The first part of this paper argues that if Craver’s ([2007a], [2007b]) popular mutual manipulability account (MM) of mechanistic constitution is embedded within Woodward’s ([2003]) interventionist theory of causation--for which it is explicitly designed--it either undermines the mechanistic research paradigm by entailing that there do not exist relationships of constitutive relevance or it gives rise to the unwanted consequence that constitution is a form of causation. The second part shows how Woodward’s theory can be adapted in such a way that (...) (MM) neither undermines the mechanistic paradigm nor reduces constitution to causation. However, it turns out that this modified theoretical embedding of (MM) makes it impossible to produce empirical evidence for constitutive relations. The paper ends by suggesting an additional criterion, the fat-handedness criterion, which, when combined with (MM), generates indirect empirical evidence for constitutive relevance. (shrink)

The evidence from randomized controlled trials (RCTs) is widely regarded as supplying the ‘gold standard’ in medicine—we may sometimes have to settle for other forms of evidence, but this is always epistemically second-best. But how well justified is the epistemic claim about the superiority of RCTs? This paper adds to my earlier (predominantly negative) analyses of the claims produced in favour of the idea that randomization plays a uniquely privileged epistemic role, by closely inspecting three related arguments from leading contributors (...) to the burgeoning field of probabilistic causality—Papineau, Cartwright and Pearl. It concludes that none of these further arguments supplies any practical reason for thinking of randomization as having unique epistemic power. IntroductionWhy the issue is of great practical importance—the ECMO casePapineau on the ‘virtues of randomization’Cartwright on causality and the ‘ideal’ randomized experimentPearl on randomization, nets and causesConclusion. (shrink)

Kim’s causal exclusion argument purports to demonstrate that the non-reductive physicalist must treat mental properties (and macro-level properties in general) as causally inert. A number of authors have attempted to resist Kim’s conclusion by utilizing the conceptual resources of Woodward’s interventionist conception of causation. The viability of these responses has been challenged by Gebharter, who argues that the causal exclusion argument is vindicated by the theory of causal Bayesian networks (CBNs). Since the interventionist conception of causation relies crucially on CBNs (...) for its foundations, Gebharter’s argument appears to cast significant doubt on interventionism’s anti-reductionist credentials. In the present article, we both (1) demonstrate that Gebharter’s CBN-theoretic formulation of the exclusion argument relies on some unmotivated and philosophically significant assumptions (especially regarding the relationship between CBNs and the metaphysics of causal relevance), and (2) use Bayesian networks to develop a general theory of causal inference for multi-level systems that can serve as the foundation for an anti-reductionist interventionist account of causation.1. (shrink)

Some machine learning models, in particular deep neural networks (DNNs), are not very well understood; nevertheless, they are frequently used in science. Does this lack of understanding pose a problem for using DNNs to understand empirical phenomena? Emily Sullivan has recently argued that understanding with DNNs is not limited by our lack of understanding of DNNs themselves. In the present paper, we will argue, _contra_ Sullivan, that our current lack of understanding of DNNs does limit our ability to understand with (...) DNNs. Sullivan’s claim hinges on which notion of understanding is at play. If we employ a weak notion of understanding, then her claim is tenable, but rather weak. If, however, we employ a strong notion of understanding, particularly explanatory understanding, then her claim is not tenable. (shrink)

The contemporary theory of epistemic democracy often draws on the Condorcet Jury Theorem to formally justify the ‘wisdom of crowds’. But this theorem is inapplicable in its current form, since one of its premises – voter independence – is notoriously violated. This premise carries responsibility for the theorem's misleading conclusion that ‘large crowds are infallible’. We prove a more useful jury theorem: under defensible premises, ‘large crowds are fallible but better than small groups’. This theorem rehabilitates the importance of deliberation (...) and education, which appear inessential in the classical jury framework. Our theorem is related to Ladha's (1993) seminal jury theorem for interchangeable (‘indistinguishable’) voters based on de Finetti's Theorem. We also prove a more general and simpler such jury theorem. (shrink)

Supporters of the autonomy of higher-level causation (or explanation) often appeal to proportionality, arguing that higher-level causes are more proportional than their lower-level realizers. Recently, measures based on information theory and causal modeling have been proposed that allow one to shed new light on proportionality and the related notion of specificity. In this paper we apply ideas from this literature to the issue of higher vs. lower-level causation (and explanation). Surprisingly, proportionality turns out to be irrelevant for the question of (...) whether higher-level causes (or explanations) can be autonomous; specificity is a much more informative notion for this purpose. (shrink)

