Some causal situations appear similar but causally different. Preemptive prevention offers such an example. However, it is difficult to capture the causal difference. In fact, it resists analysis. I discuss Collins’ s account of causal difference, and argue that it is not adequate. I also argue that the causal difference is not analyzable in terms of either dependence or production. I then examine some non-reductive account of causal difference, and claim that (...) the sense of causal difference has yet to be specified. Preemptive prevention shows that the concept of causation, whether it is reducible to something else or not, still requires some further scrutiny. (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 learning of immediate causation within a dynamic environment was examined. Participants encountered seven decision points in which they needed to choose which of three possible candidates was the cause of explosions in the environment. Each candidate was firing a weapon at random every few seconds, but only one of them produced an immediate effect. Some participants showed little learning, but most demonstrated increases in accuracy across time. On average, men showed higher accuracy and shorter latencies that were not explained (...) by differences in self-reported prior video game experience. This result suggests that prior reports of sex differences in causal choice in the game are not specific to situations involving delayed or probabilistic causal relations. (shrink)

In the last two decades few topics in philosophy of science have received as much attention as mechanistic explanation. A significant motivation for these accounts is that scientists frequently use the term “mechanism” in their explanations of biological phenomena. While scientists appeal to a variety of causal concepts in their explanations, many philosophers argue or assume that all of these concepts are well understood with the single notion of mechanism. This reveals a significant problem with mainstream mechanistic accounts– although (...) philosophers use the term “mechanism” interchangeably with other causal concepts, this is not something that scientists always do. This paper analyses two causal concepts in biology–the notions of “mechanism” and “pathway”–and how they figure in biological explanation. I argue that these concepts have unique features, that they are associated with distinct strategies of causal investigation, and that they figure in importantly different types of explanation. (shrink)

We investigated the understanding of causal systems categories—categories defined by common causal structure rather than by common domain content—among college students. We asked students who were either novices or experts in the physical sciences to sort descriptions of real-world phenomena that varied in their causal structure (e.g., negative feedback vs. causal chain) and in their content domain (e.g., economics vs. biology). Our hypothesis was that there would be a shift from domain-based sorting to causal sorting (...) with increasing expertise in the relevant domains. This prediction was borne out: The novice groups sorted primarily by domain and the expert group sorted by causal category. These results suggest that science training facilitates insight about causal structures. (shrink)

This paper centers around the notion that internal, mental representations are grounded in structural similarity, i.e., that they are so-called S-representations. We show how S-representations may be causally relevant and argue that they are distinct from mere detectors. First, using the neomechanist theory of explanation and the interventionist account of causal relevance, we provide a precise interpretation of the claim that in S-representations, structural similarity serves as a “fuel of success”, i.e., a relation that is exploitable for the representation (...) using system. Then, we discuss crucial differences between S-representations and indicators or detectors, showing that—contrary to claims made in the literature—there is an important theoretical distinction to be drawn between the two. (shrink)

The evolutionary theory of sex implies a theoretically principled account of the causal mechanisms underlying personality systems in which males pursue a relatively high-risk strategy compared to females and are thus higher on traits linked to sensation seeking and social dominance. Females are expected to be lower on these traits but higher on traits related to nurturance and attraction to long-term relationships. The data confirm this pattern of sex differences. It is thus likely that these traits have been a (...) focus of natural selection rather than the traits of gregarious/aloof and arrogant/unassuming hypothesized by Depue & Collins. (shrink)

An important function of scientific diagrams is to identify causal relationships. This commonly relies on contrasts that highlight the effects of specific difference-makers. However, causal contrast diagrams are not an obvious and easy to recognize category because they appear in many guises. In this paper, four case studies are presented to examine how causal contrast diagrams appear in a wide range of scientific reports, from experimental to observational and even purely theoretical studies. It is shown that (...) causal contrasts can be expressed in starkly different formats, including photographs of complexly visualized macromolecules as well as line graphs, bar graphs, or plots of state spaces. Despite surface differences, however, there is a measure of conceptual unity among such diagrams. In empirical studies they generally serve not only to infer and communicate specific causal claims, but also as evidence for them. The key data of some studies is given nowhere except in the diagrams. Many diagrams show multiple causal contrasts in order to demonstrate both that an effect exists and that the effect is specific -- that is, to narrowly circumscribe the phenomenon to be explained. In a large range of scientific reports, causal contrast diagrams reflect the core epistemic claims of the researchers. (shrink)

