According to orthodox causal decision theory, performing an action can give you information about factors outside of your control, but you should not take this information into account when deciding what to do. Causal decision theorists caution against an irrational policy of 'managing the news'. But, by providing information about factors outside of your control, performing an act can give you two, importantly different, kinds of good news. It can tell you that the world in which you find yourself is (...) good in ways you can't control, and it can also tell you that the act itself is in a position to make the world better. While the first kind of news does not speak in favor of performing an act, I believe that the second kind of news does. I present a revision of causal decision theory which advises you to manage the news about the good you stand to promote, while ignoring news about the good the world has provided for you. (shrink)

„Errors are the greatest obstacles to the progress of science; to correct such errors is of more practical value than to achieve new knowledge,“ asserted Eugen Bleuler. Basic error of several prevailing classification schemes of pathological conditions, as for example ICD-10, lies in confusing and mixing symptoms with diseases, what makes them unscientific. Considering the need to bring order into the chaos and light into terminological obscureness, I introduce the Causal classification of diseases originating from the notion of bodily wholeness (...) and causality of its loss. (shrink)

The Causal Exclusion Problem is raised in many domains, including in the metaphysics of macroscopic objects. If there is a complete explanation of macroscopic effects in terms of the microscopic entities that compose macroscopic objects, then the efficacy of the macroscopic will be threatened with exclusion. I argue that we can avoid the problem if we accept that macroscopic objects are ontically vague. Then, it is indeterminate which collection of microscopic entities compose them, and so information about microscopic entities is (...) insufficient to provide a complete explanation of certain properties of macroscopic objects. After outlining this solution, I consider several objections. (shrink)

The physical realm is causally closed, according to physicalists like me. But why is it causally closed, what metaphysically explains causal closure? I argue that reductive physicalists are committed to one explanation of causal closure to the exclusion of any independent explanation, and that as a result, they must give up on using a causal argument to attack mind–body dualism. Reductive physicalists should view dualism in much the way that we view the hypothesis that unicorns exist, or that the Kansas (...) City Royals won the 2003 World Series: false, but not objectionable in any distinctively causal way. My argument turns on connections between explanation, counterfactuals, and inductive confirmation. (shrink)

Discovering high-level causal relations from low-level data is an important and challenging problem that comes up frequently in the natural and social sciences. In a series of papers, Chalupka etal. (2015, 2016a, 2016b, 2017) develop a procedure forcausal feature learning (CFL) in an effortto automate this task. We argue that CFL does not recommend coarsening in cases where pragmatic considerations rule in favor of it, and recommends coarsening in cases where pragmatic considerations rule against it. We propose a new technique, (...) pragmatic causal feature learning (PCFL), which extends the original CFL algorithm in useful and intuitive ways. We show that PCFL has the same attractive measure-theoretic properties as the original CFL algorithm. We compare the performance of both methods through theoretical analysis and experiments. (shrink)

The recent literature on causality has seen the introduction of several distinctions within causality, which are thought to be important for understanding the widespread scientific practice of focusing causal explanations on a subset of the factors that are causally relevant for a phenomenon. Concepts used to draw such distinctions include, among others, stability, specificity, proportionality, or actual-difference making. In this contribution, I propose a new distinction that picks out an explanatorily salient class of causes in biological systems. Some (...) select causes in complex biological systems, I argue, have the property of enabling coherent causal control of these systems. Examples of such control variables include hormones and other signaling molecules, e.g., TOR (target of rapamycin), morphogens or the products of homeotic selector genes in embryonic pattern formation. I propose an analysis of this notion based on concepts borrowed from causal graph theory. (shrink)

Causal essentialists hold that a property essentially bears its causal and nomic relations. Further, as many causal essentialists have noted, the main motivations for causal essentialism also motivate holding that properties are individuated in terms of their causal and nomic relations. This amounts to a kind of identity of indiscernibles thesis; properties that are indiscernible with respect to their causal and nomic relations are identical. This can be compared with the more well-known identity of indiscernibles thesis, according to which particulars (...) that are qualitatively indiscernible are identical. Robert Adams has developed a well-known objection to this thesis by considering a series of possibilities involving nearly qualitatively indiscernible particulars that naturally leads to a possibility involving qualitatively indiscernible particulars. I argue that we can construct parallel cases involving a series of possibilities involving properties that are nearly indiscernible with respect to their causal and nomic relations that naturally lead to possibilities involving properties that are indiscernible with respect to their causal and nomic relations. The same features that make Adams’ argument forceful also carry over to my cases, giving us a powerful objection to the causal essentialist identity of indiscernibles thesis. (shrink)