This is part A of a paper in which we defend a semantics for counterfactuals which is probabilistic in the sense that the truth condition for counterfactuals refers to a probability measure. Because of its probabilistic nature, it allows a counterfactual ‘ifAthenB’ to be true even in the presence of relevant ‘Aand notB’-worlds, as long such exceptions are not too widely spread. The semantics is made precise and studied in different versions which are related to each other by representation theorems. (...) Despite its probabilistic nature, we show that the semantics and the resulting system of logic may be regarded as a naturalistically vindicated variant of David Lewis’ truth-conditional semantics and logic of counterfactuals. At the same time, the semantics overlaps in various ways with the non-truth-conditional suppositional theory for conditionals that derives from Ernest Adams’ work. We argue that counterfactuals have two kinds of pragmatic meanings and come attached with two types of degrees of acceptability or belief, one being suppositional, the other one being truth based as determined by our probabilistic semantics; these degrees could not always coincide due to a new triviality result for counterfactuals, and they should not be identified in the light of their different interpretation and pragmatic purpose. However, for plain assertability the difference between them does not matter. Hence, if the suppositional theory of counterfactuals is formulated with sufficient care, our truth-conditional theory of counterfactuals is consistent with it. The results of our investigation are used to assess a claim considered by Hawthorne and Hájek, that is, the thesis that most ordinary counterfactuals are false. (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)

Social scientists appeal to various “structures” in their explanations including public policies, economic systems, and social hierarchies. Significant debate surrounds the explanatory relevance of these factors for various outcomes such as health, behavioral, and economic patterns. This paper provides a causal account of social structural explanation that is motivated by Haslanger (2016). This account suggests that social structure can be explanatory in virtue of operating as a causal constraint, which is a causal factor with unique characteristics. A novel causal framework (...) is provided for understanding these explanations–this framework addresses puzzles regarding the mysterious causal influence of social structure, how to understand its relation to individual choice, and what makes it the main explanatory (and causally responsible) factor for various outcomes. (shrink)

I defend a radical interpretation of biological populations—what I call population pluralism—which holds that there are many ways that a particular grouping of individuals can be related such that the grouping satisfies the conditions necessary for those individuals to evolve together. More constraining accounts of biological populations face empirical counter-examples and conceptual difficulties. One of the most intuitive and frequently employed conditions, causal connectivity—itself beset with numerous difficulties—is best construed by considering the relevant causal relations as ‘thick’ causal concepts. I (...) argue that the fine-grained causal relations that could constitute membership in a biological population are huge in number and many are manifested by degree, and thus we can construe population membership as being defined by massively multidimensional constructs, the differences between which are largely arbitrary. I end by showing that positions in two recent debates in theoretical biology depend on a view of biological populations at odds with the pluralism defended here. (shrink)

According to the variety of evidence thesis items of evidence from independent lines of investigation are more confirmatory, ceteris paribus, than, for example, replications of analogous studies. This thesis is known to fail (Bovens and Hartmann; Claveau). However, the results obtained by Bovens and Hartmann only concern instruments whose evidence is either fully random or perfectly reliable; instead, for Claveau, unreliability is modelled as deterministic bias. In both cases, the unreliable instrument delivers totally irrelevant information. We present a model that (...) formalizes both reliability and unreliability differently. Our instruments either are reliable, but affected by random error, or are biased but not deterministically so.Bovens and Hartmann’s results are counter-intuitive in that in their model a long series of consistent reports from the same instrument does not raise suspicion of ‘too-good-to-be-true’ evidence. This happens precisely because they contemplate neither the role of systematic bias, nor unavoidable random error of reliable instruments. In our model, the variety of evidence thesis fails as well, but the area of failure is considerably smaller than for Bovens and Hartmann and Claveau, and holds for (the majority of) realistic cases (that is, where biased instruments are very biased). The essential mechanism that triggers variety of evidence thesis failure is the rate of false to true positives for the two kinds of instruments. Our emphasis is on modelling beliefs about sources of knowledge and their role in hypothesis confirmation in interaction with dimensions of evidence, such as variety and consistency. (shrink)