Causal approaches to explanation often assume that a model explains by describing features that make a difference regarding the phenomenon. Chirimuuta claims that this idea can be also used to understand non-causal explanation in computational neuroscience. She argues that mathematical principles that figure in efficient coding explanations are non-causal difference-makers. Although these principles cannot be causally altered, efficient coding models can be used to show how would the phenomenon change if the principles were modified in (...) counterpossible situations. The problem is that efficient coding models also involve difference-makers that, prima facie, cannot be characterized as non-causal in this sense. Mathematical principles always involve variables which have counterfactual relations between them. However, we cannot simply assume that these difference-makers are causal. They can also be found in paradigmatic non-causal explanations and therefore they must be characterized as non-causal in some sense. I argue that, despite appearances, Chirimuuta's view can be applied to these cases. The mentioned counterfactual relations presuppose the counterpossible conditionals that describe the modification of a relevant mathematical principle. If these conditionals are the hallmark of non-causal relations, then Chirimuuta’s criterion has the desired implication that variables in mathematical principles are non-causal difference-makers. (shrink)

Unmeasured confounding is an important threat to the validity of observational studies. A common way to deal with unmeasured confounding is to compute bounds for the causal effect of interest, that is, a range of values that is guaranteed to include the true effect, given the observed data. Recently, bounds have been proposed that are based on sensitivity parameters, which quantify the degree of unmeasured confounding on the risk ratio scale. These bounds can be used to compute an E-value, (...) that is, the degree of confounding required to explain away an observed association, on the risk ratio scale. We complement and extend this previous work by deriving analogous bounds, based on sensitivity parameters on the risk difference scale. We show that our bounds can also be used to compute an E-value, on the risk difference scale. We compare our novel bounds with previous bounds through a real data example and a simulation study. (shrink)

We are responsible for some things but not for others. In this thesis, I investigate what it takes for an entity to be responsible for something. This question has two components: agents and actions. I argue for a permissive view about agents. Entities such as groups or artificially intelligent systems may be agents in the sense required for responsibility. With respect to actions, I argue for a causal view. The relation in virtue of which agents are responsible for actions (...) is a causal one. I claim that responsibility requires causation and I develop a causal account of agency. This account is particularly apt for addressing the relationship between agency and moral responsibility and sheds light on the causal foundations of moral responsibility. (shrink)

How do people come to opposite causal judgments about societal problems, such as whether a public health policy reduced COVID‐19 cases? The current research tests an understudied cognitive mechanism in which people may agree about what actually happened (e.g., that a public health policy was implemented and COVID‐19 cases declined), but can be made to disagree about the counterfactual, or what would have happened otherwise (e.g., whether COVID‐19 cases would have declined naturally without intervention) via comparison cases. Across two (...) preregistered studies (total N = 480), participants reasoned about the implementation of a public policy that was followed by an immediate decline in novel virus cases. Study 1 shows that people's judgments about the causal impact of the policy could be pushed in opposite directions by emphasizing comparison cases that imply different counterfactual outcomes. Study 2 finds that people recognize they can use such information to influence others. Specifically, in service of persuading others to support or reject a public health policy, people systematically showed comparison cases implying the counterfactual outcome that aligned with their position. These findings were robust across samples of U.S. college students and politically and socioeconomically diverse U.S. adults. Together, these studies suggest that implied counterfactuals are a powerful tool that individuals can use to manufacture others’ causal judgments and warrant further investigation as a mechanism contributing to belief polarization. (shrink)

This article argues that centralized wage bargaining alters the causal logic in explanations of wage inequality, in the sense that common explanatory factors have different effects, given the degree of bargaining centralization. The evidence presented supports the theoretical argument. Using aggregate time-series cross-country data from fifteen capitalist democracies, the article shows that—given decentralized bargaining—trade with less developed countries, resources devoted to research and development, and government employment have inegalitarian effects on the wage distribution, whereas leftist governments and unionism compress (...) wages. However, given centralized wage bargaining these effects gradually disappear or, in some cases, change direction. (shrink)

