Provisional draft, pre-production copy of my book “The Modal Future” (forthcoming with Cambridge University Press).

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

This dissertation aims to determine the optimal level of granularity for the variables used in probabilistic causal models. These causal models are useful for generating explanations in a number of scientific contexts. In Chapter 1, I argue that there is rarely a unique level of granularity at which a given phenomenon can be causally explained, thereby rejecting various causal exclusion arguments. In Chapter 2, I consider several recent proposals for measuring the explanatory power of causal explanations, and show that these (...) measures fail to track the comparative depth of explanations given at different levels of granularity. In Chapter 3, I offer a pragmatic account of how to partition the measure space of a causal variable so as to optimally explain its effect. My account uses the decision-theoretic notion of value of information, and indexes the relative depth of an explanation to a particular agent faced with a particular decision problem. Chapter 4 applies this same decisiontheoretic framework to answer the epistemic question of how to discover constitutive relationships in nature. In Chapter 5, I describe the formal details of the relationship between random variables that are meant to be coarse-grained and fine-grained representations of the same type of phenomenon. I use this formal framework to rebut a popular argument for the view that special science probabilities can be objective chances. Chapter 6 discusses challenges related to the causal interpretation of Bayes nets that use imprecise rather than precise probabilities. (shrink)

The epistemic probability of A given B is the degree to which B evidentially supports A, or makes A plausible. This paper is a first step in answering the question of what determines the values of epistemic probabilities. I break this question into two parts: the structural question and the substantive question. Just as an object’s weight is determined by its mass and gravitational acceleration, some probabilities are determined by other, more basic ones. The structural question asks what probabilities are (...) not determined in this way—these are the basic probabilities which determine values for all other probabilities. The substantive question asks how the values of these basic probabilities are determined. I defend an answer to the structural question on which basic probabilities are the probabilities of atomic propositions conditional on potential direct explanations. I defend this against the view, implicit in orthodox mathematical treatments of probability, that basic probabilities are the unconditional probabilities of complete worlds. I then apply my answer to the structural question to clear up common confusions in expositions of Bayesianism and shed light on the “problem of the priors.”. (shrink)

Two long-standing arguments in cognitive science invoke the assumption that holistic inference is computationally infeasible. The first is Fodor’s skeptical argument toward computational modeling of ordinary inductive reasoning. The second advocates modular computational mechanisms of the kind posited by Cosmides, Tooby and Sperber. Based on advances in machine learning related to Bayes nets, as well as investigations into the structure of scientific and ordinary information, I maintain neither argument establishes its architectural conclusion. Similar considerations also undermine Fodor’s decades-long diagnosis of (...) artificial intelligence research as confounded by an inability to circumscribe the amount of information relevant to inferential processes. This diagnosis is particularly inapposite with respect to Bayes nets, since one of their strengths as machine learning systems has been their capacity to reason probabilistically about large data sets whose size overwhelms the capacities of individual human reasoners. A general moral follows from these criticisms: Insights into artificial and human cognitive systems are likely to be cultivated by focusing greater attention on the structure and density of connections among items of information that are available to them. (shrink)

Many generic sentences express stable inductive generalizations. Stable inductive generalizations are typically true for a causal reason. In this paper we investigate to what extent this is also the case for the generalizations expressed by generic sentences. More in particular, we discuss the possibility that many generic sentences of the form ‘ks have feature e’ are true because kind k have the causal power to ‘produce’ feature e. We will argue that such an analysis is quite close to a probabilistic (...) based analysis of generic sentences according to which ‘relatively many’ ks have feature e, and that, in fact, this latter type of analysis can be ‘grounded’ in terms of causal powers. We will argue, moreover, that the causal power analysis is sometimes preferred to a correlation-based analysis, because it takes the causal structure that gives rise to the probabilistic data into account. (shrink)

"Correlation is not causation" is one of the mantras of the sciences—a cautionary warning especially to fields like epidemiology and pharmacology where the seduction of compelling correlations naturally leads to causal hypotheses. The standard view from the epistemology of causation is that to tell whether one correlated variable is causing the other, one needs to intervene on the system—the best sort of intervention being a trial that is both randomized and controlled. In this paper, we argue that some purely correlational (...) data contains information that allows us to draw causal inferences: statistical noise. Methods for extracting causal knowledge from noise provide us with an alternative to randomized controlled trials that allows us to reach causal conclusions from purely correlational data. (shrink)