The appeal to expert opinion is an argument form that uses the verdict of an expert to support a position or hypothesis. A previous scheme-based treatment of the argument form is formalized within a Bayesian network that is able to capture the critical aspects of the argument form, including the central considerations of the expert's expertise and trustworthiness. We propose this as an appropriate normative framework for the argument form, enabling the development and testing of quantitative predictions as to how (...) people evaluate this argument, suggesting that such an approach might be beneficial to argumentation research generally. We subsequently present two experiments as an example of the potential for future research in this vein, demonstrating that participants' quantitative ratings of the convincingness of a proposition that has been supported with an appeal to expert opinion were broadly consistent with the predictions of the Bayesian model. (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)

What conception of causation is at work in the law? I argue that the law implicitly relies on a contrastive conception. In a liability case where the defendant's breach of duty must be shown to have caused the plaintiff's damages, it is not enough to consider what would have happened if the cause had not occurredthe law requires us to look to a specific replacement for the effect, which in this case is the hypothetical outcome in which the plaintiff came (...) off better. In place of I suggest the more explicit An explicitly contrastive approach can thus potentially help the lawyer phrase her causal question in a more explicit way, while shedding light on our conception of causation. (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)

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

The causal nature of evolution is one of the central topics in the philosophy of biology. The issue concerns whether equations used in evolutionary genetics point to some causal processes or purely phenomenological patterns. To address this question the present article builds well-defined causal models that underlie standard equations in evolutionary genetics. These models are based on minimal and biologically plausible hypotheses about selection and reproduction, and generate statistics to predict evolutionary changes. The causal reconstruction of the evolutionary principles shows (...) adaptive evolution as a genuine causal process, where fitness and selection are both causes of evolution. 1 Introduction2 The Philosophical Puzzle3 Causal Models4 Causal Foundations of Evolutionary Genetics4.1 Univariate quantitative genetics model4.1.1 The causal graph4.1.2 Structural equations4.1.3 Deriving evolutionary transition functions4.2 One-locus population genetics model5 Evolution as a Causal Process5.1 Selection as a causal process5.2 Causes of evolutionary change6 Conclusion. (shrink)

Varied evidence confirms more strongly than less varied evidence, ceteris paribus. This epistemological Variety of Evidence Thesis enjoys widespread intuitive support. We put forward a novel explication of one notion of varied evidence and the Variety of Evidence Thesis within Bayesian models of scientific inference by appealing to measures of entropy. Our explication of the Variety of Evidence Thesis holds in many of our models which also pronounce on disconfirmatory and discordant evidence. We argue that our models pronounce rightly. Against (...) a backdrop of failures of the Variety of Evidence Thesis, the intuitive case for the Variety of Evidence Thesis emerges strengthened. Our models do however not support the general case for the thesis since our explication of it fails to hold in certain cases. The parameter space of this failure is explored and an explanation for the failure is offered. (shrink)

Pearl opened the door to formally defining actual causation using causal models. His approach rests on two strategies: first, capturing the widespread intuition that X = x causes Y = y iff X = x is a Necessary Element of a Sufficient Set for Y = y, and second, showing that his definition gives intuitive answers on a wide set of problem cases. This inspired dozens of variations of his definition of actual causation, the most prominent of which are due (...) to Halpern & Pearl. Yet all of them ignore Pearl’s first strategy, and the second strategy taken by itself is unable to deliver a consensus. This paper offers a way out by going back to the first strategy: it offers six formal definitions of causal sufficiency and two interpretations of necessity. Combining the two gives twelve new definitions of actual causation. Several interesting results about these definitions and their relation to the various Halpern & Pearl definitions are presented. Afterwards the second strategy is evaluated as well. In order to maximize neutrality, the paper relies mostly on the examples and intuitions of Halpern & Pearl. One definition comes out as being superior to all others, and is therefore suggested as a new definition of actual causation. (shrink)