Causal theories of perception typically have problems in explaining deviant causal chains. They also have difficulty with other unusual putative cases of perception involving prosthetic aids, defective perception, scientifically extended cases of perception, and so on. But I show how a more adequate reflexive causal theory, in which objects or properties X cause a perceiver to acquire X-related dispositions toward that very same item X, can provide a plausible and principled perceptual explanation of all of these kinds of cases. A (...) critical discussion of David Lewis's perceptual descriptivist views is also provided, including a defense of the logical possibility of systematic misperception or perceptual error for a perceiver, in spite of its empirical improbability. (shrink)

Among the factors necessary for the occurrence of some event, which of these are selectively highlighted in its explanation and labeled as causes — and which are explanatorily omitted, or relegated to the status of background conditions? Following J. S. Mill, most have thought that only a pragmatic answer to this question was possible. In this paper I suggest we understand this ‘causal selection problem’ in causal-explanatory terms, and propose that explanatory trade-offs between abstraction and stability can provide a principled (...) solution to it. After sketching that solution, it is applied to a few biological examples, including to a debate concerning the ‘causal democracy’ of organismal development, with an anti-democratic (though not a gene-centric) moral. (shrink)

We develop a new version of the causal theory of spacetime. Whereas traditional versions of the theory seek to identify spatiotemporal relations with causal relations, the version we develop takes causal relations to be the grounds for spatiotemporal relations. Causation is thus distinct from, and more basic than, spacetime. We argue that this non-identity theory, suitably developed, avoids the challenges facing the traditional identity theory.

The epistemic theory of causality views causality as a tool that helps us to predict, explain and control our world, rather than as a relation that exists independently of our epistemic practices. In this chapter, we first provide an introduction to the epistemic theory of causality. We then outline four considerations that motivate the epistemic theory: the failure of standard theories of causality; parsimony; the epistemology of causality; and neutrality. We illustrate these four considerations in (...) the contexts of the social sciences and the cognitive sciences. We argue that the epistemic theory provides a very natural account of causality across these contexts. (shrink)

The classic formulation of causal decision theory (CDT) appeals to counterfactuals. It says that you should aim to choose an option that would have a good outcome, were you to choose it. However, this version of CDT faces trouble if the laws of nature are deterministic. After all, the standard theory of counterfactuals says that, if the laws are deterministic, then if anything—including the choice you make—were different in the present, either the laws would be violated or the distant past (...) would be changed. And as several authors have shown, it's easy to transform this upshot of the standard theory of counterfactuals into full-blown counterexamples to CDT. In response to these counterexamples, I argue here that the problem lies, not so much with CDT's guiding idea—that it's the expected causal consequences of your actions that matter for rational decision-making—but with the fact that the classic formulation of CDT doesn't pay sufficient attention to the context-sensitivity of counterfactuals. I develop a contextualist version of CDT which better accounts for this context-sensitivity. And I show that my theory avoids the problems faced by the classic formulation of CDT in determinstic worlds. (shrink)

Evidential decision theory (EDT) says that the choiceworthiness of an option depends on its evidential connections to possible outcomes. Causal decision theory (CDT) holds that it depends on your beliefs about its causal connections. While Newcomb cases support CDT, Arif Ahmed has described examples that support EDT. A new account is needed to get all cases right. I argue that an option A's choiceworthiness is determined by the probability that a good outcome ensues at possible A‐worlds that match actuality in (...) the facts causally unaffected by your decision (the “unaffected facts”). Moreover, you should evaluate A on the assumption that A is compossible with the unaffected facts. This view entails that you should use EDT when evaluating A on the assumption that the unaffected facts determine your action, but use CDT when assessing A on the opposite assumption. A's choiceworthiness equals a weighted average of these conditional assessments. The weights are determined by your beliefs about whether the unaffected fact determine your action. This account gets both Newcomb and Ahmed cases right. According to an influential view, whether you take the unaffected facts to determine your action can make a difference to whether you can regard yourself as free and the action as being under your control. While my account is neutral on this issue, it entails that whether you take the unaffected facts to determine your action is important in a different way: it matters to whether you should follow EDT or CDT. (shrink)

