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)

Much contemporary debate on the nature of mechanisms centers on the issue of modulating negative causes. One type of negative causability, which I refer to as “causation by absence,” appears difficult to incorporate into modern accounts of mechanistic explanation. This paper argues that a recent attempt to resolve this problem, proposed by Benjamin Barros, requires improvement as it overlooks the fact that not all absences qualify as sources of mechanism failure. I suggest that there are a number of (...) additional types of effects caused by absences that need to be incorporated to account for the diversity of causal connections in the biological sciences. Furthermore, it is argued that recognizing natural variability in mechanisms, such as attenuation, leads to some interesting line-drawing issues for contemporary philosophy of mechanisms. (shrink)

Hume thought that if you believed in powers, you believed in necessary connections in nature. He was then able to argue that there were none such because anything could follow anything else. But Hume wrong-footed his opponents. A power does not necessitate its manifestations: rather, it disposes towards them in a way that is less than necessary but more than purely contingent. -/- In this paper a dispositional theory of causation is offered. Causes dispose towards their effects and often (...) produce them. But a set of causes, even though they may succeed in producing an effect, cannot necessitate it since the effect could have been counteracted by some additional power. This would require a separation of our concepts of causal production and causal necessitation. The most conspicuous cases of causation are those where powers accumulate and pass a requisite threshold for an effect to occur. -/- We develop a model for representing powers as constituent vectors within an n-dimensional quality space, where composition of causes appears as vector addition. Even our resultant vector, however, has to be understood as having dispositional force only. This model throws new light on causal modality and cases of prevention, causation by absence and probabilistic causation. (shrink)

This is a brief philosophical introduction to, and an annotated translation of, the section on absence from Śālikanātha’s Pramāṇapārāyaṇa (Study of the Instruments of Knowledge), a foundational work of Prābhākara epistemology. In this section, which focuses on the epistemology of absence, Śālikanātha argues against the Bhāṭṭa view that there is a sui generis instrument of knowledge (pramāṇa) by which we learn of absence (abhāva). He does so by arguing for a subjective reductionist thesis about absence, according (...) to which the absence of a perceivable (dṛśya) object at a locus is identical with a positive state of awareness (buddhi) whose content includes the locus but not the perceivable object. If correct, Śālikanātha argues, we should therefore learn of absence in the same ways we acquire self-knowledge more generally. While developing his reductionism about absence, Śālikanātha responds to a range of concerns, including the objection that his view cannot explain causation by absence. (shrink)

The starting point in the development of probabilistic analyses of token causation has usually been the naïve intuition that, in some relevant sense, a cause raises the probability of its effect. But there are well-known examples both of non-probability-raising causation and of probability-raising non-causation. Sophisticated extant probabilistic analyses treat many such cases correctly, but only at the cost of excluding the possibilities of direct non-probability-raising causation, failures of causal transitivity, action-at-a-distance, prevention, and causation by (...) class='Hi'>absence and omission. I show that an examination of the structure of these problem cases suggests a different treatment, one which avoids the costs of extant probabilistic analyses. (shrink)

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)

I focus on token, deterministic causal claims as they feature in causal explanations. Adequately handling absences is difficult for most causal theories, including theories of causal explanation. Yet so is adequately handling cases of late preemption. The best account of absence-causal claims as they appear in causal explanations is Jonathan Schaffer's quaternary, contrastive account. Yet Schaffer's account cannot handle preemption. The account that best handles late preemption is James Woodward's interventionist account. Yet Woodward's account is inadequate when it comes (...) to absences. I propose an account that handles both absences and preemption by transposing Schaffer's account into an interventionist framework. (shrink)

Our approach aims at accounting for causal claims in terms of how the physical states of the underlying dynamical system evolve with time. Causal claims assert connections between two sets of physicals states—their truth depends on whether the two sets in question are genuinely connected by time evolution such that physical states from one set evolve with time into the states of the other set. We demonstrate the virtues of our approach by showing how it is able to account for (...) typical causes, causally relevant factors, being ‘the’ cause, and cases of overdetermination and causation by absences. (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)

This paper argues that several sorts of metaphysical and semantic indeterminacy afflict the causal relation. If, as it is plausible to hold, there is a relationship between causation and moral responsibility, then indeterminacy in the causal relation results in indeterminacy of moral responsibility more generally.