Recent epistemology of modality has seen a growing trend towards metaphysics-first approaches. Contrastingly, this paper offers a more philosophically modest account of justifying modal claims, focusing on the practices of scientific modal inferences. Two ways of making such inferences are identified and analyzed: actualist-manipulationist modality and relative modality. In AM, what is observed to be or not to be the case in actuality or under manipulations, allows us to make modal inferences. AM-based inferences are fallible, but the same holds for (...) practically all empirical inquiry. In RM, modal inferences are evaluated relative to what is kept fixed in a system, like a theory or a model. RM-based inferences are more certain but framework-dependent. While elements from both AM and RM can be found in some existing accounts of modality, it is worth highlighting them in their own right and isolating their features for closer scrutiny. This helps to establish their relevant epistemologies that are free from some strong philosophical assumptions often attached to them in the literature. We close by showing how combining these two routes amounts to a view that accounts for a rich variety of modal inferences in science. (shrink)

I introduce the notion of a ‘control variable’ which gives us a way of seeing how mental causation could be an unproblematic case of causation in general, rather than being some sui generis form of causation. Psychological variables may be the control variables for a system for which there are no physical control variables, even in a deterministic physical world. That explains how there can be psychological causation without physical causation, even in a deterministic physical world.

A core, constitutive norm of science is to remove or remedy the artefacts in one’s data. Here, we consider examples of artefacts from many fields of science (for example, astronomy, economics, electrophysiology, psychology, and systems neuroscience) and discuss their contribution to a more general evidential selection problem at the heart of the epistemology of evidence. Synthesizing and building on previously disparate discussions in many areas of the philosophy of science, we provide a novel, causal–pragmatic account that fits the examples and (...) clarifies the practices by which artefacts are discovered and remedied. (shrink)

In this paper, we identify a new and mathematically well-defined sense in which the coherence of a set of hypotheses can be truth-conducive. Our focus is not, as usual, on the probability but on the confirmation of a coherent set and its members. We show that, if evidence confirms a hypothesis, confirmation is “transmitted” to any hypotheses that are sufficiently coherent with the former hypothesis, according to some appropriate probabilistic coherence measure such as Olsson’s or Fitelson’s measure. Our findings have (...) implications for scientific methodology, as they provide a formal rationale for the method of indirect confirmation and the method of confirming theories by confirming their parts. (shrink)

In most cases, liability in tort law is all-or-nothing—a defendant is either fully liable or not at all liable for a claimant's loss. By contrast, this paper defends a causal theory of partial liability. I argue that a defendant should be held liable for a claimant's loss only to the degree to which the defendant's wrongdoing contributed to the causing of the loss. I ground this principle in a conception of tort law as a system of corrective justice and use (...) it to critically evaluate different mechanisms for “limiting” liability for consequences of wrongdoing and for “apportioning” liability between multiple wrongdoers. (shrink)

One of Stuart Glennan's most prominent contributions to the new mechanist debate consists in his reductive analysis of higher-level causation in terms of mechanisms (Glennan, 1996). In this paper I employ the causal Bayes net framework to reconstruct his analysis. This allows for specifying general assumptions which have to be satis ed to get Glennan's approach working. I show that once these assumptions are in place, they imply (against the background of the causal Bayes net machinery) that higher-level causation indeed (...) reduces to interactions between component parts of mechanisms. I also briefly discuss the plausibility of these assumptions and some consequences for the mechanism debate. (shrink)

We standardly evaluate counterfactuals and abilities in temporally asymmetric terms—by keeping the past fixed and holding the future open. Only future events depend counterfactually on what happens now. Past events do not. Conversely, past events are relevant to what abilities one has now in a way that future events are not. Lewis, Sider and others continue to evaluate counterfactuals and abilities in temporally asymmetric terms, even in cases of backwards time travel. I’ll argue that we need more temporally neutral methods. (...) The past shouldn’t always be held fixed, because backwards time travel requires backwards counterfactual dependence. Future events should sometimes be held fixed, because they’re in the causal history of the past, and agents have evidence of them independently of their decisions now. We need temporally neutral methods to maintain connections between causation, counterfactuals and evidence, and if counterfactuals are used to explain the temporal asymmetry of causation. (shrink)

How do people understand questions about cause and prevent? Some theories propose that people affirm that A causes B if A's occurrence makes a difference to B's occurrence in one way or another. Other theories propose that A causes B if some quantity or symbol gets passed in some way from A to B. The aim of our studies is to compare these theories' ability to explain judgements of causation and prevention. We describe six experiments that compare judgements for causal (...) paths that involve a mechanism, i.e. a continuous process of transmission or exchange from cause to effect, against paths that involve no mechanism yet a change in the cause nevertheless brings about a change in the effect. Our results show that people prefer to attribute cause when a mechanism links cause to effect. In contrast, prevention is sensitive both to the presence of an interruption to a causal mechanism and to a change in the outcome in the absence of a mechanism. In this sense, ‘prevent’ means something different than ‘cause not'. We discuss the implications of our results for existing theories of causation. (shrink)

