One goal of recent philosophy of mind has been to ‘naturalize’ intentionality by showing how a purely physical system could have states that represent or are about items (objects, properties, facts) in the world. The project is reductionist in spirit, the aim being to explain intentional relations—to say what they really are—and to do so in terms that do not themselves utilize intentional or semantic concepts. In this vein there are attempts to explain intentional relations in terms of causal relations, (...) informational relations, teleological or functional relations, relations involving abstract similarity or isomorphism, and various combinations thereof. What makes these accounts naturalistic is the presumed objectivity and scientific respectability of the properties appelated to in the explanans. What makes them all reductive is their shared presumption that intentionality can be explained in terms that have a wider application to intentional systems as well as to systems that have no mental properties at all. (shrink)

This paper addresses questions about how the levels of causality (generic and single-case causality) are related. One question is epistemological: can relationships at one level be evidence for relationships at the other level? We present three kinds of answer to this question, categorised according to whether inference is top-down, bottom-up, or the levels are independent. A second question is metaphysical: can relationships at one level be reduced to relationships at the other level? We present three kinds of answer to this (...) second question, categorised according to whether single-case relations are reduced to generic, generic relations are reduced to single-case, or the levels are independent. We then explore causal inference in autopsy. This is an interesting case study, we argue, because it refutes all three epistemologies and all three metaphysics. We close by sketching an account of causality that survives autopsy—the epistemic theory. (shrink)

A cause may influence its effect via multiple paths. Paradigmatically (Hesslow [1974]), taking birth control pills both decreases one’s risk of thrombosis by preventing pregnancy and increases it by producing a blood chemical. Building on Pearl ([2001]), I explicate the notion of a path-specific effect. Roughly, a path-specific effect of C on E via path P is the degree to which a change in C would change E were they to be transmitted only via P. Facts about such effects may (...) be gleaned from the structural equations commonly used to represent the causal relationships among variables. I contrast my analysis of the Hesslow case with those given by theorists of probabilistic causality, who mistakenly link it to issues of causal heterogeneity, token-causation and indeterminism. The reason probabilistic theories misdiagnose this case is that they pay inadequate attention to the structural relationships among variables. (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)

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)

I argue that information is a goal-relative concept for Bayesians. More precisely, I argue that how much information is provided by a piece of evidence depends on whether the goal is to learn the truth or to rank actions by their expected utility, and that different confirmation measures should therefore be used in different contexts. I then show how information measures may reasonably be derived from confirmation measures, and I show how to derive goal-relative non-informative and informative priors given background (...) information. Finally, I argue that my arguments have important implications for both objective and subjective Bayesianism. In particular, the Uniqueness Thesis is either false or must be modified. Moreover, objective Bayesians must concede that pragmatic factors systematically influence which priors are rational, and subjective Bayesians must concede that pragmatic factors sometimes partly determine which prior distribution most accurately represents an agent's epistemic state. (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)

Philosophers discussing causation take on, as one of their responsibilities, the task of specifying an ontology of causation. Both standard and non-standard accounts of that ontology make two assumptions: that the ontological category of causal relata admits a unique specification, and that cause and effect are of the same ontological type. These assumptions are rarely made explicit, but there is in fact little reason to think them true. It is argued here that, if the question has any interest, there are (...) some considerations in favor of rejecting Uniqueness and Uniformity, no good reasons in favor of them, but good reason to think that we are not in a position to make a decisive pronouncement, since some of the information needed to make a judgement on the matter is empirical in character. Philosophers have therefore made two mistakes about the relata of causation: one is to have accepted unwarranted restrictions on the categories pertinent to causation; the other is to have wrongly assumed that we are in a position to name them. (shrink)

Data from medical research are typically summarized with various types of outcome measures. We present three arguments in favor of absolute over relative outcome measures. The first argument is from cognitive bias: relative measures promote the reference class fallacy and the overestimation of treatment effectiveness. The second argument is decision-theoretic: absolute measures are superior to relative measures for making a decision between interventions. The third argument is causal: interpreted as measures of causal strength, absolute measures satisfy a set of desirable (...) properties, but relative measures do not. Absolute outcome measures outperform relative measures on all counts. (shrink)

