Causation is important when considering how an organism maintains health, why disease arises in a healthy person, and how one may intervene to change the course of a disease. This paper explores the form of causative relationships in health, disease and intervention, with particular regard to the pathological and biopsychosocial models. Consistent with the philosophical view of dispositionalism, we believe that objects are the fundamental relata of causation. By accepting the broad scope of the biopsychosocial model, we argue (...) that psychological and social constructs be considered objects. We think that this 'biopsychosocial dispositionalism' offers the flexibility required to describe causation throughout health, disease and intervention pathways. When constructing mechanistic chains to describe causative pathways, we argue that an object will causally connect with others through actions; transfers of energy from one object to another, initiated by the manifestation of one or more dispositional property. Finally, our analysis of causative interactions utilises the concept that a common form of interaction exists between disease and intervention pathways. This common form will always be an object, but the mode of interaction will vary with each disease. We describe how intervention may act through objects being shared between converging mechanistic chains, or through the removal and/or insertion of objects in such chains. We believe that this analysis provides novel insight to the forms of causative transactions that can occur. In addition, we hope that the findings of this analysis represent the first step towards developing a framework for appraising the composition of mechanistic theories. (shrink)

As is well-known, David Lewis’ counterfactual theory of causation is subject to serious counterexamples in ‘exceptional’ cases. What has not received due attention in the literature so far is that Lewis’ theory fails to provide necessary and sufficient conditions for causation in ‘ordinary’ cases, too. In particular, the theory suffers from the ‘problem of large causes’. It is argued that this problem may be fixed by imposing a minimization constraint, whilst this solution brings along substantial costs as (...) well. In particular, a precise formulation of minimization requires defining an ‘essential part of an event’ and/or an ‘essential subevent’. Although the possibility of such a definition is ultimately left open, some doubts are raised on whether the counterfactualists’ resources are fit for this purpose, and whether the challenge can be met without substantially departing from Lewis’ intention, which was to provide a reductive account of causation. (shrink)

Whipple disease is a rare, infectious, disease first described from a single case by Whipple in 1907. As well as characterising the clinical and pathological features of the condition, Whipple made two suggestions regarding its aetiology. These were either than the disease was caused by an infectious agent, or that it was of metabolic origin. As the disease is now thought to be caused by infection with the bacterium Tropheryma whipplei, historical reviews of the history of the disease typically mention (...) only the first of these suggestions. In this paper, we therefore revisit Whipple’s other theory. We argue that a diverse and often successful research programme was developed around this mechanism of disease causation which gave rise to many useful findings on the condition. In the later parts of this article, we then turn to discuss the surprising neglect of this period of Whipple disease research in the current literature, and conclude by offering a brief reconstruction of this early history suitable for use in a technical context. (shrink)

Causation is important when considering: how an organism maintains health; why disease arises in a healthy person; and, how one may intervene to change the course of a disease. This paper explores the form of causative relationships in health, disease and intervention, with particular regard to the pathological and biopsychosocial models. Consistent with the philosophical view of dispositionalism, we believe that objects are the fundamental relata of causation. By accepting the broad scope of the biopsychosocial model, we argue (...) that psychological and social constructs be considered objects. We think that this ‘biopsychosocial dispositionalism’ offers the flexibility required to describe causation throughout health, disease and intervention pathways. When constructing mechanistic chains to describe causative pathways, we argue that an object will causally connect with others through actions; transfers of energy from one object to another, initiated by the manifestation of one or more dispositional property. Finally, our analysis of causative interactions utilises the concept that a common form of interaction exists between disease and intervention pathways. This common form will always be an object, but the mode of interaction will vary with each disease. We describe how intervention may act through objects being shared between converging mechanistic chains, or through the removal and/or insertion of objects in such chains. We believe that this analysis provides novel insight to the forms of causative transactions that can occur. In addition, we hope that the findings of this analysis represent the first step towards developing a framework for appraising the composition of mechanistic theories. (shrink)

