Laws of nature take center stage in philosophy of science. Laws are usually believed to stand in a tight conceptual relation to many important key concepts such as causation, explanation, confirmation, determinism, counterfactuals etc. Traditionally, philosophers of science have focused on physical laws, which were taken to be at least true, universal statements that support counterfactual claims. But, although this claim about laws might be true with respect to physics, laws in the special sciences (such as biology, psychology, economics etc.) (...) appear to have—maybe not surprisingly—different features than the laws of physics. Special science laws—for instance, the economic law “Under the condition of perfect competition, an increase of demand of a commodity leads to an increase of price, given that the quantity of the supplied commodity remains constant” and, in biology, Mendel's Laws—are usually taken to “have exceptions”, to be “non-universal” or “to be ceteris paribus laws”. How and whether the laws of physics and the laws of the special sciences differ is one of the crucial questions motivating the debate on ceteris paribus laws. Another major, controversial question concerns the determination of the precise meaning of “ceteris paribus”. Philosophers have attempted to explicate the meaning of ceteris paribus clauses in different ways. The question of meaning is connected to the problem of empirical content, i.e., the question whether ceteris paribus laws have non-trivial and empirically testable content. Since many philosophers have argued that ceteris paribus laws lack empirically testable content, this problem constitutes a major challenge to a theory of ceteris paribus laws. (shrink)

Framing systematics as a field consistent with scientific inquiry entails that inferences of phylogenetic hypotheses have the goal of producing accounts of past causal events that explain differentially shared characters among organisms. Linking observations of characters to inferences occurs by way of why-questions implied by data matrices. Because of their form, why-questions require the use of common-cause theories. Such theories in phylogenetic inferences include natural selection and genetic drift. Selection or drift can explain ‘morphological’ characters but selection cannot be causally (...) applied to sequences since fitness differences cannot be directly associated with individual nucleotides or amino acids. The relation of selection to sequence data is by way of downward or top-down causation from those phenotypes upon which selection occurs. The application of phylogenetic inference to explain sequence data is thus restricted to instances where drift is the relevant theory; those nucleotides or amino acids that can be explained via downward causation are precluded from inclusion in the data matrix. The restrictions on the inclusion of sequence data in phylogenetic inferences equally apply to species hypotheses, precluding the more restrictive approach known as DNA barcoding. Not being able to discern drift and selection as relevant causal mechanisms can severely constrain the inclusion and explanations of sequence data. Implications of such exclusion are discussed in relation to the requirement of total evidence. (shrink)

Theories of explanation seek to tell us what distinctively explanatory information is. The most ambitious ones, such as the DN-account, seek to tell us what an explanation is, tout court. Less ambitious ones, such as causal theories, restrict themselves to a particular domain of inquiry. The least ambitious theories constitute outright skepticism, holding that there is no reasonably unified phenomenon to give an account of. On these views, it is impossible to give any theories of explanation at all. I argue (...) that both the less ambitious and outright skeptical varieties are committed to a certain context-sensitivity of our explanatory discourse. And though this discourse is almost certainly context-sensitive in some respects, it does not exhibit the context-sensitivity less than fully ambitious theories are committed to. Therefore, all accounts that seek to restrict themselves in scope, including causal accounts of explanation, fail. (shrink)

The dilemma of free will is that if actions are caused deterministically, then they are not free, and if they are not caused deterministically then they are not free either because then they happen by chance and are not up to the agent. I propose a conception of free will that solves this dilemma. It can be called agent causation but it differs from what Chisholm and others have called so.