The discovery of conjunctive causes--factors that act in concert to produce or prevent an effect--has been explained by purely covariational theories. Such theories assume that concomitant variations in observable events directly license causal inferences, without postulating the existence of unobservable causal relations. This article discusses problems with these theories, proposes a causal-power theory that overcomes the problems, and reports empirical evidence favoring the new theory. Unlike earlier models, the new theory derives (a) the conditions under which covariation implies conjunctive causation (...) and (b) functions relating observable events to unobservable conjunctive causal strength. This psychological theory, which concerns simple cases involving 2 binary candidate causes and a binary effect, raises questions about normative statistics for testing causal hypotheses regarding categorical data resulting from discrete variables. (shrink)

In this paper, I use interventionist causal models to identify some novel Newcomb problems, and subsequently use these problems to refine existing interventionist treatments of causal decision theory. The new Newcomb problems that make trouble for existing interventionist treatments involve so-called ‘exotic choice’—that is, decision-making contexts where the agent has evidence about the outcome of her choice. I argue that when choice is exotic, the interventionist can adequately capture causal decision-theoretic reasoning by introducing a new interventionist approach to updating on (...) exotic evidence. But I also argue that this new updating procedure is principled only if the interventionist trades in the typical interventionist conception of choice for an alternative Ramseyan conception. I end by arguing that the guide to exotic choice developed here may, despite its name, be useful in some everyday contexts. (shrink)

There is some consensus on the claim that imagination as suppositional thinking can have epistemic value insofar as it’s constrained by a principle of minimal alteration of how we know or believe reality to be – compatibly with the need to accommodate the supposition initiating the imaginative exercise. But in the philosophy of imagination there is no formally precise account of how exactly such minimal alteration is to work. I propose one. I focus on counterfactual imagination, arguing that this can (...) be modeled as simulated belief revision governed by Laplacian imaging. So understood, it can be rationally justified by accuracy considerations: it minimizes expected belief inaccuracy, as measured by the Brier score. (shrink)

The very expertise with which psychologists wield their tools for achieving laboratory control may have had the unwelcome effect of blinding psychologists to the possibilities of discovering principles of behavior without conducting experiments. When creatively interrogated, a diverse range of large, real-world data sets provides powerful diagnostic tools for revealing principles of human judgment, perception, categorization, decision-making, language use, inference, problem solving, and representation. Examples of these data sets include patterns of website links, dictionaries, logs of group interactions, collections of (...) images and image tags, text corpora, history of financial transactions, trends in twitter tag usage and propagation, patents, consumer product sales, performance in high-stakes sporting events, dialect maps, and scientific citations. The goal of this issue is to present some exemplary case studies of mining naturally existing data sets to reveal important principles and phenomena in cognitive science, and to discuss some of the underlying issues involved with conducting traditional experiments, analyses of naturally occurring data, computational modeling, and the synthesis of all three methods. (shrink)

Jim Joyce has argued that David Lewis’s formulation of causal decision theory is inadequate because it fails to apply to the “small world” decisions that people face in real life. Meanwhile, several authors have argued that causal decision theory should be developed such that it integrates the interventionist approach to causal modeling because of the expressive power afforded by the language of causal models, but, as of now, there has been little work towards this end. In this paper, I propose (...) a variant of Lewis’s causal decision theory that is intended to meet both of these demands. Specifically, I argue that Lewis’s causal decision theory can be rendered applicable to small world decisions if one analyzes his dependency hypotheses as causal hypotheses that depend on the interventionist causal modeling framework for their semantics. I then argue that this interventionist variant of Lewis’s causal decision theory is preferable to interventionist causal decision theories that purportedly generalize Lewis’s through the use of conditional probabilities. This is because Lewisian interventionist decision theory captures the causal decision theorist’s conviction that any correlation between what the agent does and cannot cause should be irrelevant to the agent’s choice, while purported generalizations do not. (shrink)