permits a sound and rigorously definable notion of ‘originating cause’ or causa causans—a type of transition event—of an outcome event. Mackie has famously suggested that causes form a family of ‘inus’ conditions, where an inus condition is ‘an insufficient but non-redundant part of an unnecessary but sufficient condition’. In this essay the needed concepts of BST theory are developed in detail, and it is then proved that the causae causantes of a given outcome event have exactly the structure of (...) a set of Mackie inus conditions. The proof requires the assumption that there is no EPR-like ‘funny business’. This seems enough to constitute a theory of ‘causation’ in at least one of its many senses. Introduction The cement of the universe Preliminaries 3.1 First definitions and postulates 3.2 Ontology: propositions 3.3 Ontology: initial events 3.4 Ontology: outcome events 3.5 Ontology: transition events 3.6 Propositional language applied to events Causae causantes 4.1 Causae causantes are basic primary transition events 4.2 Causae causantes of an outcome chain 4.3 No funny business Causae causantes and inns and inus conditions 5.1 Inns conditions of outcome chains: not quite 5.2 Inns conditions of outcome chains 5.3 Inns conditions of scattered outcome events 5.4 Inus conditions for disjunctive outcome events 5.5 Inns and inus conditions of transition events Counterfactual conditionals Appendix: Tense and modal connectives in BST. (shrink)

By contrasting Hippocratic and nineteenth century theories of disease, this paper describes important conceptual changes that have taken place in the history of medicine. Disease concepts are presented as causal networks that represent the relations among the symptoms, causes, and treatment of a disease. The transition to the germ theory of disease produced dramatic conceptual changes as the result of a radically new view of disease causation. An analogy between disease and fermentation was important for two of (...) the main developers of the germ theory of disease, Pasteur and Lister. Attention to the development of germ concepts shows the need for a referential account of conceptual change to complement a representational account. (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)

In this paper I offer an 'integrating account' of singular causation, where the term 'integrating' refers to the following program for analysing causation. There are two intuitions about causation, both of which face serious counterexamples when used as the basis for an analysis of causation. The 'process' intuition, which says that causes and effects are linked by concrete processes, runs into trouble with cases of 'misconnections', where an event which serves to prevent another fails to (...) do so on a particular occasion and yet the two events are linked by causal processes. The chance raising intuition, according to which causes raise the chance of their effects, easily accounts for misconnections but faces the problem of chance lowering causes, a problem easily accounted for by the process approach. The integrating program attempts to provide an analysis of singular causation by synthesising the two insights, so as to solve both problems. In this paper I show that extant versions of the integrating program due to Eells, Lewis, and Menzies fail to account for the chance-lowering counterexample. I offer a new diagnosis of the chance lowering case, and use that as a basis for an integrating account of causation which does solve both cases. In doing so, I accept various assumptions of the integrating program, in particular that there are no other problems with these two approaches. As an example of the process account, I focus on the recent CQ theory of Wesley Salmon (1997). (shrink)

Philosophers have long been fascinated by the connection between cause and effect: are 'causes' things we can experience, or are they concepts provided by our minds? The study of causation goes back to Aristotle, but resurged with David Hume and Immanuel Kant, and is now one of the most important topics in metaphysics. Most of the recent work done in this area has attempted to place causation in a deterministic, scientific, worldview. But what about the unpredictable and (...) chancey world we actually live in: can one theory of causation cover all instances of cause and effect? _Cause and Chance: Causation in an Indeterministic World _is a collection of specially written papers by world-class metaphysicians. Its focus is the problem facing the 'reductionist' approach to causation: the attempt to cover all types of causation, deterministic and indeterministic, with one basic theory. Contributors: Stephen Barker, Helen Beebee, Phil Dowe, Dorothy Edgington, Doug Ehring, Chris Hitchcock, Igal Kwart, Paul Noordhof, Murali Ramachandran and Michael Tooley. (shrink)

Presents an interpretation of David Hume's account of what a 'cause' is. This book emphasises on the connections between Hume's theories of cause, space and time, morals, and aesthetics.

There is, no doubt, a temptation to treat preventions, such as ‘the father’s grabbing the child prevented the accident’, and cases of ‘causation’ by omission, such as ‘the father’s inattention was the cause of the child’s accident’, as cases of genuine causation. I think they are not, and in this paper I defend a theory of what they are. More specifically, the counterfactual theory defended here is that a claim about prevention or ‘causation’ by omission should be (...) understood not as being directly about actual genuine causation but primarily as a counterfactual claim about genuine causation.1 The relation between actual causation and the mere possibility of causation allows my theory to explain both the difference and the similarity between the two notions (causation and prevention/omission). Further, the difference explains certain intuitions we have and the similarity justifies and explains the fact that for practical purposes we usually treat preventions and omissions as if they were genuine causation. Finally, the fact that this counterfactual theory of prevention and omission takes causation as primitive suggests that it is consistent with any theory of causation. This allows us to construct two arguments against what I will call genuinism, the view that cases of prevention and ‘causation’ by omission really are cases of genuine causation. In section II I show that genuinism does not account for the so-called intuition of difference. In section III I outline a number of problems that various theories of causation have with preventions and ‘causation’ by omission. These problems are ipso facto problems for genuinism, whereas I show in section V how the counterfactual theory solves those problems. Further, I answer a genuinist argument based on another type of intuition—the genuinist intuition—by showing why we have that intuition and how it should be handled (section VI). (shrink)