The chapter explores whether, or to what extent, recent work in experimental philosophy puts pressure on the idea that the concept of causation is ‘egalitarian’. Causal selection – where experimental subjects tend to rate the causal strength of (for example) a norm-violator more strongly than a non-norm-violator – is a well established phenomenon, and is in prima facie tension with an egalitarian conception of causation; it also, indirectly, puts prima facie pressure on the idea that causation is a worldly phenomenon (...) whose obtaining is independent of facts about norms. The chapter explores both the various psychological mechanisms and the broadly pragmatic approaches to explaining causal selection. It argues that the answer to the question whether or not the concept of causation is egalitarian is currently significantly empirically underdetermined, and suggests some avenues for further investigation. (shrink)

Decision-making typically requires judgments about causal relations: we need to know the causal effects of our actions and the causal relevance of various environmental factors. We investigate how several individuals' causal judgments can be aggregated into collective causal judgments. First, we consider the aggregation of causal judgments via the aggregation of probabilistic judgments, and identify the limitations of this approach. We then explore the possibility of aggregating causal judgments independently of probabilistic ones. Formally, we introduce the problem of causal-network aggregation. (...) Finally, we revisit the aggregation of probabilistic judgments when this is constrained by prior aggregation of qualitative causal judgments. (shrink)

Standard definitions of causal closure focus on where the causes in question are. In this paper, the focus is changed to where they are not. Causal closure is linked to the principle that no cause of another universe causes an event in a particular universe. This view permits the one universe to be affected by the other via an interface. An interface between universes can be seen as a domain that violates the suggested account of causal closure, suggesting a view (...) in which universes are causally closed whereas interfaces are not. On this basis, universes are not affected by other universes directly but rather indirectly. (shrink)

This paper provides a general introduction to the use of causal models in the metaphysics of causation, specifically structural equation models and directed acyclic graphs. It reviews the formal framework, lays out a method of interpretation capable of representing different underlying metaphysical relations, and describes the use of these models in analyzing causation.

Causal selection is the task of picking out, from a field of known causally relevant factors, some factors as elements of an explanation. The Causal Parity Thesis in the philosophy of biology challenges the usual ways of making such selections among different causes operating in a developing organism. The main target of this thesis is usually gene centrism, the doctrine that genes play some special role in ontogeny, which is often described in terms of information-bearing or programming. This paper is (...) concerned with the attempt of confronting the challenge coming from the Causal Parity Thesis by offering principles of causal selection that are spelled out in terms of an explicit philosophical account of causation, namely an interventionist account. I show that two such accounts that have been developed, although they contain important insights about causation in biology, nonetheless fail to provide an adequate reply to the Causal Parity challenge: Ken Waters's account of actual-difference making and Jim Woodward's account of causal specificity. A combination of the two also doesn't do the trick, nor does Laura Franklin-Hall's account of explanation (in this volume). We need additional conceptual resources. I argue that the resources we need consist in a special class of counterfactual conditionals, namely counterfactuals the antecedents of which describe biologically normal interventions. (shrink)

Causal accounts of scientific explanation are currently broadly accepted (though not universally so). My first task in this paper is to show that, even for a causal approach to explanation, significant features of explanatory practice are not determined by settling how causal facts bear on the phenomenon to be explained. I then develop a broadly causal approach to explanation that accounts for the additional features that I argue an explanation should have. This approach to explanation makes sense of several aspects (...) of actual explanatory practice, including the widespread use of equilibrium explanations, the formulation of distinct explanations for a single event, and the tight relationship between explanations of events and explanations of causal regularities. (shrink)

Modeling mechanisms is central to the biological sciences – for purposes of explanation, prediction, extrapolation, and manipulation. A closer look at the philosophical literature reveals that mechanisms are predominantly modeled in a purely qualitative way. That is, mechanistic models are conceived of as representing how certain entities and activities are spatially and temporally organized so that they bring about the behavior of the mechanism in question. Although this adequately characterizes how mechanisms are represented in biology textbooks, contemporary biological research practice (...) shows the need for quantitative, probabilistic models of mechanisms, too. In this paper we argue that the formal framework of causal graph theory is well-suited to provide us with models of biological mechanisms that incorporate quantitative and probabilistic information. On the ba-sis of an example from contemporary biological practice, namely feedback regulation of fatty acid biosynthesis in Brassica napus, we show that causal graph theoretical models can account for feedback as well as for the multi-level character of mechanisms. However, we do not claim that causal graph theoretical representations of mechanisms are advantageous in all respects and should replace common qualitative models. Rather, we endorse the more balanced view that causal graph theoretical models of mechanisms are useful for some purposes, while being insufficient for others. (shrink)