Some recent accounts of constitutive relevance have identified mechanism components with entities that are causal intermediaries between the input and output of a mechanism. I argue that on such accounts there is no distinctive inter-level form of mechanistic explanation and that this highlights an absence in the literature of a compelling argument that there are such explanations. Nevertheless, the entities that these accounts call ‘components’ do play an explanatory role. Studying causal intermediaries linking variables Xand Y provides knowledge of the (...) counterfactual conditions under which X will continue to bring about Y. This explanatory role does not depend on whether intermediate variables count as components. The question of whether there are distinctively mechanistic explanations remains open. (shrink)

To whom, if anyone, are the writings of philosophers of science relevant? There are three potential groups of people: Philosophers, Scientists, and Interested Citizens, within and beyond the academy. I argue that our discipline is potentially relevant to all three, but I particularly press the claims of the Interested Citizens. My essay is in dialogue with a characteristically insightful lecture given thirty years ago by Arthur Fine. Addressing the Philosophy of Science Association as its president, Fine argued that general philosophy (...) of science was dead, and that all the action lay in the philosophy of the special sciences. I try to identify what was correct about Fine’s diagnosis, while supplementing his message by describing fruitful projects that have since emerged. I also hope to share his subversive spirit. (shrink)

In this paper I will argue that what makes our ordinary judgements about token causation true can be explicated in terms of interferences into quasi-inertial processes. These interferences and quasi-inertial processes can in turn be fully explicated in scientific terms. In this sense the account presented here is reductive. I will furthermore argue that this version of a process-theory of causation can deal with the traditional problems that process theories have to face, such as the problem of misconnection and the (...) problem of disconnection as well as with a problem concerning the mis-classification of pre-emption cases. (shrink)

Explanations in psychiatry often integrate various factors relevant to psychopathology. Identifying genuine causes among them is theoretically and clinically important, but epistemically challenging. Woodward’s interventionism appears to provide a promising tool to achieve this. However, Woodward’s interventionism is too demanding to be applied to psychiatry. I thus introduce difference-making interventionism, which detects relevance in general rather than causation, to make interventionist reasoning viable in clinical practice. DMI mirrors the empirical reality of psychiatry even more closely than interventionism, but it needs (...) to be supplied with additional heuristics to disambiguate between causes and other difference-makers. To achieve this, I suggest employing heuristics based on multiple experiments, temporal order and scientific domain. (shrink)

Pre-emption cases have been taken by almost everyone to imply the unviability of the simple counterfactual theory of causation. Yet there is ample motivation from scientific practice to endorse a simple version of the theory if we can. There is a way in which a simple counterfactual theory, at least if understood contrastively, can be supported even while acknowledging that intuition goes firmly against it in pre-emption cases—or rather, only in some of those cases. For I present several new pre-emption (...) cases in which causal intuition does not go against the counterfactual theory, a fact that has been verified experimentally. I suggest an account of framing effects that can square the circle. Crucially, this account offers hope of theoretical salvation—but only to the counterfactual theory of causation, not to others. Again, there is (admittedly only preliminary) experimental support for this account. (shrink)

The definition of metabolic syndrome has been, and still is, extremely controversial. My purpose is not to give a solution to the associated debate but to argue that the controversy is at least partially due to the different ‘causal content’ of the various definitions: their theoretical validity and practical utility can be evaluated by reconstructing or making explicit the underlying causal structure. I will therefore propose to distinguish the alternative definitions according to the kinds of causal content they carry: definitions (...) grounded on associations, definitions presupposing a causal model built upon statistical associations, and definitions grounded on underlying mechanisms. I suggest that analysing definitions according to their causal content can be helpful in evaluating alternative definitions of some diseases. I want to show how the controversy over MetS suggests a distinction among three kinds of definitions based on how explicitly they characterise the syndrome in causal terms, and on the type of causality involved. I will call ‘type 1 definitions’ those definitions that are purely associative; ‘type 2 definitions’ the definitions based on statistical associations, plus generic medical and causal knowledge; and ‘type 3 definitions’ the definitions based on mechanisms. These kinds of definitions, although different, can be related to each other. A definition with more specific causal content may be useful in the evaluation of definitions characterised by a lower degree of causal specificity. Moreover, the identification of the type of causality involved is of help to constitute a good criterion for choosing among different definitions of a pathological entity. In section I introduce the controversy about MetS, in section I propose some remarks about medical definitions and their ‘causal import’, and in section I suggest that the different attitudes towards the definition of MetS are relevant to evaluate their explicative power. (shrink)