Causal overdetermination occupies an uncomfortable place within all the major theories of causation. A natural solution to the problems it gives rise to would be to resolve overdetermination into preemption or joint causation. However, such a solution would seem to lead to individuate events in a fragile manner. The issue of such modal fragility is addressed and it is argued that events designated as effects are always fragile in a natural way and the putative problems of adopting modal fragility (...) can be resolved. It is also studied whether causal overdetermination could work in a setting where the overdetermining causes occur in different levels of reality. Typically postulated higher-level causes are shown to contradict the definitional features of overdetermination. There is thus no reasonable role for causal overdetermination and the notion should be abandoned. (shrink)

In The Rational Imagination, Byrne proposes a mental models account of why causal and counterfactual thinking often focus on different antecedents. This review critically examines the two central propositions of her account, finding both only weakly defensible. Byrne's account is contrasted with judgment dissociation theory, which offers a functional explanation for differences in the focus of causal and counterfactual thinking.

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 book, by one of the pre-eminent philosophers of science writing today, offers the most comprehensive account available of causal asymmetries. Causation is asymmetrical in many different ways. Causes precede effects; explanations cite causes not effects. Agents use causes to manipulate their effects; they don't use effects to manipulate their causes. Effects of a common cause are correlated; causes of a common effect are not. This book explains why a relationship that is asymmetrical in one of these regards is (...) asymmetrical in the others. Hausman discovers surprising hidden connections between theories of causation and traces them all to an asymmetry of independence. This is a major book for philosophers of science that will also prove insightful to economists and statisticians. (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)

An understanding of cause--effect relationships is fundamental to the study of cognition. In this book, outstanding specialists from comparative psychology, social psychology, developmental psychology, anthropology, and philosophy present the newest developments in the study of causal cognition and discuss their different perspectives. They reflect on the role and forms of causal knowledge, both in animal and human cognition, on the development of human causal cognition from infancy, and on the relationship between individual and cultural aspects of (...) class='Hi'>causal understanding. The result is a state-of-the-art, informative, insightful, and interdisciplinary debate aimed at the non-specialist. (shrink)

This book aims to answer two main questions about Aristotle’s theory of causality and causal explanation, especially in relation to natural science: (1) How does he answer the main philosophical questions about causes to which he thinks his predecessors’ answers are flawed? (2) How do his answers bear on the main questions we confront in thinking about causality in general? The texts that deal with causality directly are analyzed against the background of his criticisms of his predecessors and his (...) broader views about explanation, highlighting their theoretically important commitments. This allows us to reveal the conceptual architecture of his theory. The basic theory is then applied to two questions about causality, one metaphysical and one epistemological. The metaphysical question is how to account for the relation between causes and what they cause, in light of a fundamental tension between different desiderata for causal explanations. Aristotle’s answer is pluralistic: he does not think that there is one metaphysical relationship between causes and what they cause even within a given mode of causality. The epistemological question asks how we grasp causes, and grasp them in a way that yields scientific understanding. Aristotle’s answer is again a pluralist one: metaphysically different phenomena demand different cognitive resources, and some are more accessible than others. Nevertheless, there is a discernible path from simpler to more sophisticated types of cognitive grasp on causality, in such a way that Aristotle can plausibly satisfy the epistemological constraints he thinks his predecessors cannot. Aristotle thus aims to provide a non-reductionist account of causality that still leaves room for a substantive conception of understanding in natural science. (shrink)

We start this paper by arguing that causality should, in analogy with force in Newtonian physics, be understood as a theoretical concept that is not explicated by a single definition, but by the axioms of a theory. Such an understanding of causality implicitly underlies the well-known theory of causal nets and has been explicitly promoted by Glymour. In this paper we investigate the explanatory warrant and empirical content of TCN. We sketch how the assumption of directed cause–effect relations can (...) be philosophically justified by an inference to the best explanation. We then ask whether the explanations provided by TCN are merely post-facto or have independently testable empirical content. To answer this question we develop a fine-grained axiomatization of TCN, including a distinction of different kinds of faithfulness. A number of theorems show that although the core axioms of TCN are empirically empty, extended versions of TCN have successively increasing empirical content. (shrink)