It is considered in some quarters that hypothesis‐driven methods are the only valuable, reliable or significant means of scientific advance. Data‐driven or ‘inductive’ advances in scientific knowledge are then seen as marginal, irrelevant, insecure or wrong‐headed, while the development of technology—which is not of itself ‘hypothesis‐led’ (beyond the recognition that such tools might be of value)—must be seen as equally irrelevant to the hypothetico‐deductive scientific agenda. We argue here that data‐ and technology‐driven programmes are not alternatives to hypothesis‐led studies in (...) scientific knowledge discovery but are complementary and iterative partners with them. Many fields are data‐rich but hypothesis‐poor. Here, computational methods of data analysis, which may be automated, provide the means of generating novel hypotheses, especially in the post‐genomic era. BioEssays 26:99–105, 2004. © 2003 Wiley Periodicals, Inc. (shrink)

Schupbach and Sprenger introduce a novel probabilistic approach to measuring the explanatory power that a given explanans exerts over a corresponding explanandum. Though we are sympathetic to their general approach, we argue that it does not adequately capture the way in which the causal explanatory power that c exerts on e varies with background knowledge. We then amend their approach so that it does capture this variance. Though our account of explanatory power is less ambitious than Schupbach and Sprenger’s in (...) the sense that it is limited to causal explanatory power, it is also more ambitious because we do not limit its domain to cases where c genuinely explains e. Instead, we claim that c causally explains e if and only if our account says that c explains e with some positive amount of causal explanatory power. 1Introduction 2The Logic of Explanatory Power 3Subjective and Nomic Distributions 3.1Actual degrees of belief 3.2The causal distribution 4Background Knowledge 4.1Conditionalization and colliders 4.2A helpful intervention 5Causal Explanatory Power 5.1The applicability of explanatory power 5.2Statistical relevance ≠ causal explanatory power 5.3Interventionist explanatory power 5.4E illustrated 6Conclusion. (shrink)

This paper presents a simple decidable logic of functional dependence LFD, based on an extension of classical propositional logic with dependence atoms plus dependence quantifiers treated as modalities, within the setting of generalized assignment semantics for first order logic. The expressive strength, complete proof calculus and meta-properties of LFD are explored. Various language extensions are presented as well, up to undecidable modal-style logics for independence and dynamic logics of changing dependence models. Finally, more concrete settings for dependence are discussed: continuous (...) dependence in topological models, linear dependence in vector spaces, and temporal dependence in dynamical systems and games. (shrink)

We argue that neuroeconomics should be a mechanistic science. We defend this view as preferable both to a revolutionary perspective, according to which classical economics is eliminated in favour of neuroeconomics, and to a classical economic perspective, according to which economics is insulated from facts about psychology and neuroscience. We argue that, like other mechanistic sciences, neuroeconomics will earn its keep to the extent that it either reconfigures how economists think about decision-making or how neuroscientists think about brain mechanisms underlying (...) behaviour. We discuss some ways that the search for mechanisms can bring about such top-down and bottom-up revision, and we consider some examples from the recent neuroeconomics literature of how varieties of progress of this sort might be achieved. (shrink)

This paper explores some issues concerning how we should think about interventions (in the sense of unconfounded manipulations) of "upper-level" variables in contexts in which these supervene on but are not identical with lower-level realizers. It is argued that we should reject the demand that interventions on upper-level variables must leave their lower-level realizers unchanged– a requirement that within an interventionist framework would imply that upper-level variables are causally inert. Instead an intervention on an upper-level variable at the same time (...) changes its lower-level realizer in a way that is consistent with the change in the upper- level variable. The lower-level realizer should not be regarded as a potential "confounder" of upper-level causal relations, as in "exclusionist" arguments. Several proposals for making this precise are considered and several pro-exclusionist arguments are criticized. (shrink)

Formal methods developed for modeling levels of selection problems have recently been applied to the investigation of major evolutionary transitions. We discuss two new tools of this kind. First, the ‘near-variant test’ can be used to compare the causal adequacy of predictively equivalent representations. Second, ‘state-variable gestalt-switching’ can be used to gain a useful dual perspective on evolutionary processes that involve both higher and lower level populations.