Using structural equations and directed graphs, Christopher Hitchcock (2007a) proposes a theory specifying the circumstances in which counterfactual dependence of one event e on another event c is necessary and sufficient for c to count as an actual cause of e. In this paper, we argue that Hitchcock is committed to a widely-endorsed folk attribution desideratum (FAD) for theories of actual causation. We then show experimentally that Hitchcock’s theory does not satisfy the FAD, and hence, it is in (...) need of revision. (shrink)

A recent paper by David Lewis, "Causation as Influence", proposes a new theory of causation. I argue against the theory, maintaining that (a) the relation asserted by a claim of the form "C was a cause of E" is distinct from the relation of causal influence, (b) the former relation depends very much, contra Lewis, on the individuation conditions for the event E, and (c) Lewis's account is unsatisfactory as an analysis of either kind of relation. The counterexamples (...) presented here provide, I suggest, some insight into the reasons for the failure of counterfactual accounts of causal relations. (shrink)

This article presents Roman Ingarden’s theory of causation, as developed in volume III of The Controversy about the Existence of the World, and defends analternative which uses some important insights of Ingarden. It rejects Ingarden’s claim that a cause is simultaneous with its effect and that a cause necessitates its effect. It uses Ingarden’s notion of ‘inclinations’ and accepts Ingarden’s claim that an event cannot necessitate a later event.

The problem of disease definition is related to theproblem of proving that a certain agent is thenecessary cause of a certain disease. Natural kindterms like ‘rheumatoid arthritis’ and ‘AIDS’ refer toessences which are discoverable rather thanpredeterminate. No statement about such diseases isa priori necessarily true. Because theories onnecessary causes involve natural kind semantics,Koch's postulates cannot be used to falsify or verifysuch theories. Instead of proving that agent A is thenecessary cause of disease D, we include A (...) in atheoretical definition of D, take this to representthe real meaning of ‘D’, and discard thepretheoretical definition. This is illustrated byKoch's own attempt to prove he had discovered thenecessary cause of tuberculosis. Methodologicalarguments about disease causation require a clear viewof our use of diagnostic terms. Medical lexicographersshould do more to provide such a view. (shrink)

A probabilistic theory of causation is a theory which holds that the central feature of causation is that causes raise the probability of their effects. In this dissertation, I defend Hans Reichenbach's original version of the probabilistic theory of causation, which analyses causal relations in terms of a three place statistical betweenness relation. Unlike most discussions of this theory, I hold that the statistical relation should be taken as a sufficient, but not as a necessary , (...) condition for causal betweenness. With this difference in interpretation, Reichenbach's theory is shown to be immune to all of the criticisms which have been raised against it in the last fifty years. ;Reichenbach's main purpose in defending a probabilistic theory of causation was to use it in giving an analysis of the direction of time. I defend this view, arguing that the arrow of causation is more basic than any of the other arrows of time---metaphysical, psychological or physical. In particular, I argue against the popular view that the direction of time is given by the physical fact that entropy only increases in one direction. I further show that the probabilistic theory of causation is particularly suited to the task of analysing the various arrows of time. In my final chapter, I also suggest that the probabilistic theory of causation may be fruitfully applied to the analysis of some important puzzles in the interpretation of quantum mechanics. (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)