“Perception is controlled hallucination,” according to proponents of predictive processing accounts of vision. I say they are right that something like this is a consequence of their view but wrong in how they have pursued the idea. The focus of my counterproposal is the causal theory of perception, which I develop in terms of a productive concept of causation. Cases of what otherwise seem like successful perception are instead mere veridical hallucination if predictive processing accounts are correct, I argue, (...) because of the role played within such accounts by absences, which cannot enter into productive causal relations. -/- I offer two arguments in support of the productive theory of perception. The first is loosely Kantian, focusing on the role that receptivity and spontaneity play in perception. The second focuses on what perception and hallucination have in common. I conclude with a series of objections and replies. (shrink)

A standard way of representing causation is with neuron diagrams. This has become popular since the influential work of David Lewis. But it should not be assumed that such representations are metaphysically neutral and amenable to any theory of causation. On the contrary, this way of representing causation already makes several Humean assumptions about what causation is, and which suit Lewis’s programme of Humean Supervenience. An alternative of a vector diagram is better suited for a powers (...) ontology. Causation should be understood as connecting property types and tokens where there are dispositions towards some properties rather than others. Such a model illustrates how an effect is typically polygenous: caused by many powers acting with each other, and sometimes against each other. It models causation as a tendency towards an effect which can be counteracted. The model can represent cases of causal complexity, interference, over-determination and causation of absence (equilibrium). (shrink)

This paper aims at bringing a new philosophical perspective to the current debate on the death penalty through a discussion of peculiar kinds of uncertainties that surround the death penalty. I focus on laying out the philosophical argument, with the aim of stimulating and restructuring the death penalty debate. I will begin by describing views about punishment that argue in favour of either retaining the death penalty (‘retentionism’) or abolishing it (‘abolitionism’). I will then argue that we should not ignore (...) the so-called “whom-question”, i.e. “To whom should we justify the system of punishment?” I identify three distinct chronological stages to address this problem, namely, “the Harm Stage”, “the Blame Stage”, and “the Danger Stage”. I will also identify four problems arising from specific kinds of uncertainties present in current death penalty debates: (1) uncertainty in harm, (2) uncertainty in blame, (3) uncertainty in rights, and (4) uncertainty in causal consequences. In the course of examining these four problems, I will propose an ‘impossibilist’ position towards the death penalty, according to which the notion of the death penalty is inherently contradictory. Finally, I will suggest that it may be possible to apply this philosophical perspective to the justice system more broadly, in particular to the maximalist approach to restorative justice. (shrink)

As Jaegwon Kim points out in his excellent new book, “reductionism” has become something of a pejorative term in philosophy and related disciplines. But originally (eg, as expressed in Ernest Nagel’s 1961 The Structure of Science) reduction was supposed to be a form of explanation, and one may wonder whether it is reasonable to reject in principle the advances in knowledge which such explanations may offer. Nagel’s own view, illustrated famously by the reduction of thermodynamics to statistical mechanics, was that (...) reduction is a relation between theories: theory A is reduced to theory B by formulating “bridge laws” which link the terminology of the theories, and using them to derive A from B. (An additional reductive claim is that Aphenomena are identical with certain B-phenomena—as when the temperature of a gas is identified with its mean molecular kinetic energy—but this kind of identity claim is, strictly speaking, independent of the claim about theories.) Applied to the case of mental states and brain states, a reduction would provide explanatory relations between psychology and neuroscience, normally supplemented with the claim that mental properties are identical with physical properties in the brain. (shrink)

Book review of 'Tropes: Properties, Objects, and Mental Causation' (2011, OUP). By DOUGLAS EHRING.

