I discuss an important feature of the notion of cause in Post. An. 1. 13, 78b13–28, which has been either neglected or misunderstood. Some have treated it as if Aristotle were introducing a false principle about explanation; others have understood the point in terms of coextensiveness of cause and effect. However, none offers a full exegesis of Aristotle's tangled argument or accounts for all of the text's peculiarities. My aim is to disentangle Aristotle's steps to show that he is arguing (...) in favour of a logical requirement for a middle term's being the appropriate cause of its explanandum. Coextensiveness between the middle term and the attribute it explains is advanced as a sine qua non condition of a middle term's being an appropriate or primary cause. This condition is not restricted either to negative causes or to middle terms in second‐figure syllogisms, but ranges over all primary causes qua primary. (shrink)

We blame faulty brakes for a car crash, or rain for our bad mood. This “merely causal” blame is usually seen as uninteresting. I argue that it is crucial for understanding the interpersonal blame with which we target ourselves and each other. The two are often difficult to distinguish, in a way that plagues philosophical discussions of blame. And interpersonal blame is distinctive, I argue, partly in its causal focus: its attention to a person as cause. I argue that this (...) causal focus helps explain several central characteristics of interpersonal blame: its tendency to exaggerate a person’s causal role, its weakening through attention to personal history or thoughts about determinism, its characteristic ‘force’ or ‘sting’, and our sense that blame is often harmful or unfair. I conclude by drawing out one implication of blame's causal focus: in a certain range of cases, blame is partly under our voluntary control. (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)

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)

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)

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)

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)

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)

Carl Hempel (1965) argued that probabilistic hypotheses are limited in what they can explain. He contended that a hypothesis cannot explain why E is true if the hypothesis says that E has a probability less than 0.5. Wesley Salmon (1971, 1984, 1990, 1998) and Richard Jeffrey (1969) argued to the contrary, contending that P can explain why E is true even when P says that E’s probability is very low. This debate concerned noncontrastive explananda. Here, a view of contrastive causal (...) explanation is described and defended. It provides a new limit on what probabilistic hypotheses can explain; the limitation is that P cannot explain why E is true rather than A if P assign E a probability that is less than or equal to the probability that P assigns to A. The view entails that a true deterministic theory and a true probabilistic theory that apply to the same explanandum partition are such that the deterministic theory explains all the true contrastive propositions constructable from that partition, whereas the probabilistic theory often fails to do so. (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)

"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 models provide a framework for making counterfactual predictions, making them useful for evaluating the truth conditions of counterfactual sentences. However, current causal models for counterfactual semantics face limitations compared to the alternative similarity-based approach: they only apply to a limited subset of counterfactuals and the connection to counterfactual logic is not straightforward. This paper argues that these limitations arise from the theory of interventions where intervening on variables requires changing structural equations rather than the values of variables. Using an (...) alternative theory of exogenous interventions, this paper extends the causal approach to counterfactuals to handle more complex counterfactuals, including backtracking counterfactuals and those with logically complex antecedents. The theory also validates familiar principles of counterfactual logic and offers an explanation for counterfactual disagreement and backtracking readings of forward counterfactuals. (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)

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)

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).

Causal claims are context sensitive. According to the old orthodoxy (Mackie 1974, Lewis 1986, inter alia), the context sensitivity of causal claims is all due to conversational pragmatics. According to the new contextualists (Hitchcock 1996, Woodward 2003, Maslen 2004, Menzies 2004, Schaffer 2005, and Hall ms), at least some of the context sensitivity of causal claims is semantic in nature. I want to discuss the prospects for causal contextualism, by asking why causal claims are context sensitive, what they are sensitive (...) to, and where they are sensitive to it. (shrink)

Causal closure arguments against interactionist dualism are currently popular amongst physicalists. Such an argument appeals to some principles of the causal closure of the physical, together with certain other premises, to conclude that at least some mental events are identical with physical events. However, it is crucial to the success of any such argument that the physical causal closure principle to which it appeals is neither too strong nor too weak by certain standards. In this paper, it is argued that (...) various forms of naturalistic dualism, of an emergentist character, are consistent with the strongest physical causal closure principles that can plausibly be advocated. (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)