When agents violate norms, they are typically judged to be more of a cause of resulting outcomes. In this paper, we suggest that norm violations also affect the causality attributed to other agents, a phenomenon we refer to as "causal superseding." We propose and test a counterfactual reasoning model of this phenomenon in four experiments. Experiments 1 and 2 provide an initial demonstration of the causal superseding effect and distinguish it from previously studied effects. Experiment 3 shows that this (...) causal superseding effect is dependent on a particular event structure, following a prediction of our counterfactual model. Experiment 4 demonstrates that causal superseding can occur with violations of non-moral norms. We propose a model of the superseding effect based on the idea of counterfactual sufficiency. (shrink)

Michael Devitt develops a hybrid causal theory of non-empty proper names and certain singular terms that semantically resemble them. He considers that the use of a name designates an object not by virtue of the different information we know about it, but by a causal network that starts from the first uses of the name to designate the object, through a "reference borrowing" from the previous uses. DOI: 10.13140/RG.2.2.35828.50564.

Causal models show promise as a foundation for the semantics of counterfactual sentences. However, current approaches face limitations compared to the alternative similarity theory: they only apply to a limited subset of counterfactuals and the connection to counterfactual logic is not straightforward. This paper addresses these difficulties using exogenous interventions, where causal interventions change the values of exogenous variables rather than structural equations. This model accommodates judgments about backtracking counterfactuals, extends to logically complex counterfactuals, and validates familiar principles of counterfactual (...) logic. This combines the interventionist intuitions of the causal approach with the logical advantages of the similarity approach. (shrink)

Causal descriptivism and its relative nominal descriptivism are critically examined. It is argued that they do not manage to undermine the principal conclusions of the new theory of reference.

When we compare the influences of two causes on an outcome, if the conclusion from every group is against that from the conflation, we think there is Simpson’s Paradox. The Existing Causal Inference Theory (ECIT) can make the overall conclusion consistent with the grouping conclusion by removing the confounder’s influence to eliminate the paradox. The ECIT uses relative risk difference Pd = max(0, (R − 1)/R) (R denotes the risk ratio) as the probability of causation. In contrast, Philosopher Fitelson uses (...) confirmation measure D (posterior probability minus prior probability) to measure the strength of causation. Fitelson concludes that from the perspective of Bayesian confirmation, we should directly accept the overall conclusion without considering the paradox. The author proposed a Bayesian confirmation measure b* similar to Pd before. To overcome the contradiction between the ECIT and Bayesian confirmation, the author uses the semantic information method with the minimum cross-entropy criterion to deduce causal confirmation measure Cc = (R − 1)/max(R, 1). Cc is like Pd but has normalizing property (between −1 and 1) and cause symmetry. It especially fits cases where a cause restrains an outcome, such as the COVID-19 vaccine controlling the infection. Some examples (about kidney stone treatments and COVID-19) reveal that Pd and Cc are more reasonable than D; Cc is more useful than Pd. (shrink)

Modern fundamental science tends to avoid the principle of physical causality and realism, replacing it with heuristically postulated and separated mathematical constructions that impose their own rules before being adjusted to measurement results. While it is officially accepted as the single possible kind of rigorous knowledge, we argue that another, explicitly extended kind of science can provide the causally complete picture of reality avoiding the glaring gaps, growing problems and persisting stagnation of the artificially reduced knowledge paradigm. The logic (...) of science development and especially its current state call for the urgently needed transition to the extended, causally complete kind of knowledge and related sustainable progress at superior creativity levels of self-aware, reason-based society. (shrink)

Recent attempts to resolve the Paradox of the Gatecrasher rest on a now familiar distinction between individual and bare statistical evidence. This paper investigates two such approaches, the causal approach to individual evidence and a recently influential (and award-winning) modal account that explicates individual evidence in terms of Nozick's notion of sensitivity. This paper offers counterexamples to both approaches, explicates a problem concerning necessary truths for the sensitivity account, and argues that either view is implausibly committed to the impossibility of (...) no-fault wrongful convictions. The paper finally concludes that the distinction between individual and bare statistical evidence cannot be maintained in terms of causation or sensitivity. We have to look elsewhere for a solution of the Paradox of the Gatecrasher. (shrink)