This paper develops axiomatic foundations for a probabilistic-interventionist theory of causal strength. Transferring methods from Bayesian confirmation theory, I proceed in three steps: I develop a framework for defining and comparing measures of causal strength; I argue that no single measure can satisfy all natural constraints; I prove two representation theorems for popular measures of causal strength: Pearl's causal effect measure and Eells' difference measure. In other words, I demonstrate these two measures can be derived from a set of plausible (...) adequacy conditions. The paper concludes by sketching future research avenues. (shrink)

This paper proposes a game-theoretic solution of the surprise examination problem. It is argued that the game of “matching pennies” provides a useful model for the interaction of a teacher who wants her exam to be surprising and students who want to avoid being surprised. A distinction is drawn between prudential and evidential versions of the problem. In both, the teacher should not assign a probability of zero to giving the exam on the last day. This representation of the problem (...) provides a diagnosis of where the backwards induction argument, which “proves” that no surprise exam is possible, is mistaken. (shrink)

The paper examines definitions of ‘cause’ in the epidemiological literature. Those definitions all describe causes as factors that make a difference to the distribution of disease or to individual health status. In the philosophical jargon, causes in epidemiology are difference-makers. Two claims are defended. First, it is argued that those definitions underpin an epistemology and a methodology that hinge upon the notion of variation, contra the dominant Humean paradigm according to which we infer causality from regularity. Second, despite the fact (...) that causes be defined in terms of ‘difference-making’, this cannot fixes the causal metaphysics. Causality in epidemiology ought to be interpreted according to the epistemic theory. In this approach relations are deemed causal depending on the evidence and on the available methods. Indeed, evidence to establish causal claims requires difference-making considerations; furthermore, those definitions of cause reflect the ‘variational’ epistemology and methodology of epidemiology. (shrink)

Empirical research has recently emerged as a key method for understanding the nature of causation, and our concept of causation. One thread of research aims to test intuitions about the nature of causation in a variety of classic cases. These experiments have principally been used to try to resolve certain debates within analytic philosophy, most notably that between proponents of transference and dependence views of causation. The other major thread of empirical research on our concept of causation has investigated the (...) role that normative considerations play in causal judgments. These experimental results suggest that philosophical accounts of our concept of causation should take a broader view of what might be relevant. For both lines of research, we describe some of the significant experiments and outline key philosophical morals that have been drawn, all while pointing out various limitations. We conclude by considering other kinds of empirical research that should be philosophically interesting for those studying the nature of causation and our concept of causation. In particular, we point towards the need for philosophical research about causal perception, causal reasoning, and causal learning, as well as ways in which this research could play a role in prescriptive metaphysics. (shrink)

Analogical reasoning addresses the question how evidence from various phenomena can be combined and made relevant for theory development and prediction. In the first part of my contribution, I review some influential accounts of analogical reasoning, both historical and contemporary, focusing in particular on Keynes, Carnap, Hesse, and more recently Bartha. In the second part, I sketch a general framework. To this purpose, a distinction between a predictive and a conceptual type of analogical reasoning is introduced. I then take up (...) a common intuition according to which analogical inferences hold if the differences between source and target concern only irrelevant circumstances. I attempt to make this idea more precise by addressing possible objections and in particular by specifying a notion of causal irrelevance based on difference making in homogeneous contexts. (shrink)

Objective probability, or objective chance, is the probability of some event occurring in the future independent of what anyone thinks. This paper presents and defends a theory of objective chance. I develop an informal analysis of objective chance, taking the common sense picture underlying our talk about the likelihood of future events as our starting point. A formal semantics is introduced, and I argue that the theory presented satisfies certain criteria of adequacy for a theory of probability.

Understanding probabilities as something other than point values has often been motivated by the need to find more realistic models for degree of belief, and in particular the idea that degree of belief should have an objective basis in “statistical knowledge of the world.” I offer here another motivation growing out of efforts to understand how chance evolves as a function of time. If the world is “chancy” in that there are non-trivial, objective, physical probabilities at the macro-level, then the (...) chance of an event e that happens at a given time is \ until it happens. But whether the chance of e goes to one continuously or not is left open. Discontinuities in such chance trajectories can have surprising and troubling consequences for probabilistic analyses of causation and accounts of how events occur in time. This, coupled with the compelling evidence for quantum discontinuities in chance’s evolution, gives rise to a “continuity bind” with respect to chance probability trajectories. I argue that a viable option for circumventing the continuity bind is to understand the probabilities “imprecisely,” that is, as intervals rather than point values. I then develop and motivate an alternative kind of continuity appropriate for interval-valued chance probability trajectories. (shrink)