Causal reasoning is one of our most central cognitive competencies, enabling us to adapt to our world. Causal knowledge allows us to predict future events, or diagnose the causes of observed facts. We plan actions and solve problems using knowledge about cause-effect relations. Without our ability to discover and empirically test causal theories, we would not have made progress in various empirical sciences. In the past decades, the important role of causal knowledge has been discovered in many areas of cognitive (...) psychology. Despite the ubiquity of causal reasoning, textbooks of cognitive psychology have neglected this growing field. The goal of The Oxford Handbook of Causal Reasoning is to fill this gap. The handbook brings together the leading researchers in the field of causal reasoning and offers state-of-the-art presentations of theories and research. It provides introductions of competing theories of causal reasoning, and discusses its role in various cognitive functions and domains. The final section presents research from neighboring fields. 1. Causal Reasoning: An Introduction Michael R. Waldmann Part I: Theories of Causal Cognition 2. Associative Accounts of Causal Cognition Mike E. Le Pelley, Oren Griffiths, and Tom Beesley 3. Rules of Causal Judgment: Mapping Statistical Information Onto Causal Beliefs José C. Perales, Andrés Catena, Antonio Cándido, and Antonio Maldonado 4. The Inferential Reasoning Theory of Causal Learning: Toward a Multi- Process Propositional Account Yannick Boddez, Jan De Houwer, and Tom Beckers 5. Causal Invariance as an Essential Constraint for Creating a Causal Representation of the World: Generalizing the Invariance of Causal Power Patricia W. Cheng and Hongjing Lu 6. The Acquisition and Use of Causal Structure Knowledge Benjamin Margolin Rottman 7. Formalizing Prior Knowledge in Causal Induction Thomas L. Griffiths 8. Causal Mechanisms Samuel G. B. Johnson and Woo-kyoung Ahn 9. Force Dynamics and Causation Phillip Wolff and Robert Thorstad 10. Mental Models and Causation P. N. Johnson- Laird and Sangeet S. Khemlani 11. Pseudocontingencies Klaus Fiedler and Florian Kutzner 12. Singular Causation David Danks 13. Cognitive Neuroscience of Causal Reasoning Joachim T. Operskalski and Aron K. Barbey Part II: Basic Cognitive Functions 14. Visual Impressions of Causality Peter White 15. Goal-Directed Actions Bernhard Hommel 16. Planning and Control Magda Osman 17. Reinforcement Learning and Causal Models Samuel J. Gershman 18. Causation and the Probability of Causal Conditionals David E. Over 19. Causal Models and Conditional Reasoning Mike Oaksford and Nick Chater 20. Concepts as Causal Models: Categorization Bob Rehder 21. Concepts as Causal Models: Induction Bob Rehder 22. Causal Explanation Tania Lombrozo and Nadya Vasilyeva 23. Diagnostic Reasoning Björn Meder and Ralf Mayrhofer 24. Inferring Causal Relations by Analogy Keith J. Holyoak and Hee-Seung Lee 25. Causal Argument Ulrike Hahn, Roland Bluhm, and Frank Zenker 26. Causality in Decision- Making York Hagmayer and Philip M. Fernbach Part III: Domains of Causal Reasoning 27. Intuitive Theories Tobias Gerstenberg and Joshua B. Tenenbaum 28. Space, Time, and Causality Marc J. Buehner 29. Causation in Legal and Moral Reasoning David A. Lagnado and Tobias Gerstenberg 30. The Role of Causal Knowledge in Reasoning About Mental Disorders Woo-kyoung Ahn, Nancy S. Kim, and Matthew S. Lebowitz 31. Causality and Causal Reasoning in Natural Language Torgrim Solstad and Oliver Bott 32. Social Attribution and Explanation Denis Hilton Part IV: Development, Phylogeny, and Culture 33. The Development of Causal Reasoning Paul Muentener and Elizabeth Bonawitz 34. Causal Reasoning in Non-Human Animals Christian Schloegl and Julia Fischer 35. Causal Cognition and Culture Andrea Bender, Sieghard Beller, and Douglas L. Medin. (shrink)

Causal knowledge unquestionably provides useful means to describe, explain and predict both natural and daily phenomena. This article addresses whether causality as such may not be ontologically primary and looks for an alternative fundamental mechanism encapsulating the information load of the causal framework. A probabilistic process view of reality asserting the struggle of natural forces is considered along with lines quoted from Nietzsche’s posthumously published notebooks and published work. Examples from scientific discoveries, in particular neurosciences, echoing his ontology are provided. (...) Furthermore, I propose a basic number game algorithm to illustrate and model the struggle of forces leading to causal inferences for an external observer. Nietzschean dynamic ontology involving the ceaseless struggle of will-to-power units accords with the emergentist approach to causation, which has been principally employed by the scientists working under the fields of thermodynamics, quantum mechanics and complex dynamical systems. (shrink)