How do people attribute responsibility in situations where the contributions of multiple agents combine to produce a joint outcome? The prevalence of over-determination in such cases makes this a difficult problem for counterfactual theories of causal responsibility. In this article, we explore a general framework for assigning responsibility in multiple agent contexts. We draw on the structural model account of actual causation (e.g., Halpern & Pearl, 2005) and its extension to responsibility judgments (Chockler & Halpern, 2004). We review the (...) main theoretical and empirical issues that arise from this literature and propose a novel model of intuitive judgments of responsibility. This model is a function of both pivotality (whether an agent made a difference to the outcome) and criticality (how important the agent is perceived to be for the outcome, before any actions are taken). The model explains empirical results from previous studies and is supported by a new experiment that manipulates both pivotality and criticality. We also discuss possible extensions of this model to deal with a broader range of causal situations. Overall, our approach emphasizes the close interrelations between causality, counterfactuals, and responsibility attributions. (shrink)

In the last 20 years, a stream of research emerged under the label of „complex problem solving“ (CPS). This research was intended to describe the way people deal with complex, dynamic, and intransparent situations. Complex computer-simulated scenarios were as stimulus material in psychological experiments. This line of research lead to subtle insights into the way how people deal with complexity and uncertainty. Besides these knowledge-rich, realistic, intransparent, complex, dynamic scenarios with many variables, a second line of research used more simple, (...) knowledge-lean scenarios with a low number of variables („minimal complex systems“, MCS) that have been proposed recently in problem-solving research for the purpose of educational assessment. In both cases, the idea behind the use of microworlds is to increase validity of problem solving tasks by presenting interactive environments that can be explored and controlled by participants while pursuing certain action goals. The main argument presented here is: both types of systems - CPS and MCS – can only be dealt with successfully if causal dependencies between input and output variables are identified and used for system control. System knowledge is necessary for control and intervention. But CPS and MCS differ in their way of how causal dependencies are identified and how the mental model is constructed; therefore, they cannot be compared directly to each other with respect to the cognitive processes that are necessary for solving the tasks. Knowledge-poor MCS tasks address only a small fraction of the cognitive processes and structures needed for knowledge-rich CPS situations. (shrink)

Causal claims in biomedical contexts are ubiquitous albeit they are not always made explicit. This paper addresses the question of what causal claims mean in the context of disease. It is argued that in medical contexts causality ought to be interpreted according to the epistemic theory. The epistemic theory offers an alternative to traditional accounts that cash out causation either in terms of “difference-making” relations or in terms of mechanisms. According to the epistemic approach, causal claims (...) tell us about which inferences (e.g., diagnoses and prognoses) are appropriate, rather than about the presence of some physical causal relation analogous to distance or gravitational attraction. It is shown that the epistemic theory has important consequences for medical practice, in particular with regard to evidence-based causal assessment. (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)

Cultural effects can influence the results of causal genetic analyses, such as Mendelian randomisation, but the potential influences of culture on genotype–phenotype associations are not currently well understood. Different genetic variants could be associated with different phenotypes in different populations, or culture could confound or influence the direction of the association between genotypes and phenotypes in different populations.

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)

The empirical literature on phenomenal causality (the notion that causality can be perceived) is reviewed. Different potential types of phenomenal causality and variables that influence phenomenal causality were considered in Part I (Hubbard 2012b) of this two-part series. In Part II, broader questions regarding properties of phenomenal causality and connections of phenomenal causality to other perceptual or cognitive phenomena (different types of phenomenal causality, effects of spatial and temporal variance, phenomenal causality in infancy, effects of object properties, naïve physics, spatial (...) localization, other illusions, amodal completion, Gestalt principles of perceptual grouping, effects of context, differences between physical and social causality, effects of learning and experience, individual differences, effects of predictability, asymmetry in phenomenal causality, differences between perceived causality and perceived force, phenomenal causality in nonhuman animals) are considered. Potential mechanisms of phenomenal causality (inference from contiguity, a priori understanding, ampliation, perceptual learning, stimulus activity, beliefs regarding kinematics, haptic experience, beliefs regarding impetus, postdiction, innateness, modularity, specific neural structures) are also considered. (shrink)

