major problems. But how can this be? How can it be that physicalist theories still have a problem explaining something (...) which their physicalism was intended to explain in the first place? If physicalism is meant to be an explanation of mental causation, then why should it still face the problem of mental causation? (shrink)

The explanatory role of natural selection is one of the long-term debates in evolutionary biology. Nevertheless, the consensus has been slippery because conceptual confusions and the absence of a unified, formal causal model that integrates different explanatory scopes of natural selection. In this study we attempt to examine two questions: (i) What can the theory of natural selection explain? and (ii) Is there a causal or explanatory model that integrates all natural selection explananda? For the first question, we argue that (...) five explananda have been assigned to the theory of natural selection and that four of them may be actually considered explananda of natural selection. For the second question, we claim that a probabilistic conception of causality and the statistical relevance concept of explanation are both good models for understanding the explanatory role of natural selection. We review the biological and philosophical disputes about the explanatory role of natural selection and formalize some explananda in probabilistic terms using classical results from population genetics. Most of these explananda have been discussed in philosophical terms but some of them have been mixed up and confused. We analyze and set the limits of these problems. (shrink)

In most academic and non-academic circles throughout history, the world and its operation have been viewed in terms of cause and effect. The principles of causation have been applied, fruitfully, across the sciences, law, medicine, and in everyday life, despite the lack of any agreed-upon framework for understanding what causation ultimately amounts to. In this engaging and accessible introduction to the topic, Douglas Kutach explains and analyses the most prominent theories and examples in the philosophy of causation. (...) The book is organized so as to respect the various cross-cutting and interdisciplinary concerns about causation, such as the reducibility of causation, its application to scientific modeling, its connection to influence and laws of nature, and its role in causal explanation. Kutach begins by presenting the four recurring distinctions in the literature on causation, proceeding through an exploration of various accounts of causation including determination, difference making and probability-raising. He concludes by carefully considering their application to the mind-body problem. _Causation_ provides a straightforward and compact survey of contemporary approaches to causation and serves as a friendly and clear guide for anyone interested in exploring the complex jungle of ideas that surround this fundamental philosophical topic. (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)

In this paper we defend the view that mechanisms are underpinned by networks of difference-making relations. First, we distinguish and criticise two different kinds of arguments in favour of an activity-based understanding of mechanism: Glennan’s metaphysics- first approach and Illari and Williamson’s science-first approach. Second, we present an alternative difference-making view of mechanism and illustrate it by looking at the history of the case of scurvy prevention. We use the case of scurvy to argue that evidence for a mechanism just (...) is evidence for difference-making relations. (shrink)

The origins and development of the problem of mental causation are outlined. The underlying presuppositions which give rise to the problem are identified. Possible strategies for solving, or dissolving the problem are examined.

Several theories of causation reject causation of or by absences. They thereby clash with much of what we think and say about what causes what. This paper examines a way in which one kind of theory, causal dispositionalism, can be modified so as to accept absence causation, while still retaining a fundamental commitment of dispositionalism. The proposal adopts parts of a strategy described by David Lewis. The paper concludes with a brief discussion of the problem of the (...) proliferation of causes. (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)