In this paper today, I would like to offer a new analysis of causation and of causal claims. It is an unorthodox one, as you will see, but I suspect that in the not too distant future it will be seen as intuitively, perhaps even trivially, true. I hardly need defend the urgency of my project. Ever since Hume, philosophers have wondered whether there are causes. This is a desperate situation. With no causes, it's hard to see (...) how brushing my teeth is likely to prevent tooth decay. Indeed, it would not be unreasonable to read Hume as an advocate of rotten teeth, which might explain the sad state that many British mouths find themselves in today. The attentive listener will have noted that I said Hume's advocacy of rotten teeth might explain the abysmal state of British oral hygiene. Of course, if Hume is right about causation then nothing explains anything, and that explains why I have been tentative in my claim. The account I would like to propose is this. The claim ‘x causes y’ is to be understood in the following way: ‘x makes y happen’. That is, to say that x is the cause of y is just to say that x makes y happen. Or, to put it more succinctly, if x is the cause of y, then x makes y happen. This is no doubt a startling claim, and one in need of further clarification and defense. To begin, I should like to contrast my analysis with another that might, on its surface, appear similar. Suppose one were to claim that 'x is the cause of y' means that x brings y about. But ‘bringing about’ is hardly an informative verbal clause, and does little ampliative work. This way of putting it lacks the opaque transparency that we’ve come to expect of philosophical analyses of causation. Now this new account is not necessarily inconsistent with other, more traditional analyses, such as Lewis and Hausman's analyses of causation in terms of counterfactuals or Eells' probabilistic theory of causation. Consider first counterfactual analyses of causation. These are efforts to account for the meaning of causal dependencies.. (shrink)

Mellor´s theory of causation has two components, one according to which causes raise their effects´ chances, and one according to which causation links facts. I argue that these two components are not independent from each other and, in particular, that Mellor´s thesis that causation links facts requires his thesis that causes raise their effects´ chances, since without the latter thesis Mellor cannot stop the slingshot argument, an argument that is a threat to any theory postulating (...) facts as the relata of causation. (shrink)

The paper begins with a discussion of Russell's view that the notion of cause is unnecessary for science and can therefore be eliminated. It is argued that this is true for theoretical physics but untrue for medicine, where the notion of cause plays a central role. Medical theories are closely connected with practical action (attempts to cure and prevent disease), whereas theoretical physics is more remote from applications. This suggests the view that causal laws are appropriate in a context (...) where there is a close connection to action. This leads to a development of an action-related theory of causality which is similar to the agency theory of Menzies and Price, but differs from it in a number of respects, one of which is the following. Menzies and Price connect ‘A causes B’ with an action to produce B by instantiating A, but, particularly in the case of medicine, the law can also be linked to the action of trying to avoid B by ensuring that A is not instantiated. The action-related theory has in common with the agency theory of Menzies and Price the ability to explain causal asymmetry in a simple fashion, but the introduction of avoidance actions together with some ideas taken from Russell enable some of the objections to agency accounts of causality to be met. Introduction Russell on causality Preliminary exposition of the action-related theory Differences between the action-related theory and the agency theory of Menzies and Price Explanation of causal asymmetry Objections to the action-related theory Extension of the theory to the indeterminate case. (shrink)

A common objection to probabilistic theories of causation is that there are prima facie causes that lower the probability of their effects. Among the many replies to this objection, little attention has been given to Mellor's (1995) indirect strategy to deny that probability-lowering factors are bona fide causes. According to Mellor, such factors do not satisfy the evidential, explanatory, and instrumental connotations of causation. The paper argues that the evidential connotation only entails an epistemically relativized (...) form of causal attribution, not causation itself, and that there are clear cases of explanation and instrumental reasoning that must appeal to negatively relevant factors. In the end, it suggests a more liberal interpretation of causation that restores its connotations. Una objeción común a las teorías probabilísticas de la causalidad es que aparentemente existen causas que disminuyen la probabilidad de sus efectos. Entre las muchas respuestas a esta objeción, se le ha dado poca atención a la estrategia indirecta de D. H. Mellor (1995) para negar que un factor que disminuya la probabilidad de un efecto sea una causa legítima. Según Mellor, tales factores no satisfacen las connotaciones evidenciales, explicativas e instrumentales de la causalidad. El artículo argumenta que la connotación evidencial sólo implica una forma epistémicamente relativizada de atribución causal y no la causalidad misma, y que hay casos claros de explicación y razonamiento instrumental que deben apelar a factores negativamente relevantes. Se sugiere una interpretación más liberal de la causalidad que reinstaura sus connotaciones. (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)

A discussion of Aristotle’s thought on determinism and culpability, Necessity, Cause, and Blame also reveals Richard Sorabji’s own philosophical commitments. He makes the original argument here that Aristotle separates the notions of necessity and cause, rejecting both the idea that all events are necessarily determined as well as the idea that a non-necessitated event must also be non-caused. In support of this argument, Sorabji engages in a wide-ranging discussion of explanation, time, free will, essence, and purpose in nature. He also (...) provides historical perspective, arguing that these problems remain intimately bound up with modern controversies. “ Necessity, Cause and Blame would be counted by all as one of Sorabji’s finest. The book is essential for philosophers—both specialists on the Greeks and modern thinkers about free will—and also compelling for non-specialists.”—Martha Nussbaum “Original and important . . . The book relates Aristotle’s discussions to both the contemporary debates on determinism and causation and the ancient ones. It is especially detailed on Stoic arguments about necessity . . . and on the social and legal background to Aristotle’s thought.”— Choice “It is difficult to convey the extraordinary richness of this book. . . . A Greekless philosopher could read it with pleasure . . . At the same time, its learning and scholarship are enormous.”—G. E. M. Anscombe, Times Literary Supplement. (shrink)