A major criticism of David Lewis’ counterfactual theory of causation is that it allows too many things to count as causes, especially since Lewis allows, in addition to events, absences to be causes as well. Peter Menzies has advanced this concern under the title “the problem of profligate causation.” In this paper, I argue that the problem of profligate causation provides resources for exposing a tension between Lewis’ acceptance of absence causation and his modal realism. (...) The result is a different problem of profligate causation—one that attacks the internal consistency of Lewisian metaphysics rather than employing common sense judgments or intuitions that conflict with Lewis’ extensive list of causes. (shrink)

Eyal Shahar’s essay review [1] of James Penston’s remarkable book [2] seems more inspired playful academic provocation than review or essay, expressing dramatic views of impossible validity. The account given of modern biostatistical causation reveals the slide from science into the intellectual confusion and non-science RCTs have created: “…. the purpose of medical research is to estimate the magnitude of the effect of a causal contrast, for example the probability ratio of a binary outcome …” But Shahar’s world is (...) simultaneously not probabilistic, but of absolute uncertainty: “We should have no confidence in any type of evidence ….. We should have no confidence at all”. Shahar’s "Causal contrast" is attractive. It seems to make sense, but bypasses in two words the means of establishing causation by the scientific method. This phrase assumes a numeric statistically significant “contrast” is causal rather than a potential correlation requiring further investigation. The concept of “causal contrast” is a slippery slope from sense into biostatistical non-science. This can be illustrated with an hypothetical RCT where 100% of interventions exhibit a posited treatment effect and 0% of placebo controls. Internal validity is seemingly quite reasonably assumed satisfied (common-sense dictating the likelihood of an awesome magnificent fraud, bias or plain error of the magnitude required is infinitesimal). Scientific method appears satisfied. The RCT demonstrates: (1) strict regularity of outcome in the presence of posited cause; (2) the absence of outcome in its absence and (3) an intervention (experiment) showing the direction of causation is from posited cause to posited effect. Now travel further down the slope from science. Assume 50% of interventions and 0% of controls are positive. We compromise scientific method, but justify this by assuming a large subgroup which we say surely must on these figures be exhibiting the posited treatment effect. But what of 10% of interventions and 9% of placebo controls exhibiting the posited treatment effect? Our biostatistician says the 1% “causal contrast” is statistically significant. But we have: (1) minimal evidence of regularity; (2) the posited outcome irrespective of presence of posited cause and (3) our intervention is at the highest equivocal in demonstrating any form of causation. This is not science. It is, however, where biostatistics has unthinkingly taken us, as Penston has shown comprehensively [2]. We, the audience of published medical research, are now for the 10% / 9% example well down the slope from science. An unattractive hypothesis results requiring numerous assumptions similar to these:- "There is a 'contrast' which is ‘causal’, albeit the method employed is not scientific. An effect of the intervention has been observed in a very small subgroup. This subgroup is susceptible to treatment. The similar number of placebo controls exhibiting the outcome sought is irrelevant, because the 1% difference between intervention and controls is statistically significant. The statistical analysis is valid and reliable. The RCT’s internal validity is sufficiently satisfied. No funding or bias or fraud has affected the results or their analysis.” As Penston notes: “Confirming and refuting the results of research is crucial to science …. But … there’s no way of testing the results of any particular large-scale RCT or epidemiological study. Each study … is left hanging in the air, unsupported.” It gets worse. To identify a rare serious adverse reaction of a frequency of 1:10,000 can require a trial of 200,000 or larger split between controls and interventions. This is not done. But for every 100 who prospectively benefit from the intervention, 9,900 also receive it. And for every 100 benefiting one person (who likely gains no benefit) will suffer a serious unidentified adverse reaction. This is also without taking account of more common adverse reactions whether serious or otherwise. References [1] Shahar, E. (2011) Research and medicine: human conjectures at every turn. International Journal of Person Centered Medicine 1 (2), 250-253. [2] Penston, J. (2010). stats.con: How we’ve been fooled by statistics-based research in medicine. London: The London Press, UK. (shrink)

Many philosophers maintain that causation is to be explicated in terms of a kind of dependence between cause and effect. These “dependence” theories are opposed by “production” accounts which hold that there is some more fundamental causal “oomph”. A wide range of experimental research on everyday causal judgments seems to indicate that ordinary people operate primarily with a dependence-based notion of causation. For example, people tend to say that absences and double preventers are causes. We argue that the (...) impression that commonsense causal discourse is largely dependence-based is the result of focusing on a very narrow class of causal verbs. Almost all of the vignette-based experimental work on causal judgment has been prosecuted using the word “cause”. But much ordinary causal discourse involves special causal verbs, such as “burn” and “crack”. We find that these verbs display a quite different pattern from the verb “cause”. For instance, for absences and double preventers (Studies 1-3), we find that while people are inclined to say that X caused Y to burn, turn, crack or start, they are less inclined to think that X burned, turned, cracked or started Y. In Study 4, we find that for chains involving a distal and proximal event, people are inclined to say that the distal event is not a special cause of the outcome, though it is a “cause” of the outcome. Together, we find a surprising double dissociation between “cause” and a stock of special causal verbs. We conclude by suggesting that much commonsense causal judgment, which heavily trades in special causal verbs, might be better captured by production-based accounts of causation. (shrink)