Our scientific theories, like our cognitive structures in general, consist of propositions linked by evidential, explanatory, probabilistic, and logical connections. Those theoretical webs ‘impinge on the world at their edges,’ subject to a continuing barrage of incoming evidence. Our credences in the various elements of those structures change in response to that continuing barrage of evidence, as do the perceived connections between them. Here we model scientific theories as Bayesian nets, with credences at nodes and conditional links between them modelled (...) as conditional probabilities. We update those networks, in terms of both credences at nodes and conditional probabilities at links, through a temporal barrage of random incoming evidence. Robust patterns of punctuated equilibrium, suggestive of ‘normal science’ alternating with ‘paradigm shifts,’ emerge prominently in that change dynamics. The suggestion is that at least some of the phenomena at the core of the Kuhnian tradition are predictable in the typical dynamics of scientific theory change captured as Bayesian nets under even a random evidence barrage. (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)

Much of the modern philosophy of causation has been governed by two ideas: (i) causes make their effects inevitable; (ii) a cause is something that makes a difference to whether its effect occurs. I focus on explaining the origin of idea (ii) and its connection to (i). On my view, the frequent attempts to turn (ii) into an analysis of causation are wrongheaded. Patterns of difference-making aren't what makes causal claims true. They merely provide a useful test for causal claims. (...) Moreover, what justifies us in using them as a test is idea (i). That's how (i) and (ii) are connected. (shrink)

Evolutionary transitions in individuality (ETIs) are events during which individuals at a given level of organization (particles) interact to form higher-level entities (collectives) which are then recognized as new individuals at that level. ETIs are intimately related to levels of selection, which, following Okasha, can be approached from two different perspectives. One, referred to as ‘synchronic’, asks whether selection occurs at the collective level while the partitioning of particles into collectives is taken for granted. The other, referred to as ‘diachronic’, (...) asks about the origins of the partitioning of particles into collectives. After having presented the two perspectives and a classical formalism used to deal with the levels-of-selection question in the literature, namely the multilevel version of the Price equation, I show that because this formalism treats the levels-of-selection question from a synchronic perspective, it is inadequate to explain ETIs. This is because a fundamental aspect of ETIs is the origin of collectives. From there, I develop a framework for levels of selection compatible with the diachronic perspective. This framework relies on the distinction between what I call, on the one hand, a ‘functional aggregative collective trait’, and on the other hand, a ‘functional non-aggregative collective trait’. After having presented this distinction, I implement it in the Price equation, leading to a new statistical partitioning of this equation which, I argue, represents a causal decomposition more relevant for ETIs. Finally, I exploit this partitioning to explain the critical stages of an ETI. In addition to its explanatory power, a measure of the degree of functional non-aggregativity could be used as a proxy for the degree of individuality of a collective. (shrink)

Galles & Pearl (l998) claimed that s [possible-worlds] framework.s framework. Recursive models are shown to correspond precisely to a subclass of (possible-world) counterfactual structures. On the other hand, a slight generalization of recursive models, models where all equations have unique solutions, is shown to be incomparable in expressive power to counterfactual structures, despite the fact that the Galles and Pearl arguments should apply to them as well. The problem with the Galles and Pearl argument is identified: an axiom that they (...) viewed as irrelevant, because it involved disjunction (which was not in their language), is not irrelevant at all. (shrink)

The framework of causal Bayes nets, currently influential in several scientific disciplines, provides a rich formalism to study the connection between causality and probability from an epistemological perspective. This article compares three assumptions in the literature that seem to constrain the connection between causality and probability in the style of Occam's razor. The trio includes two minimality assumptions—one formulated by Spirtes, Glymour, and Scheines (SGS) and the other due to Pearl—and the more well-known faithfulness or stability assumption. In terms of (...) logical strength, it is fairly obvious that the three form a sequence of increasingly stronger assumptions. The focus of this article, however, is to investigate the nature of their relative strength. The comparative analysis reveals an important sense in which Pearl's minimality assumption is as strong as the faithfulness assumption and identifies a useful condition under which it is as safe as SGS's relatively secure minimality assumption. Both findings have notable implications for the theory and practice of causal inference. 1 Introduction2 Background: Inference of Causal Structure in Markovian Causal Models3 Three Assumptions of Simplicity4 A Comparison of P-minimality and Faithfulness5 A Comparison of P-minimality and SGS-minimality6 Methodological Formulations and Prior Knowledge of Causal Order7 Conclusion. (shrink)