The problem of the man who met death in Damascus appeared in the infancy of the theory of rational choice known as causal decision theory. A straightforward, unadorned version of causal decision theory is presented here and applied, along with Brian Skyrms’ deliberation dynamics, to Death in Damascus and similar problems. Decision instability is a fascinating topic, but not a source of difficulty for causal decision theory. Andy Egan’s purported counterexample to causal decision theory, Murder Lesion, is considered; a simple (...) response shows how Murder Lesion and similar examples fail to be counterexamples, and clarifies the use of the unadorned theory in problems of decision instability. I compare unadorned causal decision theory to previous treatments by Frank Arntzenius and by Jim Joyce, and recommend a well-founded heuristic that all three accounts can endorse. Whatever course deliberation takes, causal decision theory is consistently a good guide to rational action. (shrink)

Despite being a milestone in the history of statistical causal inference, Sewall Wright’s 1918 invention of path analysis did not receive much immediate attention from the statistical and scientific community. Through a careful historical analysis, this paper reveals some previously overlooked philosophical issues concerning the history of causal inference. Placing the invention of path analysis in a broader historical and intellectual context, I portray the scientific community’s initial lack of interest in the method as a natural consequence of relevant scientific (...) and philosophical conditions. In addition to Karl Pearson’s positivist refutation of causation, I contend that the acceptance of path analysis faced several other challenges, including the introduction of a new formalism, conceptual barriers to causal inference, and the lack of model-based statistical thinking. The presence of these challenges shows that the delayed progress in causal inference in the early twentieth century was inevitable. (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)

Causal reasoning and game-theoretic reasoning are fundamental topics in artificial intelligence, among many other disciplines: this paper is concerned with their intersection. Despite their importance, a formal framework that supports both these forms of reasoning has, until now, been lacking. We offer a solution in the form of (structural) causal games, which can be seen as extending Pearl's causal hierarchy to the game-theoretic domain, or as extending Koller and Milch's multi-agent influence diagrams to the causal domain. We then consider three (...) key questions: i) How can the (causal) dependencies in games - either between variables, or between strategies - be modelled in a uniform, principled manner? ii) How may causal queries be computed in causal games, and what assumptions does this require? iii) How do causal games compare to existing formalisms? To address question i), we introduce mechanised games, which encode dependencies between agents' decision rules and the distributions governing the game. In response to question ii), we present definitions of predictions, interventions, and counterfactuals, and discuss the assumptions required for each. Regarding question iii), we describe correspondences between causal games and other formalisms, and explain how causal games can be used to answer queries that other causal or game-theoretic models do not support. Finally, we highlight possible applications of causal games, aided by an extensive open-source Python library. (shrink)

Causal selection is the task of picking out, from a field of known causally relevant factors, some factors as elements of an explanation. The Causal Parity Thesis in the philosophy of biology challenges the usual ways of making such selections among different causes operating in a developing organism. The main target of this thesis is usually gene centrism, the doctrine that genes play some special role in ontogeny, which is often described in terms of information-bearing or programming. This paper is (...) concerned with the attempt of confronting the challenge coming from the Causal Parity Thesis by offering principles of causal selection that are spelled out in terms of an explicit philosophical account of causation, namely an interventionist account. I show that two such accounts that have been developed, although they contain important insights about causation in biology, nonetheless fail to provide an adequate reply to the Causal Parity challenge: Ken Waters's account of actual-difference making and Jim Woodward's account of causal specificity. A combination of the two also doesn't do the trick, nor does Laura Franklin-Hall's account of explanation (in this volume). We need additional conceptual resources. I argue that the resources we need consist in a special class of counterfactual conditionals, namely counterfactuals the antecedents of which describe biologically normal interventions. (shrink)

Aristotle grants perceptible qualities the power to generate sense perception in animals. But it is unclear whether, for him, these qualities can produce any effect other than perception. In this paper I address this issue through a novel approach. To show that they can produce non-perceptual effects, I explore contexts in his extant works where qualities appear to do causal work in nature without leading to perception in animals. This inquiry aims to demonstrate that Aristotle’s realism about qualities survives a (...) potential threat posed by views that dispute the qualities’ causal efficacy outside perception. (shrink)

I develop an account of ecological role functions—the functions of species within ecosystems—which is informed by alternative regime phenomena in ecology. My account is a causal-role theory which includes a counterfactual sensitivity condition. The account tracks and explains a distinction ecologists make between functions and various activities which are not functions. My counterfactual sensitivity condition resolves the liberality problem often attributed to causal-role theories of function, while also illuminating the explanatory centrality of role functions within ecology.