A new series entitled Oxford Philosophical Concepts (OPC) made its debut in November 2014. As the series’ Editor Christia Mercer notes, this series is an attempt to respond to the call for and the tendency of many philosophers to invigorate the discipline. To that end each volume will rethink a central concept in the history of philosophy, e.g. efficient causation, health, evil, eternity, etc. “Each OPC volume is a history of its concept in that it tells a story about (...) changing solutions to specific philosophical problems” (xiii). The series presents itself as innovative along three main lines: its reexamination of the so-called “canon,” its reconsidering the value of interdisciplinary exchanges, and its encouraging philosophers to move beyond the current borders of philosophy. By engaging with non-Western traditions and carefully considering topics and materials which are not strictly philosophical, the collections from this series aim to render the history of philosophy accessible to a wide audience. -/- The first OPC volume to appear in print is “Efficient Causation – A History” edited by Tad Schmaltz. Using careful historical and philosophical analysis as well as interdisciplinary reflections this anthology proposes to tell the story of how efficient causation, equated nowadays with “causation” tout court, came to play its prominent role in our philosophical and scientific vocabulary. Eleven contributions cover the period from Ancient times (Aristotle and the Stoics), through the Middle Ages (both the Western and the Islamic traditions), passing through the Early Modern times (represented here by Descartes, Spinoza, Leibniz, Malebranche, Berkeley and Hume), all the way to Kant and finally contemporary philosophers (classified into two opposing camps: Humean and Neo-Aristotelian). There are also four reflections which explore the applications of the notion of efficient causation to areas different from philosophy, especially the arts (literature, music, painting, etc.). (shrink)

Absences pose a dilemma for theories of causation. Allowing them to be causes seems to make theories too permissive (Lewis, 2000). Banning them from being causes seems to make theories too restrictive (Schaffer, 2000, 2004). An increasingly popular approach to this dilemma is to acknowledge that norms can affect which absences count as causes (e.g., Thomson, 2003; McGrath, 2005; Henne et al., 2017; Willemsen, 2018). In this article, I distinguish between two influential implementations of such ‘abnormality’ approaches and argue (...) that so-called ‘double-prevention mechanisms’ provide counterexamples against both. (shrink)

In order to defend mental explanations dualists may appeal to dispositions (powers). By accepting a powers theory of causation, a dualist can more plausibly defend mental explanations that are given independently of physical explanations. Accepting a power-based theory still comes with a price. Absences and double preventers are not causes in a powers theory, and solutions based on them can only defend their explanatory relevance in mental explanations. There is still a chance that such mental explanations can be causal (...) explanations, though they do not refer to real causes. (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)

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)

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)

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.

In this paper, I consider the implications of grief for philosophical theorising about absence experience. I argue that whilst some absence experiences that occur in grief might be explained by extant philosophical accounts of absence experience, others need different treatment. I propose that grieving subjects' descriptions of feeling as if the world seems empty or a part of them seems missing can be understood as referring to a distinctive type of absence experience. In these profound (...) class='Hi'>absence experiences, I will argue, the absence of a person as a condition on various possibilities is made manifest in the structure of experience over time. Thus, by paying close attention to grief, we can see that even accounts of absence experience that are presented as in competition with one another may not be so, and that to explain all kinds of absence experience we sometimes need to appeal to something overlooked in other accounts, and which is neither straightforwardly perceptual or cognitive. I also suggest that we would have good reason to take such experiences to be part of and not merely psychological effects of grief. (shrink)