Causal compatibilism claims that even though physics is causally closed, and even though mental properties are multiply realizable and are not identical to physical causal properties, mental properties are causal properties nonetheless. This position asserts that there is genuine causation at multiple descriptive/ontological levels; physics-level causal claims are not really incompatible with mentalistic causal claims. I articulate and defend a version of causal compatibilism that incorporates three key contentions. First, causation crucially involves robust patterns (...) of counterfactual dependence among properties.Second, often several distinct such patterns, all subsuming a single phenomenon, exist at different descriptive/ontological levels (e.g., microphysical, neurobiological, macrobiological, and psychological). Third, the concept of causation is governed by an implicit contextual parameter that normally determines a specific descriptive/ontological level as the contextually relevant level, for the context-sensitive semantic evaluation of causal statements. (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)

Think of some environmentally unfriendly choices – taking the car instead of public transport or driving an SUV, just binning something recyclable, using lots of plastic bags, buying an enormous television, washing clothes in hot water, replacing something when you could make do with last year's model, heating rooms you don't use or leaving the heating high when you could put on another layer of clothing, flying for holidays, wasting food and water, eating a lot of beef, installing a patio (...) heater, maybe even, as some have said lately, owning a dog. Think about your own choices, instances in which you take an action which enlarges your carbon footprint when you might have done otherwise without much trouble. Is there consolation in the thought that it makes no difference what you do? (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)

Scientific models describe natural phenomena at different levels of abstraction. Abstract descriptions can provide the basis for interventions on the system and explanation of observed phenomena at a level of granularity that is coarser than the most fundamental account of the system. Beckers and Halpern (2019), building on work of Rubenstein et al. (2017), developed an account of abstraction for causal models that is exact. Here we extend this account to the more realistic case where an abstract causal (...) model offers only an approximation of the underlying system. We show how the resulting account handles the discrepancy that can arise between low- and high-level causal models of the same system, and in the process provide an account of how one causal model approximates another, a topic of independent interest. Finally, we extend the account of approximate abstractions to probabilistic causal models, indicating how and where uncertainty can enter into an approximate abstraction. (shrink)

Causal selection and priority are at the heart of discussions of the causal parity thesis, which says that all causes of a given effect are on a par, and that any justified priority assigned to a given cause results from causal explanatory interests. In theories of causation that provide necessary and sufficient conditions for the truth of causal claims, status as cause is an either/or issue: either a given cause satisfies the conditions or it does not. (...) Consequently, assessments of causal parity and priority require more resources, which can either be additional or part of the causal analysis itself. While adding resources in terms of a theory of causal explanation has been standard, here we develop a unified conceptual analysis that includes a range of different precise causal concepts that allows for assessments of causal priority in terms of different kinds of causal relevance. (shrink)

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

It is argued that in deterministic contexts evidence for causal relations states whether a boundary condition makes a difference or not to a phenomenon. In order to substantiate the analysis, I show that this difference/indifference making is the basic type of evidence required for eliminative induction in the tradition of Francis Bacon and John Stuart Mill. To this purpose, an account of eliminative induction is proposed with two distinguishing features: it includes a method to establish the (...) class='Hi'>causal irrelevance of boundary conditions by means of indifference making, which is called strict method of agreement, and it introduces the notion of a background against which causal statements are evaluated. Causal statements thus become three-place-relations postulating the relevance or irrelevance of a circumstance C to the examined phenomenon P with respect to a background B of further conditions. To underline the importance of evidence in terms of difference/indifference making, I sketch two areas, in which eliminative induction is extensively used in natural and engineering sciences. One concerns exploratory experiments, the other engineering design methods. Given that a method is discussed that has been used for centuries, I make no claims to novelty in this paper, but hope that the combined discussion of several topics that are still somewhat underrepresented in the philosophy of science literature is of some merit. (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)