In this note, I will discuss one issue concerning the main argument of Mind in a Physical World (Kim, 1998), the Causal Exclusion Argument. The issue is whether it is a consequence of the Causal Exclusion Argument that all macro level causation (that is, causation above the level of fundamental physics) is an illusion, with all of the apparent causal powers of mental and other macro properties draining into the bottom level of physics. I will argue that such a consequence (...) would give us reason to reject the Causal Exclusion Argument. But there is also a stronger challenge, the charge that, if there is no bottom level of physics, the Causal Exclusion Argument has the consequence that “causal powers would drain away into a bottomless pit and there wouldn’t be any causation anywhere.” (81--page numbers that are not attributed to other works are to Kim, 1998). (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)

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)

This paper poses an original puzzle about the relationship between causation and moral responsibility called The Moral Difference Puzzle. Using the puzzle, the paper argues for three related ideas: (1) the existence of a new sort of moral luck; (2) an intractable conflict between the causal concepts used in moral assessment; and (3) inability of leading theories of causation to capture the sorts of causal differences that matter for moral evaluation of agents’ causal contributions to outcomes.

This paper argues that several sorts of metaphysical and semantic indeterminacy afflict the causal relation. If, as it is plausible to hold, there is a relationship between causation and moral responsibility, then indeterminacy in the causal relation results in indeterminacy of moral responsibility more generally.

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)

En este artículo abordo críticamente la aseveración de David Papineau según la cual la evidencia fisiológica acumulada es suficiente para adoptar razonablemente el Principio del Cierre Causal de lo Físico y la vía negativa, viz. entender físico como no mental, como solución al dilema de Hempel. Comenzaremos restando fuerza a tal afirmación revisando el trabajo de W. Penfield y J. Eccles, dos importantes neurocientíficos y declarados dualistas. No obstante, luego nos centraremos en el trabajo de B. Libet en el que (...) se demostraría que los movimientos voluntarios están realmente determinados por causas enteramente fisiológicas, lo cual constituiría una pieza fundamental de evidencia a favor de Papineau. Nuestro análisis mostrará que no se siguen tales conclusiones. Esto tendrá consecuencias negativas para el Cierre Causal de lo Físico y con ello para el Argumento Causal para el Fisicalismo del cual el mencionado principio es premisa clave. (shrink)

Causal selection has to do with the distinction we make between background conditions and “the” true cause or causes of some outcome of interest. A longstanding consensus in philosophy views causal selection as lacking any objective rationale and as guided, instead, by arbitrary, pragmatic, and non-scientific considerations. I argue against this position in the context of causal selection for disease traits. In this domain, causes are selected on the basis of the type of causal control they exhibit over a disease (...) of interest. My analysis clarifies the principled rationale that guides this selection and how it involves both pragmatic and objective considerations, which have been overlooked in the extant literature. (shrink)

The systems studied in the special sciences are often said to be causally autonomous, in the sense that their higher-level properties have causal powers that are independent of the causal powers of their more basic physical properties. This view was espoused by the British emergentists, who claimed that systems achieving a certain level of organizational complexity have distinctive causal powers that emerge from their constituent elements but do not derive from them. More recently, non-reductive physicalists have espoused a similar view (...) about the causal autonomy of special-science properties. They argue that since these properties can typically have multiple physical realizations, they are not identical to physical properties, and further they possess causal powers that differ from those of their physical realisers. Despite the orthodoxy of this view, it is hard to find a clear exposition of its meaning or a defence of it in terms of a well-motivated account of causation. In this paper, we aim to address this gap in the literature by clarifying what is implied by the doctrine of the causal autonomy of special-science properties and by defending the doctrine using a prominent theory of causation from the philosophy of science. (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)

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)

This paper applies Causal Modeling Semantics (CMS, e.g., Galles and Pearl 1998; Pearl 2000; Halpern 2000) to the evaluation of the probability of counterfactuals with disjunctive antecedents. Standard CMS is limited to evaluating (the probability of) counterfactuals whose antecedent is a conjunction of atomic formulas. We extend this framework to disjunctive antecedents, and more generally, to any Boolean combinations of atomic formulas. Our main idea is to assign a probability to a counterfactual ( A ∨ B ) > C at (...) a causal model M by looking at the probability of C in those submodels that truthmake A ∨ B (Briggs 2012; Fine 2016, 2017). The probability of p (( A ∨ B ) > C ) is then calculated as the average of the probability of C in the truthmaking submodels, weighted by the inverse distance to the original model M. The latter is calculated on the basis of a proposal by Eva et al. (2019). Apart from solving a major problem in the research on counterfactuals, our paper shows how work in semantics, causal inference and formal epistemology can be fruitfully combined. (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)

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.