This paper defends a counterfactual account of explanation, according to which successful explanation requires tracing patterns of counterfactual dependence of a special sort, involving what I call active counterfactuals. Explanations having this feature must appeal to generalizations that are invariant--stable under certain sorts of changes. These ideas are illustrated by examples drawn from physics and econometrics.

This article defends the use of interventionist counterfactuals to elucidate causal and explanatory claims against criticisms advanced by James Bogen and Peter Machamer. Against Bogen, I argue that counterfactual claims concerning what would happen under interventions are meaningful and have determinate truth values, even in a deterministic world. I also argue, against both Machamer and Bogen, that we need to appeal to counterfactuals to capture the notions like causal relevance and causal mechanism. Contrary to what both authors suppose, counterfactuals are (...) not "unscientific" - a substantial tradition within statistics and the causal modelling literature makes heavy use of them. (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)

A common strategy for simplifying complex systems involves partitioning them into subsystems whose behaviors are roughly independent of one another at shorter timescales. Dynamic causal models clarify how doing so reveals a system’s nonequilibrium causal relationships. Here I use these models to elucidate the idealizations and abstractions involved in representing a system at a timescale. The models reveal that key features of causal representations—such as which variables are exogenous—may vary with the timescale at which a system is considered. This has (...) implications for debates regarding which systems can be represented causally. (shrink)

Causal representations are distinguished from non-causal ones by their ability to predict the results of interventions. This widely-accepted view suggests the following adequacy condition for causal models: a causal model is adequate only if it does not contain variables regarding which it makes systematically false predictions about the results of interventions. Here I argue that this condition should be rejected. For a class of equilibrium systems, there will be two incompatible causal models depending on whether one intervenes upon a certain (...) variable to fix its value, or ‘lets go’ of the variable and allows it to vary. The latter model will fail to predict the result of interventions on the let-go-of variable. I argue that there is no basis for preferring one of these models to the other, and thus that models failing to predict interventions on particular variables can be just as adequate as those making no such false predictions. This undermines a key argument against relying upon causal models inferred from equilibrium data. (shrink)

Causal representations are distinguished from non-causal ones by their ability to predict the results of interventions. This widely-accepted view suggests the following adequacy condition for causal models: a causal model is adequate only if it does not contain variables regarding which it makes systematically false predictions about the results of interventions. Here I argue that this condition should be rejected. For a class of equilibrium systems, there will be two incompatible causal models depending on whether one intervenes upon a certain (...) variable to fix its value, or ‘lets go’ of the variable and allows it to vary. The latter model will fail to predict the result of interventions on the let-go-of variable. I argue that there is no basis for preferring one of these models to the other, and thus that models failing to predict interventions on particular variables can be just as adequate as those making no such false predictions. This undermines a key argument (Dash in Caveats for causal reasoning with equilibrium models. University of Pittsburgh. PhD thesis, 2003) against relying upon causal models inferred from equilibrium data. (shrink)

In the current literature on scientific explanation unification became unfashionable in favour of causal approaches. We want to bring unification back into the picture. In this paper we demonstrate that resemblance questions do occur in scientific practice and that they cannot be properly answered without unification. Our examples show that resemblance questions about particular facts demand what we call causal network unification, while resemblance questions about regularities require what we call mechanism unification. We clarify how these types of unification relate (...) to Philip Kitcher’s account, but also to causal and mechanistic accounts of explanation. (shrink)