Analyses of singular causation often make use of the idea that a cause increases the probability of its effect. Of particular salience in such accounts are the values of the probability function of the effect, conditional on the presence and absence of the putative cause, analysed around the times of the events in question: causes are characterized by the effect’s probability function being greater when conditionalized upon them. Put this way, it becomes clearer that the ‘behaviour’ of probability functions in (...) small intervals about the times in question ought to be of concern. In this article, I make an extended case that causal theorists employing the ‘probability raising’ idea should pay attention to the continuity question. Specifically, if the probability functions are ‘jumping about’ in ways typical of discontinuous functions, then the stability of the relevant probability increase is called into question. The rub, however, is that sweeping requirements for either continuity or discontinuity are problematic and, as I argue, this constitutes a ‘continuity bind’. Hence more subtle considerations and constraints are needed, two of which I consider: utilizing discontinuous first derivatives of continuous probability functions, and abandoning point probability for imprecise probability. _1_ Introduction _2_ Probability Trajectories and Continuity _2.1_ Probability trajectories _2.2_ Causation as discontinuous jumps _2.3_ Against systematic discontinuity _3_ Broader Discontinuity Concerns _4_ The Continuity Bind _4.1_ Retaining continuity with discontinuous first derivatives _4.2_ Imprecise probability trajectories _5_ Concluding Remarks Appendix. (shrink)

A definition of causation as probability-raising is threatened by two kinds of counterexample: first, when a cause lowers the probability of its effect; and second, when the probability of an effect is raised by a non-cause. In this paper, I present an account that deals successfully with problem cases of both these kinds. In doing so, I also explore some novel implications of incorporating into the metaphysical investigation considerations of causal psychology.

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)

The principle of the common cause claims that if an improbable coincidence has occurred, there must exist a common cause. This is generally taken to mean that positive correlations between non-causally related events should disappear when conditioning on the action of some underlying common cause. The extended interpretation of the principle, by contrast, urges that common causes should be called for in order to explain positive deviations between the estimated correlation of two events and the expected value of their correlation. (...) The aim of this paper is to provide the extended reading of the principle with a general probabilistic model, capturing the simultaneous action of a system of multiple common causes. To this end, two distinct models are elaborated, and the necessary and sufficient conditions for their existence are determined. (shrink)

The existing philosophical views on what is the meaning of causality adequate to medicine are vastly divided. We approach this question and offer two arguments in favor of pluralism regarding concepts of causality. First, we analyze the three main types of research designs (randomized-controlled trials, observational epidemiology and laboratory research). We argue, using examples, that they allow for making causal conclusions that are best understood differently in each case (in agreement with a version of manipulationist, probabilistic and mechanistic definitions, respectively). (...) Second, we analyze clinical practice and argue that these manipulationist, probabilistic and mechanistic causal claims can be used as evidence for different therapeutic decisions. We differentiate among ‘predicting’ that does not change the relata of causal claims, (mechanistic) ‘interferences’, and ‘interventions’ in the strict sense that act on causes to change effects. The central conclusion is that causal claims agreeing with diverse concepts of causality can deliver evidence for different types of therapeutic decisions. (shrink)

It is often natural to compare two events by describing one as ‘more of a cause’ of some effect than the other. But what do such comparisons amount to, exactly? This paper aims to provide a guided tour of the recent literature on ‘degrees of causation’. Section 2 looks at what I call ‘dependence measures’, which arise from thinking of causes as difference‐makers. Section 3 looks at what I call ‘production measures’, which arise from thinking of causes as jointly sufficient (...) for their effects. Finally, section 4 examines the important question of whether there is any sense in which an agent is more responsible for an outcome in virtue of her action being more of a cause of it. I describe a puzzle that emerges from this question, and explore various strategies for resolving it. (shrink)

Much of the philosophical literature on causation has focused on the concept of actual causation, sometimes called token causation. In particular, it is this notion of actual causation that many philosophical theories of causation have attempted to capture.2 In this paper, we address the question: what purpose does this concept serve? As we shall see in the next section, one does not need this concept for purposes of prediction or rational deliberation. What then could the purpose be? We will argue (...) that one can gain an important clue here by looking at the ways in which causal judgments are shaped by people‘s understanding of norms. (shrink)

In recent years, there has been a philosophical cottage industry producing arguments that our concept of causation is not univocal: that there are in fact two concepts of causation, corresponding to distinct species of causal relation. Papers written in this tradition have borne titles like “Two Concepts of Cause” and “Two Concepts of Causation”. With due apologies to Charles Dickens, I hereby make my own contribution to this genre.