Jaegwon Kim’s influential exclusion argument attempts to demonstrate the inconsistency of nonreductive materialism in the philosophy of mind. Kim’s argument begins by showing that the three main theses of nonreductive materialism, plus two additional considerations, lead to a specific and familiar picture of mental causation. The exclusion argument can succeed only if, as Kim claims, this picture is not one of genuine causal overdetermination. Accordingly, one can resist Kim’s conclusion by denying this claim, maintaining instead that the effects of the (...) mental are always causally overdetermined. I call this strategy the ‘ overdetermination challenge’. One of the main aims of this paper is to show that the overdetermination challenge is the most appropriate response to Kim’s exclusion argument, at least in its latest form. I argue that Kim fails to adequately respond to the overdetermination challenge, thus failing to prevent his opponents from reasonably maintaining that the effects of the mental are always causally overdetermined. Interestingly, this discussion reveals a curious dialectical feature of Kim’s latest response to the overdetermination challenge: if it succeeds, then a new, simpler and more compact version of the exclusion argument is available. While I argue against the consequent of this conditional, thereby also rejecting the antecedent, this dialectical feature should be of interest to philosophers on either side of this debate. (shrink)

Some non-reductionists claim that so-called ‘exclusion arguments’ against their position rely on a notion of causal sufficiency that is particularly problematic. I argue that such concerns about the role of causal sufficiency in exclusion arguments are relatively superficial since exclusionists can address them by reformulating exclusion arguments in terms of physical sufficiency. The resulting exclusion arguments still face familiar problems, but these are not related to the choice between causal sufficiency and physical sufficiency. The upshot is that objections to the (...) notion of causal sufficiency can be answered in a straightforward fashion and that such objections therefore do not pose a serious threat to exclusion arguments. (shrink)

The causal impacts of genes and environment on any one biological trait are inextricably entangled, and consequently it is widely accepted that it makes no sense in singleton cases to privilege either factor for particular credit. On the other hand, at a population level it may well be the case that one of the factors is responsible for more variation than the other. Standard methodological practice in biology uses the statistical technique of analysis of variance to measure this latter kind (...) of causal efficacy. In this paper, I argue that: 1) analysis of variance is in fact badly suited to this role; and. (shrink)

Causation appears to present us with an interpretative difficulty. While arguably a redundant relation given fundamental physics, it is nevertheless apparently pragmatically indispensable. This chapter revisits certain arguments made previously by the author for these claims with the benefit of hindsight, starting with the role of causal models in the human sciences, and attempting to explain why it is not possible to straightforwardly ground such models in fundamental physics. This suggests that further constraints, going beyond physics, are needed to legitimate (...) such models. These supplementary constraints could be reified, but that would seem to conflict with the completeness of physics. A response is to emphasize the practical role of causal talk, and the author suggests that a fictionalist approach might be worth exploring. After clarifying fictionalism as a general approach, they carry out in some detail the project of clarifying what a fictionalist attitude to causation would involve. (shrink)

Given the importance of the principle of causality for the demonstration of God’s existence, this paper attempts to justify the evidence and necessity of the principle of causality, by following Fr. Fabro’s Thomistic defense—based on the notion of participation—but adding a particular emphasis on the notion of “being which is not per se,” this latter as an explanatory notion of the notion of “being which is by participation.” The introductory remarks touch upon two misunderstandings regarding the notion of (...) participation employed as a subject of the principle of causality: the first, considering “participated being” as a synonym of “received being,” and the second, the confusion, regarding the notion of being by participation, between its notional dependence on the notion of being as a whole and its real dependence on the real intensive Being. Then, in the first point, the defense of the principle of causality is distinguished from other related problems, like the particular applications of this principle. In the second and main point, we try to justify the necessity of being caused in the being which is experienced as being by participation, as follows: 1) that which is something by participation is not this something per se; 2) now, that which is not per se, either is not or is per aliud, 3) Therefore, that which is something by participation is per aliud. In the third and last point, we endeavor to justify the Thomism of our defense and of our emphasis on this notion of “being which is not per se” by considering two texts of St. Thomas. (shrink)