In a recent article in this journal, Federica Russo and Jon Williamson argue that an analysis of causality in terms of probabilistic relationships does not do justice to the use of mechanistic evidence to support causal claims. I will present Ronald Giere's theory of probabilistic causation, and show that it can account for the use of mechanistic evidence (both in the health sciences—on which Russo and Williamson focus—and elsewhere). I also review some other probabilistic theories of causation (of Suppes, Eells, (...) and Humphreys) and show that they cannot account for the use of mechanistic evidence. I argue that these theories are also inferior to Giere's theory in other respects. (shrink)

The goal of research in social epidemiology is not simply conceptual clarification or theoretical understanding, but more importantly it is to contribute to, and enhance the health of populations (and so, too, the people who constitute those populations). Undoubtedly, understanding how various individual risk factors such as smoking and obesity affect the health of people does contribute to this goal. However, what is distinctive of much on-going work in social epidemiology is the view that analyses making use of individual-level variables (...) is not enough. In the spirit of Durkheim and Weber, S. Leonard Syme makes this point by writing that just “as bad water and food may be harmful to our health, unhealthful forces in our society may be detrimental to our capacity to make choices and to form opinions” conducive to health and well-being. Advocates of upstream (distal) causes of adverse health outcomes propose to identify the most important of these “unhealthful forces” as the fundamental causes of adverse health outcomes. However, without a clear, theoretically precise and well-grounded understanding of the characteristics of fundamental causes, there is little hope in applying the statistical tools of the health sciences to hypotheses about fundamental causes, their outcomes, and policies intended to enhance the health of populations. This paper begins the process of characterizing the social epidemiological concept of fundamental cause in a theoretically respectable and robust way. (shrink)

The failure to recognize a correlation as spurious can lead people to adopt strategies to bring about a specific outcome that manipulate something other than a cause of the outcome. However, in a 2008 paper appearing in the journal Analysis, Bert Leuridan, Erik Weber and Maarten Van Dyck suggest that knowledge of spurious correlations can, at least sometimes, justify adopting a strategy aiming at bringing about some change. This claim is surprising and, if true, throws into question the claim of (...) Nancy Cartwright and others that knowledge of laws of association is insufficient for distinguishing effective and ineffective strategies. This paper examines the nature of spurious correlations and their value in crafting strategies for change. The conclusion of the paper is that while knowledge of a spurious correlation may have practical value, the value depends on either having knowledge of the causal structure underlying the correlation or it depends on the use of ‘causal criteria’. (shrink)

Nancy Cartwright begins her recent book, Hunting Causes and Using Them, by noting that while a few years ago real causal claims were in dispute, nowadays “causality is back, and with a vengeance.” In the case of the social sciences, Keith Morrison writes that “Social science asks ‘why?’. Detecting causality or its corollary—prediction—is the jewel in the crown of social science research.” With respect to the health sciences, Judea Pearl writes that the “research questions that motivate most studies in the (...) health sciences are causal in nature.” However, not all data used by people interested in making causal claims come from experiments that use random assignment to control and treatment groups. Indeed, much research in the social and health science depends on non-experimental, observational data. Thus, one of the most important problems in the social and health sciences concerns making warranted causal claims using non-experimental, observational data; viz., “Can observational data be used to make etiological inferences leading to warranted causal claims?” This paper examines one method of warranting causal claims that is especially widespread in epidemiology and the health sciences generally—the use of causal criteria. It is argued that cases of complex causation generally, and redundant causation—both causal overdetermination and causal preemption—specifically, undermine the use of such criteria to warrant causal claims. (shrink)

Pluralism with respect to the structure of explanations of facts is not uncommon. Wesley Salmon, for instance, distinguished two types of explanation: causal explanations (which provide insight in the causes of the fact we want to explain) and unification explanations (which fit the explanandum into a unified world view). The pluralism which Salmon and others have defended is compatible with several positions about the exact relation between these two types of explanations. We distinguish four such positions, and argue in favour (...) of one of them. We also compare our results with the views of some authors who have recently written on this subject. (shrink)