An influential tradition in the philosophy of causation has it that all token causal facts are, or are reducible to, facts about difference-making. Challenges to this tradition have typically focused on pre-emption cases, in which a cause apparently fails to make a difference to its effect. However, a novel challenge to the difference-making approach has recently been issued by Alyssa Ney. Ney defends causal foundationalism, which she characterizes as the thesis that facts about difference-making depend upon facts about physical causation. (...) She takes this to imply that causation is not fundamentally a matter of difference-making. In this paper, I defend the difference-making approach against Ney’s argument. I also offer some positive reasons for thinking, pace Ney, that causation is fundamentally a matter of difference-making. (shrink)

In their article 'Causes and Explanations: A Structural-Model Approach. Part I: Causes', Joseph Halpern and Judea Pearl draw upon structural equation models to develop an attractive analysis of 'actual cause'. Their analysis is designed for the case of deterministic causation. I show that their account can be naturally extended to provide an elegant treatment of probabilistic causation.

ABSTRACT Joseph Halpern and Judea Pearl draw upon structural equation models to develop an attractive analysis of ‘actual cause’. Their analysis is designed for the case of deterministic causation. I show that their account can be naturally extended to provide an elegant treatment of probabilistic causation. 1Introduction 2Preemption 3Structural Equation Models 4The Halpern and Pearl Definition of ‘Actual Cause’ 5Preemption Again 6The Probabilistic Case 7Probabilistic Causal Models 8A Proposed Probabilistic Extension of Halpern and Pearl’s Definition 9Twardy and Korb’s Account 10Probabilistic (...) Fizzling 11Conclusion. (shrink)

I explore the problem of ``probabilistic causal preemption'' in the context of a``propensity trajectory'' theory of singular probabilistic causation. This involvesa particular conception of events and a substantive thesis concerning events soconceived.

This paper considers the applicability of standard accounts of causation to living systems. In particular it examines critically the increasing tendency to equate causal explanation with the identification of a mechanism. A range of differences between living systems and paradigm mechanisms are identified and discussed. While in principle it might be possible to accommodate an account of mechanism to these features, the attempt to do so risks reducing the idea of a mechanism to vacuity. It is proposed that the solution (...) to this problem requires the development of a philosophical account of process adequate to apply to living systems. (shrink)

This paper considers the applicability of standard accounts of causation to living systems. In particular it examines critically the increasing tendency to equate causal explanation with the identification of a mechanism. A range of differences between living systems and paradigm mechanisms are identified and discussed. While in principle it might be possible to accommodate an account of mechanism to these features, the attempt to do so risks reducing the idea of a mechanism to vacuity. It is proposed that the solution (...) to this problem requires the development of a philosophical account of process adequate to apply to living systems. (shrink)

This paper considers the applicability of standard accounts of causation to living systems. In particular it examines critically the increasing tendency to equate causal explanation with the identification of a mechanism. A range of differences between living systems and paradigm mechanisms are identified and discussed. While in principle it might be possible to accommodate an account of mechanism to these features, the attempt to do so risks reducing the idea of a mechanism to vacuity. It is proposed that the solution (...) to this problem requires the development of a philosophical account of process adequate to apply to living systems. (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)

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

Does one’s causal responsibility increase the degree of one’s moral responsibility? The proponents of resultant moral luck hold that it does. Until quite recently, the causation literature has almost exclusively been interested in the binary question of whether one factor is a cause of an outcome. Naturally, the debate over resultant moral luck also revolved around this binary question. However, we have seen an increased interest in the question of degrees of causation in recent years. And some philosophers have already (...) explored various implications of a graded notion of causation on resultant moral luck. In this paper, I will do the same. But the implications that I will draw attention to are bad news for resultant moral luck. I will show that resultant moral luck entails some implausible results that leave resultant moral luck more indefensible than it was previously thought be. I will also show that what is typically taken to be the positive argument in favor of resultant moral luck fails. I will conclude that we should reject resultant moral luck. (NOTE: Email me for a copy.). (shrink)

Critics of functional explanations in social science maintain that such explanations are illegitimate unless a mechanism is specified. Others argue that mechanisms are not necessary for causal inference and that functional explanations are a type of causal claim that raise no special difficulties for testing. I show that there is indeed a special problem that confronts testing functional explanations resulting from their connection to second-order causal claims. I explain how mechanisms can resolve this difficulty, but argue that this does not (...) provide support for methodological individualism since it is not necessary that the mechanisms be described in terms of individual interactions. (shrink)