ABSTRACT: A systematic reconstruction of Chrysippus’ theory of causes, grounded on the Stoic tenets that causes are bodies, that they are relative, and that all causation can ultimately be traced back to the one ‘active principle’ which pervades all things. I argue that Chrysippus neither developed a finished taxonomy of causes, nor intended to do so, and that he did not have a set of technical terms for mutually exclusive classes of causes. Rather, the various (...) adjectives which he used for causes had the function of describing or explaining particular features of certain causes in particular philosophical contexts. I challenge the sometimes assumed close connection of Chrysippus’ notion of causation with explanation. I show that the standard view that the distinction between proximate and auxiliary causes and perfect and principal causes corresponds to the distinction between internal and external determining factors is not born out by the evidence, and argue that causes of the two types were not thought to co-operate, but rather conceived of as alternatives. (shrink)

ABSTRACT This article studies the theory of animal seeds as purely material entities in the early seventeenth-century medical writings of Antonio Ponce Santacruz, royal physician to the Spanish king Philipp IV. Santacruz adopts the theory of the eduction of substantial forms from the potentiality of matter, according to which new kinds of causal powers can arise out of material composites of a certain complexity. Santacruz stands out among the late Aristotelian defenders of eduction theory because he applies the concept of (...) an instrument of direction developed by the medieval Avicenna commentator Gentile da Foligno and gives a novel turn to this concept by interpreting animal seeds as separate instruments. The article situates Santacruz's theory in the context of early modern debates about the concept of the eduction of forms, as well as in the context of early modern debates about the concept of separate instruments. Particular attention is paid to Santacruz's responses to the biological views of Julius Caesar Scaliger and Thomas Feyens. Santacruz's response to Scaliger turns out to be central for his explication of the eduction relation, and Santacruz's response to Feyens turns out to be central for his explication of the nature of instrumental causation. (shrink)

_ Source: _Volume 10, Issue 3, pp 349 - 369 A theory of causation suitable for historiography must accommodate the many types of causal claims historians make. In this paper, I examine the advantages of applying D. K. Lewis’s counterfactual theory of causation to the philosophy of historiography. I contend that Lewis’s possible world semantics offers a superior framework for making sense of historical causation, and that it lays the foundation for historians to look at history as (...) causal series of events, remaining agnostic as to whether there may be historical regularities or laws. Lewis’s theory can also accommodate important notions often used by historians, such as absences as causes, historical necessity and contingency, and the role they play in the formulation of historical counterfactuals. (shrink)

In this doctoral thesis, I will argue that in his De motu (1721, ‘On motion’), Bishop George Berkeley (c.1684–1753) develops a pragmatist theory of causation regarding mechanical theories outlined previously with Newtonianism. I place chief emphasis on the importance of logic and mathematics in Berkeley’s scientific approach, on which the other levels of semantics, epistemology, and mechanics build up. On my rendering, Berkeley’s pragmatic method to conceive or mathematically imagine causation makes sense in terms of mechanical (...) class='Hi'>causes or ‘mathematical hypotheses’. For the mechanist maintains the usefulness and truthfulness of causation by the following definition. Definition. A pragmatist theory of causation is one which holds that: 1 Causal terms are indispensable in scientific deliberation for their usefulness; they cannot be eliminated [contra reductionism]. 2 What a cause is is defined by one’s temporal deliberative practices, independent of a temporal structure that theories hold [contra structuralism]. 3 Causal laws (theories formulated in causal terms) are genuinely true, not fictitious, when one confirms and deduces them [contra instrumentalism]. By justifying this definition, I will object to three rival readings—reductionism, structuralism, and instrumentalism—to my reading of Berkeley as a pragmatist about causation. In particular, my pragmatist reading criticises the most popular instrumentalist reading because, according to the latter, talk of causal terms like forces can be false or merely fictitious inasmuch as one can hold the utility of theories in mechanical practices. The instrumentalist reading is then compatible with mathematical formalism, according to which it is not truth or meaning that counts as formal manipulation or game of meaningless symbols, thereby eschewing a platonist attitude towards mathematical objects. However, I rebut the formalistic instrumentalism from Berkeley’s logical and realist standpoint, maintaining the irreducibility of occult qualities that mathematical objects have in their formulation from hypotheses to propositions. Light shall be shed on the tenet I propose that law-propositions formulated in hypothetical, causal terms must be true, neither false nor fictitious, when we (1) frame, (2) confirm, and (3) express them to the extent of our discursive thinking (in three steps). [339 words]. (shrink)