The ‘no-difference problem’ challenges us to explain in which way the occurrence of an aggregate effect gives us reason to act in a specific way, although our individual actions make no difference to the effect’s occurrence. When discussing this problem, philosophers usually distinguish between so-called ‘triggering cases’, where the aggregate effect in question is brought about upon reaching a precise threshold, and ‘non-triggering cases’, in which no such precise threshold exists. However, despite their relevant differences, it is widely assumed not (...) only that both categories of cases confront us with the same moral problem, but also that this problem should be solved in the same way no matter which category we are considering. In this paper, I argue that this assumption is mistaken by showing that non-triggering cases pose very different moral problems than triggering cases unless very specific and, arguably, unlikely assumptions in neighbouring debates about causation and decision-making under indeterminacy hold. (shrink)

Meek and Glymour use the graphical approach to causal modeling to argue that one and the same norm of rational choice can be used to deliver both causal-decision-theoretic verdicts and evidential-decision-theoretic verdicts. Specifically, they argue that if an agent maximizes conditional expected utility, then the agent will follow the causal decision theorist’s advice when she represents herself as intervening, and will follow the evidential decision theorist’s advice when she represents herself as not intervening. Since Meek and Glymour take no stand (...) on whether agents should represent themselves as intervening, they provide more general advice than standard causal decision theorists and evidential decision theorists. But I argue here that even Meek and Glymour’s advice is not sufficiently general. This is because their advice is not sensitive to the distinct ways in which agents can fail to intervene, and there are decision-making contexts in which agents can reasonably have non-extreme confidence that they are intervening. I then show that the most natural extension of Meek and Glymour’s framework fails, but offer a generalization of my “Interventionist Decision Theory” that does not suffer from the same problems. (shrink)

Woodward present an argument for the Causal Markov Condition (CMC) on the basis of a principle they dub ‘modularity’ ([1999, 2004]). I show that the conclusion of their argument is not in fact the CMC but a substantially weaker proposition. In addition, I show that their argument is invalid and trace this invalidity to two features of modularity, namely, that it is stated in terms of pairwise independence and ‘arrow-breaking’ interventions. Hausman & Woodward's argument can be rendered valid through a (...) reformulation of modularity, but it is doubtful that the argument so revised provides any substantially new insight regarding the basis of the CMC. Introduction The CMC versus Hausman & Woodward's conclusion Hausman & Woodward's argument Modularity and independent error terms Conclusion Appendix: D-separation. (shrink)

I argue that Hume’s philosophy of time is relationist in the following two senses. 1) Standard definition of relationism. Time is a succession of indivisible moments. Hence there is no time independent of change. Time is a relational, not substantial feature of the world. 2) Rigid relationism. There is no evidence of uniform natural standard for synchronization of clocks. No absolute temporal metric is available. There are countless times, and no time is privileged. Combining 1) and 2) shows that Hume’s (...) ontology of time is thoroughly relationist. (shrink)

Normic Laws and the Significance of Nonmonotonic Reasoning for Philosophy of Science. Normic laws have the form ‘if A then normally B’. They have been discovered in the explanation debate, but were considered as empirically vacuous (§1). I argue that the prototypical (or ideal) normality of normic laws implies statistical normality (§2), whence normic laws have empirical content. In §3–4 I explain why reasoning from normic laws is nonmonotonic, and why the understanding of the individual case is so important here. (...) After sketching some foundations of nonmonotonic reasoning as developed by AI-researchers (§5), Iargue that normic laws are also the best way to understand ceteris paribus laws (§6). §7 deals with the difference between physical and non-physical disciplines and §9 with the difference between normicity and approximation. In §8 it is shown how nonmonotonic reasoning provides a new understanding of the protection of theories against falsification by auxiliary hypotheses. §10, finally, gives a system- and evolution-theoretical explanation of the deeper reason for the omnipresence of normic laws in practice and science, and forthe connection between ideal and statistical normality. (shrink)