In this paper I analyze the process by which modelers in systems biology arrive at an adequate representation of the biological structures thought to underlie data gathered from high-throughput experiments. Contrary to views that causal claims and explanations are rare in systems biology, I argue that in many studies of gene regulatory networks modelers aim at a representation of causal structure. In addressing modeling challenges, they draw on assumptions informed by theory and pragmatic considerations in a manner that is guided (...) by an interventionist conception of causal structure. While doubts have been raised about the applicability of this notion of causality to complex biological systems, it is here seen to be an adequate guide to inquiry. (shrink)

This book addresses key conceptual issues relating to the modern scientific and engineering use of computer simulations. It analyses a broad set of questions, from the nature of computer simulations to their epistemological power, including the many scientific, social and ethics implications of using computer simulations. The book is written in an easily accessible narrative, one that weaves together philosophical questions and scientific technicalities. It will thus appeal equally to all academic scientists, engineers, and researchers in industry interested in questions (...) related to the general practice of computer simulations. (shrink)

To whom, if anyone, are the writings of philosophers of science relevant? There are three potential groups of people: Philosophers, Scientists, and Interested Citizens, within and beyond the academy. I argue that our discipline is potentially relevant to all three, but I particularly press the claims of the Interested Citizens. My essay is in dialogue with a characteristically insightful lecture given thirty years ago by Arthur Fine. Addressing the Philosophy of Science Association as its president, Fine argued that general philosophy (...) of science was dead, and that all the action lay in the philosophy of the special sciences. I try to identify what was correct about Fine’s diagnosis, while supplementing his message by describing fruitful projects that have since emerged. I also hope to share his subversive spirit. (shrink)

While ideal interventions are acknowledged by many as valuable tools for the analysis of causation, recent discussions have shown that, since there are no ideal interventions on upper-level phenomena that non-reductively supervene on their underlying mechanisms, interventions cannot—contrary to a popular opinion—ground an informative analysis of constitution. This has led some to abandon the project of analyzing constitution in interventionist terms. By contrast, this paper defines the notion of a horizontally surgical intervention, and argues that, when combined with some innocuous (...) metaphysical principles about the relation between upper and lower levels of mechanisms, that notion delivers a sufficient condition for constitution. This, in turn, strengthens the case for an interventionist analysis of constitution. (shrink)

The free-energy principle states that all systems that minimize their free energy resist a tendency to physical disintegration. Originally proposed to account for perception, learning, and action, the free-energy principle has been applied to the evolution, development, morphology, anatomy and function of the brain, and has been called a postulate, an unfalsifiable principle, a natural law, and an imperative. While it might afford a theoretical foundation for understanding the relationship between environment, life, and mind, its epistemic status is unclear. Also (...) unclear is how the free-energy principle relates to prominent theoretical approaches to life science phenomena, such as organicism and mechanism. This paper clarifies both issues, and identifies limits and prospects for the free-energy principle as a first principle in the life sciences. (shrink)

Realism is generally assumed as the correct position with regards to psychological research and the measurement of psychological attributes in psychometrics. Borsboom et al., 203–219 2003), for instance, argued that the choice of a reflective measurement model necessarily implies a commitment to the existence of psychological constructs as well as a commitment to the belief that empirical testing of measurement models can justify their correspondence with real causal structures. Hood :739–761 2013) deemphasized Borsboom et al.’s position and argued that the (...) choice of a reflective measurement model does not necessarily require ontological commitments, though, in his view, it does necessitate a commitment to minimal epistemic realism. Although these arguments are formulated with regard to psychological research, they can actually be generalized to other disciplines in social sciences that use similar methodologies and statistical techniques. In Hood’s opinion, empiricism does not suffice to provide an adequate account of the choice of reflective measurement models given that this choice requires an appeal to causal explanations. In this paper, we argue against Hood and answer this challenge, providing epistemic foundations for social science research that do not appeal to realism. (shrink)