This paper sketches a causal account of scientific explanation designed to sustain the judgment that high-level, detail-sparse explanations—particularly those offered in biology—can be at least as explanatorily valuable as lower-level counterparts. The motivating idea is that complete explanations maximize causal economy: they cite those aspects of an event’s causal run-up that offer the biggest-bang-for-your-buck, by costing less (in virtue of being abstract) and delivering more (in virtue making the event stable or robust).

People more frequently select norm-violating factors, relative to norm- conforming ones, as the cause of some outcome. Until recently, this abnormal-selection effect has been studied using retrospective vignette-based paradigms. We use a novel set of video stimuli to investigate this effect for prospective causal judgments—i.e., judgments about the cause of some future outcome. Four experiments show that people more frequently select norm- violating factors, relative to norm-conforming ones, as the cause of some future outcome. We show that the abnormal-selection effects (...) are not primarily explained by the perception of agency (Experiment 4). We discuss these results in relation to recent efforts to model causal judgment. (shrink)

In previous work I have argued that talk about negative events should not be taken at face value: typically, what we are inclined to think of as a negative event (John’s failure to go jogging) is just an ordinary, positive event (his going to the movie instead); it is a positive event under a negative description. Here I consider more closely the difficulties that arise in those cases where no positive event seems available to do the job, as with putative (...) cases of causation by omission. In particular, I elaborate on Helen Beebee’s idea that not all causal explanations are reports of causation. When we mention John’s failure to turn off the gas as an explanans of why there was an explosion, we do not say what caused the explosion. We do not mention any of the relevant causes. We just remark that one sort of event that was supposed to occur, and whose occurrence would have prevented the explosion, did not in fact occur. (shrink)

Causal exclusion arguments are taken to threaten the autonomy of the special sciences, and the causal efficacy of mental properties. A recent line of response to these arguments has appealed to “independently plausible” and “well grounded” theories of causation to rebut key premises. In this paper I consider two papers which proceed in this vein and show that they share a common feature: they both require causes to be proportional to their effects. I argue that this feature is a bug, (...) and one that generalises: any attempt to rescue the autonomy of the special sciences, or the efficacy of the mental, from exclusion worries had better not look to proportionality for help. (shrink)

Abstract In this paper I consider an easier-to-read and improved to a certain extent version of the causal chance-based analysis of counterfactuals that I proposed and argued for in my A Theory of Counterfactuals. Sections 2, 3 and 4 form Part I: In it, I survey the analysis of the core counterfactuals (in which, very roughly, the antecedent is compatible with history prior to it). In section 2 I go through the three main aspects of this analysis, which are the (...) following. First, it is a causal analysis, in that it requires that intermediate events to which the antecedent event is not a cause be preserved in the main truth-condition schema. Second, it highlights the central notion to the semantics of counterfactuals on the account presented here -- the notion of the counterfactual probability of a given counterfactual, which is the probability of the consequent given the following: the antecedent, the prior history, and the preserved intermediate events. Third, it considers the truth conditions for counterfactuals of this sort as consisting in this counterfactual probability being higher than a threshold. In section 3, I re-formulate the analysis of preservational counterfactuals in terms of the notion of being a cause, which ends up being quite compact. In section 4 I illustrate this analysis by showing how it handles two examples that have been considered puzzling – Morgenbesser's counterfactual and Edgington's counterfactual. Sections 5 and on constitute Part II: Its main initial thrust is provided in section 5, where I present the main lines of the extension of the theory from the core counterfactuals (analyzed in part I) to counterfactuals (roughly) whose antecedents are not compatible with their prior history. In this part II, I elaborate on counterfactuals that don't belong to the core, and more specifically on so-called reconstructional counterfactuals (as opposed to the preservational counterfactuals, which constitute the core counterfactual-type). The heart of the analysis is formulated in terms of processes leading to the antecedent (event/state), and more specifically in terms of processes likely to have led to the antecedent, a notion which is analyzed entirely in terms of chance. It covers so-called reconstructional counterfactuals as opposed to the core, so-called preservational counterfactuals, which are analyzed in sections 2 and 3 of part I. The counterfactual probability of such reconstructional counterfactuals is determined via the probability of possible processes leading to the antecedent weighed, primarily and roughly, by the conditional probability of the antecedent given such process: The counterfactual probability is thus, very roughly, a weighted sum for all processes most likely to have led to the antecedent, diverging at a fixed time. In section 6 I explain and elaborate further on the main points in section 5. In section 7 I illustrate the reconstructional analysis. I specify counterfactuals which are so-called process-pointers, since their consequent specifies stages in processes likely to have led to their antecedent. I argue that so-called backtracking counterfactuals are process-pointers counterfactuals, which fit into the reconstructional analysis, and do not call for a separate reading. I then illustrate cases where a speaker unwittingly employs a certain counterfactual while charitably construable as intending to assert (or ‘having in mind’) another. Here I also cover the issue of how to construe what one can take as back-tracking counterfactuals, or counterfactuals of the reconstructional sort, and more specifically, which divergence point they should be taken as alluding to (prior to which the history is held fixed). Some such cases also give rise to what one can take as a dual reading of a counterfactual between preservational and reconstructional readings. Such cases may yield an ambiguity, where in many cases one construal is dominant. In section 8 I illustrate the analysis by applying it to the famous Bizet-Verdi counterfactuals. This detailed analysis of counterfactuals (designed for the indeterministic case) has three main distinctive elements: its being chance-based, its causal aspect, and the use it makes of processes most likely to have led to the antecedent-event. This analysis is couched in a very different conceptual base from, and is an alternative account to, analyses in terms of the standard notion of closeness or distance of possible worlds, which is the main feature of the Stalnaker-Lewis-type analyses of counterfactuals. This notion of closeness or distance plays no role whatsoever in the analysis presented here. (This notion of closeness has been left open by Stalnaker, and to significant extent also by Lewis's second account.) . (shrink)