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

Two key ideas of scientific explanation−explanation as causal information and explanation as unification-have frequently been set into mutual opposition. This paper proposes a “dialectical solution” to this conflict, by arguing that causal explanations are preferable to non-causal ones, because they lead to a higherdegree of unification at the level of explaining statistical regularities. The core axioms of the theory of causal nets (TC) are justified because they offer the best if not the only unifying explanation of two statistical phenomena: screening (...) off and linking up. Alternative explanations of the two phenomena are discussed and it isshown why they don’t work. It is demonstrated that although the core axioms of TC are empirically vacuous, extended versions of TC have empirical content by means of which they can generate independently testable predictions.Con frecuencia se han planteado como contrapuestas dos ideas clave en la explicacion cientifica (explicacion como informacion causal y explicacion como unificacion). El presente articulo propone una “solucion dialectica” argumentando que las explicaciones causales son preferibles a las no-causales porque aquellas comportan un mayor grado de unificacion en la explicacion de regularidades estadisticas. Los axiomas centrales de la teoria de redes causales (TC) estan justificados porque ofrecen la mejor, si no la unica, explicacion unificada de dos fenomenos estadisticos: neutralizacion (screening off) y vinculacion (linking up). Se discuten las explicaciones alternativas de estos dos fenomenos y se razona por que no funcionan. Se demuestra ademas que aunque los axiomas centrales de TC son empiricamente vacuos, las versiones extendidas de TC tienen un contenido empirico gracias al cual pueden generar predicciones independientemente contrastables. (shrink)

We start this paper by arguing that causality should, in analogy with force in Newtonian physics, be understood as a theoretical concept that is not explicated by a single definition, but by the axioms of a theory. Such an understanding of causality implicitly underlies the well-known theory of causal nets and has been explicitly promoted by Glymour. In this paper we investigate the explanatory warrant and empirical content of TCN. We sketch how the assumption of directed cause–effect relations can be (...) philosophically justified by an inference to the best explanation. We then ask whether the explanations provided by TCN are merely post-facto or have independently testable empirical content. To answer this question we develop a fine-grained axiomatization of TCN, including a distinction of different kinds of faithfulness. A number of theorems show that although the core axioms of TCN are empirically empty, extended versions of TCN have successively increasing empirical content. (shrink)

For nearly as long as the word “correlation” has been part of statistical parlance, students have been warned that correlation does not prove causation, and that only experimental studies, e.g., randomized clinical trials, can establish the existence of a causal relationship. Over the last few decades, somewhat of a consensus has emerged between statisticians, computer scientists, and philosophers on how to represent causal claims and connect them to probabilistic relations. One strand of this work studies the conditions under which evidence (...) accumulated from non-experimental (observational) studies can be used to infer a causal relationship. In this paper, I compare the typical conditions required to infer that one variable is a direct cause of another in observational and experimental studies. I argue that they are essentially the same. (shrink)

Cartwright (Synthese 121(1/2):3–27, 1999a; The dappled world, Cambridge University Press, Cambridge, 1999b) attacked the view that causal relations conform to the Markov condition by providing a counterexample in which a common cause does not screen off its effects: the prominent chemical factory. In this paper we suggest a new way to handle counterexamples to Markov causation such as the chemical factory. We argue that Cartwright’s as well as similar scenarios feature a certain kind of non-causal dependence that kicks in once (...) the common cause occurs. We then develop a representation of this specific kind of non-causal dependence that allows for modeling the problematic scenarios in such a way that the Markov condition is not violated anymore. (shrink)

Batterman and Rice ([2014]) argue that minimal models possess explanatory power that cannot be captured by what they call ‘common features’ approaches to explanation. Minimal models are explanatory, according to Batterman and Rice, not in virtue of accurately representing relevant features, but in virtue of answering three questions that provide a ‘story about why large classes of features are irrelevant to the explanandum phenomenon’ ([2014], p. 356). In this article, I argue, first, that a method (the renormalization group) they propose (...) to answer the three questions cannot answer them, at least not by itself. Second, I argue that answers to the three questions are unnecessary to account for the explanatoriness of their minimal models. Finally, I argue that a common features account, what I call the ‘generalized ontic conception of explanation’, can capture the explanatoriness of minimal models. (shrink)