The Agency and the Manipulability theory of causation, in spite of significant differences, share at least three claims. First, that manipulation – roughly, that by manipulating causes we bring about effects – is a central notion for causation; second, that such a notion of manipulation allows a reductive – i.e. general and comprehensive – account of causation; third, that this view has its forefathers in the works of Collingwood, Gasking and von Wright. This paper mainly challenges (...) the third claim and argues that the misreading of those authors leads to a more dangerous consequence: a confusion between epistemological, metaphysical and methodological issues about causation. (shrink)

What is the connection between causation and responsibility? Is there a best way to theorize philosophically about causation? Which factors determine and influence what we judge to be the cause of something? Bringing together interdisciplinary research from experimental philosophy, traditional philosophy and psychology, this collection showcases the most recent developments and approaches to questions about causation. Chapters discuss the diverse theoretical ramifications of empirical findings in experimental philosophy of causation, providing a comprehensive survey of key issues (...) such as the perception and learning of causal relations, omission, normative considerations, mechanism, voluntariness and legal theories of causation. With novel contributions from both experts and rising stars, Advances in Experimental Philosophy of Causation demonstrates the value of empirical work and opens new domains of inquiry at the cutting edge of the field. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:On Concepts and Theories of AddictionLennart Nordenfelt (bio)Keywordsaddiction, disease, will power, autonomy, holistic view of healthThe article "A Liberal Account of Addiction" is a good piece of analytic philosophy applied to psychiatry. It is well-informed both with regard to empirical matters and philosophical conceptualization. The arguments are often—but, as I will show, not always—quite convincing. The conclusions of the paper also have crucial consequences for practice, for the (...) treatment of patients, and for social policy.The authors argue that current scientific understandings of the problem of addiction are fundamentally flawed. They distinguish between two main positions in science: The Disease View and the Willpower View. According to the Disease View, drug-seeking behavior is the direct result of some physiological change in the drug seeker's brain. According to the Willpower View, the addict is no longer rational; he or she uses drugs as a result of a fundamentally non-voluntary process.The authors dismiss the Disease View in the following way. They first note that drug addicts are in many ways rational planners. The addicts may have to think a lot to find the best ways to find the heroin, cigarettes, or alcohol, and they normally act according to this planning. They are not in any simple sense "caused" to act in a particular way. Moreover, referring to recent neurological literature, the authors note that the changes caused by drug addiction—which have to do with activating reward pathways in the brain—are identical with the outcomes of many other human activities that we do not call addiction. "In fact, any pleasurable experience causes dopamine to be released within the brain, activating these reward pathways" (Foddy and Savulescu 2010, 4). These experiences can be the result of coffee drinking, sexual activity, and physical exercise. Thus, the physical changes in the brain are not effects peculiar to the pharmacology of the drugs; they are instead the effects of the pleasure that the subject has experienced.The argument against the Willpower View is lengthy and more involved. The proponent of the Willpower View must argue that there is some flaw in the subject's autonomy. The drug addict is in some sense unable to avoid taking the drug. The authors of the present article scrutinize this idea on the basis of distinguishing between different senses of autonomy: Substantive autonomy and procedural autonomy. They state that we must here be talking about procedural autonomy, namely, autonomy regarded as dependent only on our capacity to process information and make choices in accordance with our preferences. We cannot, as in the case of substantive autonomy, require that the preferences themselves be reasonable. [End Page 27] In such a case, many of our ordinary actions would be judged non-autonomous.The most reasonable Willpower accounts rely on the idea that addicted people in some sense lack self-control. The authors cite different interpretations of the concept of lacking self- control and they conclude that "none of these … theories can say that addicts are necessarily lacking in self-control unless they also make unreasonable normative or false factual claims about the nature of drug- or pleasure-oriented choices" (Foddy and Savulescu 2010, 10). For instance, according to one interpretation the subject does not endorse his own desire for drugs, but takes the drug anyway. According to another interpretation, the addict regrets taking the drug after having done so. Against such claims the authors claim that many addicts indeed endorse their desires for drugs and many addicts do not regret their addictive behavior.So what is the positive account proposed by the authors? They put forward what they call a Liberal View. It contains three claims about addiction: First, we do not know whether an addict values anything more than the satisfaction of his addictive desires; second, we do not know whether an addict behaves autonomously when he uses drugs; and third, addictive desires are just strong regular desires.According to the Liberal View, one has to accept that the addicts may have drug taking as their highest priority and that they do not have any reduced procedural autonomy. The authors say: "Once we abandon normative bias, we must accept... (shrink)