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)

Any property has two sorts of causal features: “forward‐looking” ones, having to do with what its instantiation can contribute to causing, and ldquo;backward‐looking” ones, having to do with how its instantiation can be caused. Such features of a property are essential to it, and properties sharing all of their causal features are identical. Causal necessity is thus a special case of metaphysical necessity. Appeals to imaginability have no more force against this view than they do against the Kripkean view that (...) statements like “Gold is an element” are metaphysically necessary. (shrink)

In psychiatry, pharmacological drugs play an important experimental role in attempts to identify the neurobiological causes of mental disorders. Besides being developed in applied contexts as potential treatments for patients with mental disorders, pharmacological drugs play a crucial role in research contexts as experimental instruments that facilitate the formulation and revision of neurobiological theories of psychopathology. This paper examines the various epistemic functions that pharmacological drugs serve in the discovery, refinement, testing, and elaboration of neurobiological theories of mental disorders. I (...) articulate this thesis with reference to the history of antipsychotic drugs and the evolution of the dopamine hypothesis of schizophrenia in the second half of the twentieth century. I argue that interventions with psychiatric patients through the medium of antipsychotic drugs provide researchers with information and evidence about the neurobiological causes of schizophrenia. This analysis highlights the importance of pharmacological drugs as research tools in the generation of psychiatric knowledge and the dynamic relationship between practical and theoretical contexts in psychiatry. (shrink)

It is natural to think of remembering in terms of causation: I can recall a recent dinner with a friend because I experienced that dinner. Some fifty years ago, Martin and Deutscher (1966) turned this basic thought into a full-fledged theory of memory, a theory that came to dominate the landscape in the philosophy of memory. Remembering, Martin and Deutscher argue, requires the existence of a specific sort of causal connection between the rememberer's original experience of an event and his (...) later representation of that event: a causal connection sustained by a memory trace. In recent years, it has become apparent that this reference to memory traces may be out of step with memory science. Contemporary proponents of the causal theory are thus confronted with the question: is it possible to develop an empirically adequate version of the theory, or is it time to move beyond it? This chapter traces the recent history of the causal theory, showing how increased awareness of the theory’s problems has led to the development of modified version of the causal theory and ultimately to the emergence of postcausal theories. (shrink)

The purpose of this paper is to address a well-known dilemma for physicalism. If mental properties are type identical to physical properties, then their causal efficacy is secure, but at the cost of ruling out mentality in creatures very different to ourselves. On the other hand, if mental properties are multiply realizable, then all kinds of creatures can instantiate them, but then they seem to be causally redundant. The causal exclusion problem depends on the widely held principle that realized properties (...) inherit their causal powers from their realizers. While this principle holds for functional realization, it fails on a broader notion of realization that permits the realization of complex qualitative properties such as spatial and temporal patterns. Such properties are best seen as dependent powerful qualities, which have their causal roles in virtue of being the qualities they are, and do not inherit powers from their realizers. Recent studies have identified one such property—neural synchrony—as a correlate of consciousness. If synchrony is also partially constitutive of consciousness, then phenomenal properties are both multiply realizable and causally novel. I outline a version of representationalism about consciousness on which this constitution claim holds. (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 essay presents a novel counterexample to Causal Decision Theory (CDT). Its interest is that it generates a case in which CDT violates the very principles that motivated it in the first place. The essay argues that the objection applies to all extant formulations of CDT and that the only way out for that theory is a modification of it that entails incompatibilism. The essay invites the reader to find this consequence of CDT a reason to reject it.

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)

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)

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)

This paper develops an argument against causal decision theory. I formulate a principle of preference, which I call the Guaranteed Principle. I argue that the preferences of rational agents satisfy the Guaranteed Principle, that the preferences of agents who embody causal decision theory do not, and hence that causal decision theory is false.