Modern medicine is often said to have originated with nineteenth century germ theory, which attributed diseases to bacterial contagions. The success of this theory is often associated with an underlying principle referred to as the “doctrine of specific etiology”. This doctrine refers to specificity at the level of disease causation or etiology. While the importance of this doctrine is frequently emphasized in the philosophical, historical, and medical literature, these sources lack a clear account of the types of specificity that it (...) involves and why exactly they matter. This paper argues that nineteenth century germ theory involves two types of specificity at the level of etiology. One type receives significant attention in the literature, but its influence on modern medicine has been misunderstood. A second type is present in this model, but it has been completely overlooked in the extant literature. My analysis clarifies how these types of specificity led to a novel conception of etiology that continues to figure in medicine today. (shrink)

I argue that the best interpretation of the general theory of relativity has need of a causal entity, and causal structure that is not reducible to light cone structure. I suggest that this causal interpretation of GTR helps defeat a key premise in one of the most popular arguments for causal reductionism, viz., the argument from physics.

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)

Are we entering a major new phase of modern science, one in which our standard, human modes of reasoning and understanding, including heuristics, have decreasing value? The new methods challenge human intelligibility. The digital revolution inspires such claims, but they are not new. During several historical periods, scientific progress has challenged traditional concepts of reasoning and rationality, intelligence and intelligibility, explanation and knowledge. The increasing intelligence of machine learning and networking is a deliberately sought, somewhat alien intelligence. As such, it (...) challenges the traditional, heuristic foresight of expert researchers. Nonetheless, science remains human-centered in important ways—and yet many of our ordinary human epistemic activities are alien to ourselves. This fact has always been the source of “the discovery problem”. It generalizes to the problem of understanding expert scientific practice. Ironically, scientific progress plunges us ever deeper into complexities beyond our grasp. But how is progress possible without traditional realism and the intelligibility realism requires? Pragmatic flexibility offers an answer. (shrink)

Backtracking counterfactuals are problem cases for the standard, similarity based, theories of counterfactuals e.g., Lewis. These theories usually need to employ extra-assumptions to deal with those cases. Hiddleston, 632–657, 2005) proposes a causal theory of counterfactuals that, supposedly, deals well with backtracking. The main advantage of the causal theory is that it provides a unified account for backtracking and non-backtracking counterfactuals. In this paper, I present a backtracking counterfactual that is a problem case for Hiddleston’s account. Then I propose an (...) informational theory of counterfactuals, which deals well with this problem case while maintaining the main advantage of Hiddleston’s account. In addition, the informational theory offers a general theory of backtracking that provides clues for the semantics and epistemology of counterfactuals. I propose that backtracking is reasonable when the state of affairs expressed in the antecedent of a counterfactual transmits less information about an event in the past than the actual state of affairs. (shrink)

It is sometimes thought that randomized study group allocation is uniquely proficient at producing comparison groups that are evenly balanced for all confounding causes. Philosophers have argued that in real randomized controlled trials this balance assumption typically fails. But is the balance assumption an important ideal? I run a thought experiment, the CONFOUND study, to answer this question. I then suggest a new account of causal inference in ideal and real comparative group studies that helps clarify the roles of confounding (...) variables and randomization. 1Confounders and Causes2The Balance Assumption3The CONFOUND Study 3.1CONFOUND 13.2CONFOUND 24Disjunction C and the Ideal Study 4.1The ultimate ‘other cause’: C4.2The ideal comparative group study4.3Required conditions for causal inference5Confounders as Causes, Confounders as Correlates6Summary. (shrink)

The relationship between psychological states and the brain remains an unresolved issue in philosophy of psychology. One appealing solution that has been influential both in science and in philosophy is Dennett’s concept of the intentional stance, according to which beliefs and desires are real and objective phenomena, but not necessarily states of the brain. A fundamental shortcoming of this approach is that it does not seem to leave any causal role for beliefs and desires in influencing behavior. In this paper, (...) I show that intentional states ascribed from the intentional stance should be seen as real causes, develop this to an independently plausible ontological position, and present a response to the latest interventionist causal exclusion worries. (shrink)