This dissertation presents a new interpretation of Rene Descartes' views on body/body causation by examining them within their historical context. Although Descartes gives the impression that his views constitute a complete break with those of his predecessors, he draws on both Scholastic Aristotelian concepts of the efficient cause and existing anti-Aristotelian views. ;The combination of Aristotelian and anti-Aristotelian elements in Descartes' theory of causation creates a tension in his claims about the relationship between the first cause, God, and (...) the secondary causes, created things. To make sense of Descartes' position on secondary causation I study the 16th and 17th century debates on secondary causation, God's concurrence, and the action of efficient causes. I examine the Aristotelian commentaries of the Jesuit philosophers Francisco Suarez, Francisco Toledo, Antonio Rubio and the Coimbran Commentators. I also analyze the anti-Aristotelian views on nature and causation found in Sebastian Basson's textbook on natural philosophy. ;The Jesuit philosophers, like Descartes, deny that the extendedness and impenetrability of matter requires the existence of occult forces to penetrate the matter and exercise causality. Rather they argue that causality is exercised by a thing's form and that causal interaction requires only contiguity not penetration. They also downplay the importance of the final cause, making the efficient cause prior in the study of nature. While Descartes rejects their hylomorphism, he agrees with the Jesuits that there are secondary efficient causes which determine God's action, causing a specific kind of effect. However, for Descartes the secondary causes are the laws of nature, not individual substances. ;Descartes' reduction of all natural change to the local motion of material particles is reminiscent of Basson's anti-Aristotelian natural philosophy. Basson reacts against the Jesuit view of secondary causation, arguing that it commits them to attributing cognition to physical causes. His own account of natural causation contains both mechanistic elements, which we find in a more developed form in Descartes' philosophy, and Neoplatonic and Stoic elements which Descartes rejects. (shrink)

I will argue for the similarity between some aspects of Aristotle’s doctrine of causes and a particular kind of interventionist theory of causality. The interventionist account hypothesizes that there is a connection between causation and human intervention: the idea of a causal relation between two events is generated by the reflection of human beings on their own operating. This view is remindful of the Aristotelian concept of αἴτιον, which is linked to the figure of the αἴτιος, the person (...) who is responsible of an action. Aristotle conceives of the efficient cause as the active element which, in the φύσις, gives rise to movement and imposes the form, in analogy with the active element that in τέχνη operates the production: the craftsman. This analogy suggests that Aristotle conceives of the causation on the basis of the human ability to modify the environment with aims. Within the debate on the manipulative theory the classical accounts worked out by Collingwood, Gasking and von Wright have been recently criticized by Woodward. von Wright’s reductive account explains causation on the basis of human free action, while Woodward regards this reduction as a dangerous move which makes causal explanations too much anthropomorphic. I will show that Aristotle’s doctrine of causes is more similar to von Wright’s account and that the Aristotelian analysis of becoming supports von Wright’s reductive interventionism against Woodward’s criticism. Furthermore, I will draw a comparison between interventionism and dispositionalism, where the latter is another contemporary account of causation that claims Aristotelian roots. (shrink)

I will argue for the similarity between some aspects of Aristotle’s doctrine of causes and a particular kind of interventionist theory of causality. The interventionist account hypothesizes that there is a connection between causation and human intervention: the idea of a causal relation between two events is generated by the reflection of human beings on their own operating. This view is remindful of the Aristotelian concept of αἴτιον, which is linked to the figure of the αἴτιος, the person (...) who is responsible of an action. Aristotle conceives of the efficient cause as the active element which, in the φύσις, gives rise to movement and imposes the form, in analogy with the active element that in τέχνη operates the production: the craftsman. This analogy suggests that Aristotle conceives of the causation on the basis of the human ability to modify the environment with aims. Within the debate on the manipulative theory the classical accounts worked out by Collingwood, Gasking and von Wright have been recently criticized by Woodward. von Wright’s reductive account explains causation on the basis of human free action, while Woodward regards this reduction as a dangerous move which makes causal explanations too much anthropomorphic. I will show that Aristotle’s doctrine of causes is more similar to von Wright’s account and that the Aristotelian analysis of becoming supports von Wright’s reductive interventionism against Woodward’s criticism. Furthermore, I will draw a comparison between interventionism and dispositionalism, where the latter is another contemporary account of causation that claims Aristotelian roots. (shrink)