Causation is a macroscopic phenomenon. The temporal asymmetry displayed by causation must somehow emerge along with other asymmetric macroscopic phenomena like entropy increase and the arrow of radiation. I shall approach this issue by considering ‘causal inference’ techniques that allow causal relations to be inferred from sets of observed correlations. I shall show that these techniques are best explained by a reduction of causation to structures of equations with probabilistically independent exogenous terms. This exogenous probabilistic independence imposes a recursive order (...) on these equations and a consequent distinction between dependent and independent variables that lines up with the temporal asymmetry of causation. (shrink)

Jaegwon Kim argues that unreduced mental causes are excluded from efficacy because physical causes are sufficient in themselves. One response to this causal exclusion argument is to embrace some form of overdetermination. In this paper I consider two forms of overdetermination. Independent overdetermination suggests that two individually sufficient causes bring about one effect. This model fails because the sufficiency of one cause renders the other cause unnecessary. Dependent overdetermination suggests that a physical cause is necessary and sufficient for a given (...) effect, but it necessitates a mental cause of the effect as well. This model fails because the necessity of the mental cause renders the physical cause individually insufficient. (shrink)

Causal analysis in the social sciences takes advantage of a variety of methods and of a multi-fold source of information and evidence. This pluralistic methodology and source of information raises the question of whether we should accordingly have a pluralistic metaphysics and epistemology. This paper focuses on epistemology and argues that a pluralistic methodology and evidence don’t entail a pluralistic epistemology. It will be shown that causal models employ a single rationale of testing, based on the notion of variation. Further, (...) I shall argue that this monistic epistemology is also involved in alternative philosophical theories of causation. (shrink)

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

This is my first professional philosophical essay. I wrote "The twofold meaning of being" in 1996 when I was a student of Nunzio Incardona at University of Palermo (Italy) and before my degree thesis, "The difference in Aristotle’s Metaphysics". It still waits to be published.

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)

What are scientific theories and how should they be represented? In this article, I propose a causal–structural account, according to which scientific theories are to be represented as sets of interrelated causal and credal nets. In contrast with other accounts of scientific theories (such as Sneedian structuralism, Kitcher’s unificationist view, and Darden’s theory of theoretical components), this leaves room for causality to play a substantial role. As a result, an interesting account of explanation is provided, which sheds light on explanatory (...) unification within a causalist framework. The theory of classical genetics is used as a case study. 1 Introduction2 The Theory of Classical Genetics3 Three Philosophical Accounts of the Theory of Classical Genetics3.1 The structuralist account3.2 Kitcher’s unificationism3.3 Darden and theory change in science4 A Common Lacuna: Where is Causality?5 Woodward’s Interventionist Account of Causation6 Causal Bayes Nets and Their Interrelations6.1 Causal Bayes nets6.2 Relations among causal nets6.3 Credal nets and their interrelations7 The Theory of the Gene and its Causal Graph8 A First Exemplar: Stem Length in Pea Plants8.1 Three crosses on stem length in pea plants8.2 The causal graph for stem length in pea plants8.3 Morgan’s explanatory principles and the credal net for stem length in pea plants9 Explaining Mendel’s Crosses: A Causal–Structural Account10 Monohybrid Crosses with Complete Dominance11 Exemplars,Explanatory Patterns, Generic Credal Nets, and Mechanism Schemas12 Incomplete Dominance13 Anomalies14 Multi-hybrid Crosses with Independent Assortment15 Multi-hybrid Crosses with Linkage and Crossing-Over16 Double Crossing-Over and the Linear Order of the Gene17 Causal–Structural Explanation18 Explanatory Unification19 Concluding Remarks. (shrink)

Backtracking influence is influence that zigzags in time. For example, backtracking influence exists when an event E_1 makes an event E_2 more likely by way of a nomic connection that goes from E_1 back in time to an event C and then forward in time to E_2. I contend that in our local region of spacetime, at least, backtracking influence is redundant in the sense that any existing backtracking influence exerted by E_1 on E_2 is equivalent to E_1's temporally direct (...) influence on E_2. I prove the redundancy of backtracking influence using several plausible physical principles without assuming any fundamental temporal or causal asymmetry. This explanation can play a prominent role in an account of why causation appears to be objectively asymmetric regardless of whether the fundamental laws are symmetric. (shrink)