Analyses of factual causation face perennial problems, including preemption, overdetermination, and omissions. Arguably, the thorniest, are cases of omissive overdetermination, involving two independent omissions, each sufficient for the harm, and neither, independently, making a difference. A famous example is Saunders, where pedestrian was hit by a driver of a rental car who never pressed on the (unbeknownst to the driver) defective (and, negligently, never inspected) brakes. Causal intuitions in such cases are messy, reflected in disagreement about which omission (...) mattered. What these analyses mistakenly take for granted, is that at issue is the 'efficacy' of each omission. I argue, on the contrary, the puzzle of omissive overdetermination favors taking the act/omission distinction seriously. Factual causation, properly understood precludes omissions (i.e. omissions are not causal). Of course, the law also attaches liability to omissions, but this works differently from liability for real causes (e.g. omissions have a duty requirement, they also respond differentially to difference-making considerations). The manner in which liability attaches for omissions differs from that of straightforward causal liability, and is entirely dependent on the underlying causal structure. Attention to that structure (e.g. that the driver's hitting the pedestrian with his car is what actually caused the injury) sheds light on which omissions matter (e.g. driver's failure to press on the brakes) and why (because that failure removes a defense the driver would have to liability for the accident he caused). Other cases, where the parties' connection is entirely omissive (e.g. two physicians fail to detect independently lethal conditions), come out differently (tracking moralized elements). The analysis offered makes better sense of both why omissive determination cases are puzzling and how to resolve them. (shrink)

Causal pluralism is currently a hot topic in philosophy. However, the consequences of this view on causation for scientific knowledge and scientific methodology are heavily underexposed in the present debate. My aim in this paper is to argue that an epistemological-methodological point of view should be valued as a line of approach on its own and to demonstrate how epistemological- methodological causal pluralism differs in its scope from conceptual and metaphysical causal pluralism. Further, I defend epistemological-methodological (...) class='Hi'>causal pluralism and try to illustrate that scientific practice needs diverse causal concepts in diverse domains, and even diverse causal concepts within singular domains. (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)

Behavior genetics is a controversial science. For decades, scholars have sought to understand the role of heredity in human behavior and life-course outcomes. Recently, technological advances and the rapid expansion of genomic databases have facilitated the discovery of genes associated with human phenotypes such as educational attainment and substance use disorders. To maximize the potential of this flourishing science, and to minimize potential harms, careful analysis of what it would mean for genes to be causes of human behavior is needed. (...) In this paper, we advance a framework for identifying instances of genetic causes, interpreting those causal relationships, and applying them to advance causal knowledge more generally in the social sciences. Central to thinking about genes as causes is counterfactual reasoning, the cornerstone of causal thinking in statistics, medicine, and philosophy. We argue that within-family genetic effects represent the product of a counterfactual comparison in the same way as average treatment effects (ATEs) from randomized controlled trials (RCTs). Both ATEs from RCTs and within-family genetic effects are shallow causes: They operate within intricate causal systems (non-unitary), produce heterogeneous effects across individuals (non-uniform), and are not mechanistically informative (non-explanatory). Despite these limitations, shallow causal knowledge can be used to improve understanding of the etiology of human behavior and to explore sources of heterogeneity and fade-out in treatment effects. (shrink)

The causal Bayes net framework specifies a set of axioms for causal discovery. This article explores the set of causal variables that function as relata in these axioms. Spirtes showed how a causal system can be equivalently described by two different sets of variables that stand in a non-trivial translation-relation to each other, suggesting that there is no “correct” set of causal variables. I extend Spirtes’ result to the general framework of linear structural equation models (...) and then explore to what extent the possibility to intervene or a preference for simpler causal systems may help in selecting among sets of causal variables. (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)

This paper distinguishes between causal isolation robustness analysis and independent determination robustness analysis and suggests that the triangulation of the results of different epistemic means or activities serves different functions in them. Circadian clock research is presented as a case of causal isolation robustness analysis: in this field researchers made use of the notion of robustness to isolate the assumed mechanism behind the circadian rhythm. However, in contrast to the earlier philosophical case studies on causal isolation robustness (...) analysis (Weisberg and Reisman in Philos Sci 75:106–131, 2008 ; Kuorikoski et al. in Br J Philos Sci 61:541–567, 2010 ), robustness analysis in the circadian clock research did not remain in the level of mathematical modeling, but it combined it with experimentation on model organisms and a new type of model, a synthetic model. (shrink)