In this paper, I argue that absences pose a challenge to our understanding of physicalism that has not been properly appreciated. I do this by setting out a thought experiment involving a being in whom absence properties occupy the causal roles that functionalists take to define mental properties, in which case these absence properties realize the being’s mental properties. Such a being should be compatible with the truth of physicalism, I argue, even though its mental properties are neither (...) themselves physical properties nor are they realized/grounded in physical properties—instead, they are realized/grounded in (nonphysical) absence properties. I argue that the case serves as a counterexample to leading formulations of physicalism that appeal to realization or grounding, but not to standard supervenience-based formulations of physicalism, because the latter typically include negative truths in their supervenience base in addition to physical truths. I show how realization- and grounding-based formulations of physicalism might be revised to handle the problem, but also recommend that we rethink how we understand physicalism and the role that negative entities can play for physicalists. (shrink)

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.

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 this paper, I take a critical look at Sartorio’s book Causation and Free Will (2016). Sartorio offers a rich defence of an actual-sequence view of freedom, which pays close attention to issues in the philosophy of causation and how they relate to freedom. I argue that although this focus on causation is illuminating, Sartorio’s project nevertheless runs into some serious difficulties. Perhaps most worrying amongst them is whether the agent-based reason-sensitivity account, offered by Sartorio, is consistent (...) with Frankfurt-style cases – the very cases which are provided as the sole reason to endorse an actual-sequence view of freedom. I suggest that given that powers and causation are so intimately bound together, the debate is skewed somewhat by thinking of these as rivals. (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)

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)

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)

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 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.

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)

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)

This dissertation begins by addressing the question of when a causal model is apt for deciding questions of actual causation with respect to some target situation. I first provide relevant background about causal models, explain what makes them promising as a tool for analyzing actual causation, and motivate the need for a theory of aptness as part of such an analysis (Chapter 1). I then define what it is for a model on a given interpretation to be accurate (...) of, that is, say only true things about, some target situation. This involves a systematization of various representational principles mentioned and/or discussed throughout the literature into a method of interpretation, which I propose be taken as standard (Chapter 2). Next, I explain and address two reasons for which accuracy as I’ve defined it is insufficient for aptness. The first reason – already discussed in the literature – is the problem of structural isomorphs. In response, I propose the aptness condition of Explicit Partial Mediation (Chapter 3). The second reason – which has yet to be noticed – is the problem of the indeterminacy of accuracy. As I demonstrate, a model is accurate of a target situation only relative to a set of background possibilities – what I call a modal profile. It follows that a model represents a situation only relative to some modal profile or other. I go on to discuss the ramifications of this observation for a theory of actual causation in terms of models. I argue that the relativity be taken at face value and built into our metaphysical account of causation, resulting in a view that I call causal relativism (Chapter 4). I explore one advantage of this view in detail: that the resulting account can defend the principle of strong proportionality against several objections (Chapter 5). Finally, I apply the earlier discussion of aptness to attempts to provide a semantics of counterfactuals in terms of causal models – an interventionist semantics. I show how just as a similarity semantics relies on an opaque notion of similarity, an interventionist semantics relies on an analogous notion of aptness. The challenge of articulating aptness thus undermines the claim that an interventionist semantics avoids representational problems inherent in a similarity semantics (Chapter 6). I close with a recap and suggestions for future research (Chapter 7). -/- . (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 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)

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.

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)

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)

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

Extant research has shown that ordinary causal judgments are sensitive to normative factors. For instance, agents who violate a norm are standardly deemed more causal than norm-conforming agents in identical situations. In this paper, we explore two competing explanations for the Norm Effect: the Responsibility View and the Bias View. According to the former, the Norm Effect arises because ordinary causal judgment is intimately intertwined with moral responsibility. According to the alternative view, the Norm Effect is the result of a (...) blame-driven bias. In a series of five preregistered experiments (N = 2688), we present evidence that predominantly favours the Bias View. In particular, and against predictions made by the Responsibility View, we show that participants deem agents who violate nonpertinent or silly norms – norms that do not relate to the outcome at hand – as more causal, and that this effect cannot be explained in terms of plausible mediators such as the agent’s foreknowledge and desire, or the foreseeability of harm. We close with a discussion regarding the implications of these findings, in as regards the just assessment of proximate cause in the law. (shrink)