In this chapter, we outline the range of argument forms involving causation that can be found in everyday discourse. We also survey empirical work concerned with the generation and evaluation of such arguments. This survey makes clear that there is presently no unified body of research concerned with causal argument. We highlight the benefits of a unified treatment both for those interested in causal cognition and those interested in argumentation, and identify the key challenges that must be met for a (...) full understanding of causal argumentation. (shrink)

One primary goal for metaphysical theories of natural kinds is to account for their epistemic fruitfulness. According to cluster theories of natural kinds, this epistemic fruitfulness is grounded in the regular and stable co- occurrence of a broad set of properties. In this paper, I defend the view that such a cluster theory is insufficient to adequately account for the epistemic fruitfulness of kinds. I argue that cluster theories can indeed account for the projectibility of natural kinds, but not for (...) several other epistemic operations that natural kinds support. Natural kinds also play a role in scientific explanations and categorizations. A theory of natural kinds can only account for these additional kind-based epistemic practices if it also analyzes their causal structure. (shrink)

The development of causal modelling since the 1950s has been accompanied by a number of controversies, the most striking of which concerns the Markov condition. Reichenbach's conjunctive forks did satisfy the Markov condition, while Salmon's interactive forks did not. Subsequently some experts in the field have argued that adequate causal models should always satisfy the Markov condition, while others have claimed that non-Markovian causal models are needed in some cases. This paper argues for the second position by considering the multi-causal (...) forks, which are widespread in contemporary medicine (Section 2). A non-Markovian causal model for such forks is introduced and shown to be mathematically tractable (Sections 6, 7, and 8). The paper also gives a general discussion of the controversy about the Markov condition (Section 1), and of the related controversy about probabilistic causality (Sections 3, 4, and 5). (shrink)

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)

The paper contains a novel realist account of causal production and the necessary connection between cause and effect. I argue that the asymmetric relation between causally connected events must be regarded as a product of a symmetric interaction between two or more entities. All the entities involved contribute to the producing, and so count as parts of the cause, and they all suffer a change, and so count as parts of the effect. Cause and effect, on this account, are two (...) different states of the very same compound substance, or system, one coming to exist out of the other. (shrink)

In this paper, I consider Sterba’s recent criticism of skeptical theism in context of his argument from evil. I show that Sterba’s criticism of skeptical theism shares an undesirable trait with all past criticisms of skeptical theism: it fails. This is largely due to his focus on causal connections and his neglect of logical connections. Because of this, his argument remains vulnerable to skeptical theism.