According to manipulationist accounts of causal explanation, to explain an event is to show how it could be changed by intervening on its cause. The relevant change must be a ‘serious possibility’ claims Woodward 2003, distinct from mere logical or physical possibility—approximating something I call ‘scientific possibility’. This idea creates significant difficulties: background knowledge is necessary for judgments of possibility. Yet the primary vehicles of explanation in manipulationism are ‘invariant’ generalisations, and these are not well adapted to encoding such knowledge, (...) especially in the social sciences, as some of it is non-causal. Ceteris paribus (CP) laws or generalisations labour under no such difficulty. A survey of research methods such as case and comparative studies, randomised control trials, ethnography, and structural equation modeling, suggests that it would be more difficult and in some instances impossible to try to represent the output of each method in invariant generalisations; and that this is because in each method causal and non-causal background knowledge mesh in a way that cannot easily be accounted for in manipulationist terms. Ceteris paribus-generalisations being superior in this regard, a theory of explanation based on the latter is a better fit for social science. (shrink)

Debates about explanation in the social sciences often proceed without any clear idea what an 'account' of explanation should do. In this paper I take a stance - what I will call contextualism - that denies there are purely formal and conceptual constraints on explanation and takes standards of explanation to be substantive empirical claims, paradigmatically claims about causation. I then use this standpoint to argue for position on issues in the philosophy of social science concerning reduction, idealized models, social (...) mechanisms, functional explanations, inference to the best explanation and interpretive understanding. (shrink)

It is often argued that if a mentalproperty supervenes on a physical property, then (1)the mental property M ``inherits'''' its causal efficacyfrom the physical property P and (2) the causalefficacy of M reduces to that of P. However, once weunderstand the supervenience thesis and the concept ofcausation probabilistically, it turns out that we caninfer the causal efficacy of M from that of P andvice versa if and only if a certain condition, whichI call the ``line-up'''' thesis, holds. I argue that (...) thesupervenience thesis entails neither this conditionnor its denial. I also argue that even when theline-up thesis holds true, reductionism about thecausal efficacy of the mental property doesn''tfollow. (shrink)

The connection between the probabilities of conditionals and the corresponding conditional probabilities has long been explored in the philosophical literature, but its implementation faces both technical obstacles and objections on empirical grounds. In this paper I ?rst outline the motivation for the probabilistic turn and Lewis’ triviality results, which stand in the way of what would seem to be its most straightforward implementation. I then focus on Richard Jeffrey’s ’random-variable’ approach, which circumvents these problems by giving up the notion that (...) conditionals denote propositions in the usual sense. Even so, however, the random-variable approach makes counterintuitive predictions in simple cases of embedded conditionals. I propose to address this problem by enriching the model with an explicit representation of causal dependencies. The addition of such causal information not only remedies the shortcomings of Jeffrey’s conditional, but also opens up the possibility of a uni?ed probabilistic account of indicative and counterfactual conditionals. (shrink)

Anti-realists typically contend that truth is epistemically constrained. Truth, they say, cannot outstrip our capacity to know. Some anti-realists are also willing to make a further claim: if truth is epistemically constrained, classical logic is to be given up in favour of intuitionistic logic. Here we shall be concerned with one argument in support of this thesis - Crispin Wright's Basic Revisionary Argument, first presented in his Truth and Objectivity. We argue that the reasoning involved in the argument, if correct, (...) validates a parallel argument that leads to conclusions that are unacceptable to classicists and intuitionists alike. (shrink)

There are simple mechanical systems that elude causal representation. We describe one that cannot be represented in a single directed acyclic graph. Our case suggests limitations on the use of causal graphs for causal inference and makes salient the point that causal relations among variables depend upon details of causal setups, including values of variables.