Many investigations into the world, including philosophical ones, aim to discover causal knowledge, and many experimental methods have been developed to assist in causal discovery. More recently, algorithms have emerged that can also learn causal structure from purely or mostly observational data, as well as experimental data. These methods have started to be applied in various philosophical contexts, such as debates about our concepts of free will and determinism. This paper provides a “user's guide” to these methods, though not in (...) the sense of specifying exact button presses in a software package. Instead, we explain the larger “pipeline” within which these methods are used and discuss key steps in moving from initial research idea to validated causal structure. (shrink)

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)

ABSTRACT Darwin claims in the Origin that similarity is evidence for common ancestry, but that adaptive similarities are ‘almost valueless’ as evidence. This second claim seems reasonable for some adaptive similarities but not for others. Here we clarify and evaluate these and related matters by using the law of likelihood as an analytic tool and by considering mathematical models of three evolutionary processes: directional selection, stabilizing selection, and drift. Our results apply both to Darwin’s theory of evolution and to modern (...) evolutionary biology. _1_ Introduction _2_ The Likelihood Framework _3_ A Sufficient Condition for a Similarity to Favour Common Ancestry over Separate Ancestry _4_ The 1/p Criterion and Its Limitations _5_ Directional Selection versus Drift _6_ Stabilizing Selection versus Drift _7_ Going beyond Two Taxa _8_ Conclusions Appendix. (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)

This paper discusses von Wright's theory of causation from Explanation and Understanding and Causality and Determinism in contemporary context. I argue that there are two important common points that von Wright's view shares with the version of manipulability currently supported by Woodward: the analysis of causal relations in a system modelled on controlled experiments, and the explanation of manipulability through counterfactuals - with focus on the counterfactual account of unmanipulable causes. These points also mark von Wright's departure from previous action-based (...) theories of causation. Owing to these two features, I argue that, upon classifying different versions of manipulability theories, von Wright's view should be placed closer to the interventionist approach than to the agency theory, where it currently stands. Furthermore, given its relevance in contemporary context, which this paper aims to establish, I claim that von Wright's theory can be employed to solve present problems connected to manipulability approaches to causation. (shrink)

It has become a popular view among non-reductive physicalists that it is possible to devise empirical tests generating evidence for the causal efficacy of the mental, whereby the exclusion worries that have haunted the position of non-reductive physicalism for decades can be dissolved once and for all. This paper aims to show that these evidentialist hopes are vain. I argue that, if the mental is taken to supervene non-reductively on the physical, there cannot exist empirical evidence for its causal efficacy. (...) While causal structures without non-reductive supervenience relations can be conclusively identified in ideal discovery circumstances, it is impossible, in principle, to generate evidence that would favour models with mental causation over models without. Ascribing causal efficacy to the mental, for the non-reductive physicalist, is a modelling choice that must be made on the basis of metaphysical background theories or pragmatic maxims guiding the selection among empirically indistinguishable models. (shrink)

Recent approaches to causal modelling rely upon the causal Markov condition, which specifies which probability distributions are compatible with a directed acyclic graph. Further principles are required in order to choose among the large number of DAGs compatible with a given probability distribution. Here we present a principle that we call frugality. This principle tells one to choose the DAG with the fewest causal arrows. We argue that frugality has several desirable properties compared to the other principles that have been (...) suggested, including the well-known causal faithfulness condition. _1_ Introduction _2_ The Causal Markov Condition _3_ Faithfulness _4_ Frugality _4.1_ Basic independences and frugality _4.2_ General properties of directed acyclic graphs satisfying frugality _4.3_ Connection to minimality assumptions _5_ Frugality as a Parsimony Principle _6_ Conclusion Appendix. (shrink)