Is the common cause principle merely one of a set of useful heuristics for discovering causal relations, or is it rather a piece of heavy duty metaphysics, capable of grounding the direction of causation itself? Since the principle was introduced in Reichenbach’s groundbreaking work The Direction of Time (1956), there have been a series of attempts to pursue the latter program—to take the probabilistic relationships constitutive of the principle of the common cause and use them to ground the direction (...) of causation. These attempts have not all explicitly appealed to the principle as originally formulated; it has also appeared in the guise of independence conditions, counterfactual overdetermination, and, in the causal modelling literature, as the causal markov condition. In this paper, I identify a set of difficulties for grounding the asymmetry of causation on the principle and its descendents. The first difficulty, concerning what I call the vertical placement of causation, consists of a tension between considerations that drive towards the macroscopic scale, and considerations that drive towards the microscopic scale—the worry is that these considerations cannot both be comfortably accommodated. The second difficulty consists of a novel potential counterexample to the principle based on the familiar Einstein Podolsky Rosen (EPR) correlations in quantum mechanics. (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)

Epidemiologists’ discussions on causation are not always very enlightening with regard to the notion of ‘cause’ in epidemiology. Epidemiologists rightly work from a science-based approach to causation in epidemiology, but largely disagree about the matter. Disagreement may be partly due to confusion of the question of useful concepts for causal inference in epidemiological practice with the question of the metaphysical presuppositions of causal concepts used in epidemiology. In other words, epidemiologists seem to confuse the practical results of epidemiological (...) research at the population level with the metaphysical views about the reality of disease causation at the individual level in their writings on causation. (shrink)

Why do people get sick? I argue that a disease explanation is best thought of as causal network instantiation, where a causal network describes the interrelations among multiple factors, and instantiation consists of observational or hypothetical assignment of factors to the patient whose disease is being explained. This paper first discusses inference from correlation to causation, integrating recent psychological discussions of causal reasoning with epidemiological approaches to understanding disease causation, particularly concerning ulcers and lung cancer. It then shows (...) how causal mechanisms represented by causal networks can contribute to reasoning involving correlation and causation. The understanding of causation and causal mechanisms provides the basis for a presentation of the causal network instantiation model of medical explanation. (shrink)

The paper argues that the reconciliation of the Causal Theory of Perception with Disjunctivism requires the rejection of causal particularism – the idea that the ontology of causation is always and everywhere an ontology of particulars (e.g., events). The so-called ‘Humean Principle’ that causes must be distinct from their effects is argued to be a genuine barrier to any purported reconciliation, provided causal particularism is retained; but extensive arguments are provided for the rejection of causal particularism. It is (...) then explained how the reconciliation of the causal theory with disjunctivism can proceed on the basis of an ontology of facts. (shrink)

Sungho Choi has criticised Michael Strevens's counterexample to DavidLewis's final theory of "token" causation, causation as "influence." Iargue that, even if Choi's points are correct, Strevens's counterexampleremains useful in revealing a shortcoming of Lewis's theory. Thisshortcoming is that Lewis's theory does not properly account for*degrees* of causation. That is, even if Choi's points are correct,Lewis's theory does not capture an intuition we have about the*comparative* causal statuses of those events involved in Strevens'scounterexample (we might, for example, intuit (...) that Sylvie's ball-firingis *as much*/*more*/*less* a cause of the jar's shattering as/than isBruno's ball-firing). (shrink)

The paper argues that the reconciliation of the Causal Theory of Perception with Disjunctivism requires the rejection of causal particularism – the idea that the ontology of causation is always and everywhere an ontology of particulars (e.g., events). The so-called ‘Humean Principle’ that causes must be distinct from their effects is argued to be a genuine barrier to any purported reconciliation, provided causal particularism is retained; but extensive arguments are provided for the rejection of causal particularism. It is (...) then explained how the reconciliation of the causal theory with disjunctivism can proceed on the basis of an ontology of facts. (shrink)