A finer-grained delineation of a given explanandum reveals a nexus of closely related causal and non- causal explanations, complementing one another in ways that yield further explanatory traction on the phenomenon in question. By taking a narrower construal of what counts as a causal explanation, a new class of distinctively mathematical explanations pops into focus; Lange’s characterization of distinctively mathematical explanations can be extended to cover these. This new class of distinctively mathematical explanations is illustrated with the Lotka-Volterra equations. There (...) are at least two distinct ways those equations might hold of a system, one of which yields straightforwardly causal explanations, but the other of which yields explanations that are distinctively mathematical in terms of nomological strength. In the first, one first picks out a system or class of systems, finds that the equations hold in a causal -explanatory way; in the second, one starts with the equations and explanations that must apply to any system of which the equations hold, and only then turns to the world to see of what, if any, systems it does in fact hold. Using this new way in which a model might hold of a system, I highlight four specific avenues by which causal and non- causal explanations can complement one another. (shrink)

Agent-causal libertarians maintain we are irreducible agents who, by acting, settle matters that aren’t already settled. This implies that the neural matters underlying the exercise of our agency don’t conform to deterministic laws, but it does not appear to exclude the possibility that they conform to statistical laws. However, Pereboom (Noûs 29:21–45, 1995; Living without free will, Cambridge University Press, Cambridge, 2001; in: Nadelhoffer (ed) The future of punishment, Oxford University Press, New York, 2013) has argued that, if these neural (...) matters conform to either statistical or deterministic physical laws, the complete conformity of an irreducible agent’s settling of matters with what should be expected given the applicable laws would involve coincidences too wild to be credible. Here, I show that Pereboom’s argument depends on the assumption that, at times, the antecedent probability certain behavior will occur applies in each of a number of occasions, and is incapable of changing as a result of what one does from one occasion to the next. There is, however, no evidence this assumption is true. The upshot is the wild coincidence objection is an empirical objection lacking empirical support. Thus, it isn’t a compelling argument against agent-causal libertarianism. (shrink)

This paper argues that causal idealism, the view that causation is a product of mental activity, should be considered a competetitor to contemporary views that incorporate human thought and agency into the causal relation. Weighing contextualism, contrastivism, or pragmatism about causation against causal idealism results in at least a tie with respect to the virtues of these theories.

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)

In the ‘Refutation of Idealism’ chapter of the first Critique, Kant argues that the conditions required for having certain kinds of mental episodes are sufficient to guarantee that there are ‘objects in space’ outside us. A perennially influential way of reading this compressed argument is as a kind of causal inference: in order for us to make justified judgements about the order of our inner states, those states must be caused by the successive states of objects in space outside us. (...) Here I consider the best recent versions of this reading, and argue that each suffers from apparently fatal flaws. -/- . (shrink)

In this thesis, I give a metascientific account of causality in medicine. I begin with two historical cases of causal discovery. These are the discovery of the causation of Burkitt’s lymphoma by the Epstein-Barr virus, and of the various viral causes suggested for cervical cancer. These historical cases then support a philosophical discussion of causality in medicine. This begins with an introduction to the Russo- Williamson thesis (RWT), and discussion of a range of counter-arguments against it. Despite these, (...) I argue that the RWT is historically workable, given a small number of modifications. I then expand Russo and Williamson’s account. I first develop their suggestion that causal relationships in medicine require some kind of evidence of mechanism. I begin with a number of accounts of mechanisms and produce a range of consensus features of them. I then develop this consensus position by reference to the two historical case studies with an eye to their operational competence. In particular, I suggest that it is mechanistic models and their representations which we are concerned with in medicine, rather than the mechanism as it exists in the world. -/- I then employ these mechanistic models to give an account of the sorts of evidence used in formulating and evaluating causal claims. Again, I use the two human viral oncogenesis cases to give this account. I characterise and distinguish evidence of mechanism from evidence of difference-making, and relate this to mechanistic models. I then suggest the relationship between types of evidence presents us with a means of tackling the reference-class problem. This sets the scene for the final chapter. Here, I suggest the manner in which these two different classes of evidence become integrated is also reflected in the way that developing research programmes change as their associated causal claims develop. (shrink)