In a single-iteration fake barn case, the agent correctly identifies an object of interest on the first try, despite the presence of nearby lookalikes that could have mislead her. In a multiple-iteration fake barn case, the agent first encounters several fakes, misidentifies each of them, and then encounters and correctly identifies a genuine item of interest. Prior work has established that people tend to attribute knowledge in single-iteration fake barn cases, but multiple-iteration cases have not been tested. However, some theorists (...) contend that multiple-iteration cases are more important and will elicit a strong tendency to deny knowledge. Here I report a behavioural experiment investigating knowledge judgments in multiple-iteration fake barn cases. The main finding is that people tend to attribute knowledge in these cases too. Ironically, the results indicate that the presence of fakes could prevent iterated errors from lowering knowledge attributions. The results also provide evidence that ordinary knowledge attributions are based on attributions of cognitive ability. (shrink)

Some explanations appeal to facts about the causal structure of a system in order to shed light on a particular phenomenon; these are explanations which do more than cite the causes X and Y of some state-of-affairs Z, but rather appeal to “macro-level” causal features—for example the fact that A causes B as well as C, or perhaps that D is a strong inhibitor of E—in order to explain Z. Appeals to these kinds of “macro-level” causal features appear in a (...) wide variety of social scientific and biological research; statements about features such as “patriarchy,” “healthcare infrastructure,” and “functioning DNA repair mechanism,” for instance, can be understood as claims about what would be different in a system with a different causal structure. I suggest interpreting counterfactual questions involving structural features as questions about alternative parameter settings of causal models, and propose an extension of the usual interventionist framework for causal explanation which enables scientists to explore the consequences of interventions on “macro-level” structure. (shrink)

Existing research suggests that people's judgments of actual causation can be influenced by the degree to which they regard certain events as normal. We develop an explanation for this phenomenon that draws on standard tools from the literature on graphical causal models and, in particular, on the idea of probabilistic sampling. Using these tools, we propose a new measure of actual causal strength. This measure accurately captures three effects of normality on causal judgment that have been observed in existing studies. (...) More importantly, the measure predicts a new effect ("abnormal deflation"). Two studies show that people's judgments do, in fact, show this new effect. Taken together, the patterns of people's causal judgments thereby provide support for the proposed explanation. (shrink)

Various results show the ‘formal equivalence’ of kin and group selectionist methodologies, but this does not preclude there being a real and useful distinction between kin and group selection processes. I distinguish individual- and population-centred approaches to drawing such a distinction, and I proceed to develop the latter. On the account I advance, the differences between kin and group selection are differences of degree in the structural properties of populations. A spatial metaphor provides a useful framework for thinking about these (...) differences: kin and group selection may be conceptualized as large, overlapping regions of K - G space. I then consider some implications of the account, defend it from possible objections, and further argue that the structural features characteristic of both kin and group selection may recur at multiple levels of biological organization. (shrink)

The issue of causal comparability in the social sciences underlies matters of both generalization and extrapolation. After critiquing two existing interpretations of comparability, due to Hitchcock and Hausman, I propose a distinction between ontological and epistemic comparability. While the former refers to whether two cases are actually comparable, the latter respects that in cases of incomplete information, we need to rely on whatever evidence we have of comparability. I argue, using a political science case study, that in those cases of (...) imperfect information, an epistemic homogeneity criterion can be an adequate justification for generalization. (shrink)

This article assesses how people reason with categories whose features are related in causal cycles. Whereas models based on causal graphical models have enjoyed success modeling category-based judgments as well as a number of other cognitive phenomena, CGMs are only able to represent causal structures that are acyclic. A number of new formalisms that allow cycles are introduced and evaluated. Dynamic Bayesian networks represent cycles by unfolding them over time. Chain graphs augment CGMs by allowing the presence of undirected links (...) that model feedback relations between variables. Unfolded chain graphs are chain graphs that unfold over time. An existing model of causal cycles is also evaluated. Four experiments in which subjects reason about categories with cyclically related features provided evidence against DBNs and alpha centrality and for the two types of chain graphs. Chain graphs—a mechanism for representing the equilibrium distribution of a dynamic system—may thus be good candidates for modeling how people reason causally with complex systems. Applications of chain graphs to areas of cognition other than category-based judgments are discussed. (shrink)