Economists reason causally. Like many other scientists, they aim at formulating justified causal claims about their object of study. This thesis contributes to our understanding of how causal reasoning proceeds in economics. By using the research on the causes of unemployment as a case study, three questions are adressed. What are the meanings of causal claims? How can a causal claim be adequately supported by evidence? How are causal beliefs affected by incoming facts? In the process of answering these semantic, (...) epistemic and dynamical questions, the richness of causal reasoning in economics is brought to the foreground. In the part on semantics, it is argued that the meaning of causal generalizations in policy-oriented economics is best captured by using the concept of ‘inferential relation’ rather than the one of ‘referential relation’. This part contributes to develop an inferentialist semantics by distinguishing among types of inferential relations. In the part on epistemology, it is argued that justification in sciences like economics often relies, and ought to rely, on evidential variety―i.e. the combination of evidence from multiple sources. An interpretation of independence among evidential sources is offered: two evidential sources are fully independent if and only if the reasons why they would be unreliable do not overlap. It is then shown that the variety-of-evidence thesis does not hold under extreme circumstances. The part on dynamics focuses on deviant-case study. A storyline is provided for what deviant-case study aims at and how it proceeds in what is characterized as an ‘eclectic science’. (shrink)

One goal of recent philosophy of mind has been to ‘naturalize’ intentionality by showing how a purely physical system could have states that represent or are about items in the world. The project is reductionist in spirit, the aim being to explain intentional relations—to say what they really are—and to do so in terms that do not themselves utilize intentional or semantic concepts. In this vein there are attempts to explain intentional relations in terms of causal relations, informational relations, teleological (...) or functional relations, relations involving abstract similarity or isomorphism, and various combinations thereof. What makes these accounts naturalistic is the presumed objectivity and scientific respectability of the properties appelated to in the explanans. What makes them all reductive is their shared presumption that intentionality can be explained in terms that have a wider application to intentional systems as well as to systems that have no mental properties at all. (shrink)

I am very grateful to Stephan Leuenberger, Erica Shumener and Naomi Thompson for their excellent and thoughtful commentaries on Making Things Up. I have learned a lot from thinking through their replies. As it happens, they focus on pretty disparate aspects of the book: necessitation, relative fundamentality, and what builds the building facts, respectively. I will thus engage with their remarks separately.

For a long time, regularity accounts of causation have virtually vanished from the scene. Problems encountered within other theoretical frameworks have recently induced authors working on causation, laws of nature, or methodologies of causal reasoning – as e.g. May (Kausales Schliessen. Eine Untersuchung über kausale Erklärungen und Theorienbildung. Ph.D. thesis, Universität Hamburg, Hamburg, 1999), Ragin (Fuzzy-set social science. Chicago: University of Chicago Press, 2000), Graßhoff and May (Causal regularities. In W. Spohn, M. Ledwig, & M. Esfeld (Eds.), Current issues in (...) causation (pp. 85–114). Paderborn: Mentis, 2001), Swartz (The concept of physical law (2nd ed.). http://www.sfu.ca/philosophy/physical-law/, 2003), Halpin (Erkenntnis, 58, 137–168, 2003) – to direct their attention back to regularity theoretic analyses. In light of the latest proposals of regularity theories, the paper at hand therefore reassesses the criticism raised against regularity accounts since the INUS theory of causation of Mackie (The cement of the universe. A study of causation. Oxford: Clarendon Press, 1974). It is shown that most of these objections target strikingly over-simplified regularity theoretic sketches. By outlining ways to refute these objections it is argued that the prevalent conviction as to the overall failure of regularity theories has been hasty. (shrink)

The essential precondition of implementing interventionist techniques of causal reasoning is that particular variables are identified as so-called intervention variables. While the pertinent literature standardly brackets the question how this can be accomplished in concrete contexts of causal discovery, the first part of this paper shows that the interventionist nature of variables cannot, in principle, be established based only on an interventionist notion of causation. The second part then demonstrates that standard observational methods that draw on Bayesian networks identify intervention (...) variables only if they also answer the questions that can be answered by interventionist techniques—which are thus rendered dispensable. The paper concludes by suggesting a way of identifying intervention variables that allows for exploiting the whole inferential potential of interventionist techniques. (shrink)