In the recent literature on causal and non-causal scientific explanations, there is an intuitive assumption according to which an explanation is non-causal by virtue of being abstract. In this context, to be ‘abstract’ means that the explanans in question leaves out many or almost all causal microphysical details of the target system. After motivating this assumption, we argue that the abstractness assumption, in placing the abstract and the causal character of an explanation in tension, is misguided in ways that are (...) independent of which view of causation or causal explanation one takes to be most accurate. On major accounts of causation, as well as on major accounts of causal explanation, the abstractness of an explanation is not sufficient for it being non-causal. That is, explanations are not non-causal by dint of being abstract. (shrink)

Kin selection and multilevel selection are alternative approaches for studying the evolution of social behaviour, the relation between which has long been a source of controversy. Many recent theorists regard the two approaches as ultimately equivalent, on the grounds that gene frequency change can be correctly expressed using either. However, this shows only that the two are formally equivalent, not that they offer equally good causal representations of the evolutionary process. This article articulates the notion of an ‘adequate causal representation’ (...) using causal graphs, and then seeks to identify circumstances under which kin and multilevel selection do and do not satisfy the test of causal adequacy. 1 Introduction2 The KS and MLS Approaches2.1 The MLS decomposition2.2 The KS decomposition3 Equivalence and Causality4 Two Problem Cases4.1 The non-social trait case4.2 Genotypic selection with meiotic drive5 Casual Adequacy: A Graphical Approach5.1 The basic idea5.2 Graphs with individual and group variables5.3 Cases where KS is causally adequate5.4 Cases where MLS is causally adequate6 Discussion6.1 Relation to previous work. (shrink)

Recently the functional model of reduction has become something like the standard model of reduction in philosophy of mind. In this paper, I argue that the functional model fails as an account of reduction due to problems related to three key concepts: functionalization, realization and causation. I further argue that if we try to revise the model in order to make it more coherent and scientifically plausible, the result is merely a simplified version of what in philosophy of science is (...) known as mechanistic explanation. Hence, instead of analyzing reduction in philosophy of mind in terms of functional reduction, it should be analyzed in terms of mechanistic explanation. (shrink)

The first part of this paper finds Craver’s (2007) mutual manipulability theory (MM) of constitution inadequate, as it definitionally ties constitution to the feasibility of idealized experiments, which, however, are unrealizable in principle. As an alternative, the second part develops an abductive theory of constitution (NDC), which exploits the fact that phenomena and their constituents are unbreakably coupled via common causes. The best explanation for this common-cause coupling is the existence of an additional dependence relation, viz. constitution. Apart from adequately (...) capturing the essential characteristics of constitution missed by MM, NDC has important ramifications for constitutional discovery—most notably, that there is no experimentum crucis for constitution, not even under ideal discovery circumstances. (shrink)

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)

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)

ABSTRACT Contrastive and deviant/default accounts of causation are becoming increasingly common. However, discussions of these accounts have neglected important questions, including how the context determines the contrasts, and what shared knowledge is necessary for this to be possible. I address these questions, using organic chemistry as a case study. Focusing on one example—nucleophilic substitution—I show that the kinds of causal claims that can be made about an organic reaction depend on how the reaction is modelled, and argue that paying attention (...) to the various ways that reactions are modelled has important implications for our understanding of causation. _1_ Introduction _2_ General Contrastive Causal Claims in Organic Chemistry _3_ Deviant Causal Claims in Organic Chemistry _4_ Nucleophilic Substitution Reactions _5_ The Causal Modelling Tradition _5.1_ The type/token distinction _6_ Competing Reactions _6.1_ Type- and token-causal claims, variables, and values of variables _7_ Disambiguation of ‘Reaction’ _8_ Reaction Kinds _9_ Specific Reactions _9.1_ Specific reactions and token-causal claims _9.2_ Specific reactions and type-causal claims _10_ Implications _10.1_ Kinds of causal claim _10.2_ Contrastive and deviant causal claims _10.3_ Model relativity. (shrink)

Comparisons of causal efficacy are ubiquitous in the practice of science and indeed everyday life. I focus on just one aspect of this task – one to my knowledge nowhere yet addressed satisfactorily – namely, comparing the efficacies of two causes that work in apparently incommensurable ways. Contrary to common opinion I argue that, to be comparable, it is neither necessary nor sufficient that two causes also be commensurable.