A phenome occurs through the many pathways of the complex net of interaction between the phenome and its environment; therefore researching and understanding how it arises requires investigation into many possible causes that are in constant interaction with each other. The most comprehensive investigations in biology are the ones in which many biologists from different sub-areas—evolutionary biology, developmental biology, molecular biology, physiology, genetics, epigenetics, ecology—have collaborated. Still, biologists do not always need to collaborate or look for the most comprehensive explanations. (...) A more standard investigation in biology occurs within a single subarea, and uses well-defined experiments with very specific conditions. This paper is about causation and related explanation in plant phenome research and its relevance to Aristotle’s Theory of Four Causes. I argue that there are causes which resemble Aristotle’s formal, material, and efficient causes in phenotype explanation and occurrence; but causes which resemble Aristotle’s final causes occur in phenotype explanation only, not in the occurrence. (shrink)

This essay, written by a biologist, a microbial ecologist, a biological anthropologist, and an anthropologist‐historian, examines tensions and translations in microbiome research on animals in the laboratory and field. The authors trace how research questions and findings in the laboratory are extrapolated into the field and vice versa, and the shifting evidentiary standards that these research settings require. Showing how complexities of microbiomes challenge traditional standards of causation, the authors contend that these challenges require new approaches (...) to inferences used in ecology, anthropology, and history. As social scientists incorporate investigations of microbial life into their human studies, microbiome researchers venture into field settings to develop mechanistic understandings about the functions of complex microbial communities. These efforts generate new possibilities for cross‐fertilizations and inference frameworks to interpret microbiome findings. Microbiome research should integrate multiple scales, levels of variability, and other disciplinary approaches to tackle questions spanning conditions from the laboratory to the field. (shrink)

Many researchers consider cancer to have molecular causes, namely mutated genes that result in abnormal cell proliferation (e.g. Weinberg 1998). For others, the causes of cancer are to be found not at the molecular level but at the tissue level where carcinogenesis consists of disrupted tissue organization with downward causation effects on cells and cellular components (e.g. Sonnenschein and Soto 2008). In this contribution, I ponder how to make sense of such downward causation claims. Adopting a manipulationist account (...) of causation (Woodward 2003), I propose a formal definition of downward causation and discuss further requirements (in light of Baumgartner 2009). I then show that such an account cannot be mobilized in support of non-reductive physicalism (contrary to Raatikainen 2010). However, I also argue that such downward causation claims might point at particularly interesting dynamic properties of causal relationships that might prove salient in characterizing causal relationships (following Woodward 2010). (shrink)

Many researchers consider cancer to have molecular causes, namely mutated genes that result in abnormal cell proliferation (e.g. Weinberg 1998); yet for others, the causes of cancer are to be found not at the molecular level but at the tissue level and carcinogenesis would consist in a disrupted tissue organization with downward causation effects on cells and cellular components (e.g. Sonnenschein & Soto 2008). In this contribution, I ponder how to make sense of such downward causation claims. Adopting (...) a manipulationist account of causation (Woodward 2003), I propose a formal definition of downward causation, and discuss further requirements (in light of Baumgartner 2009). I then show that such an account cannot be mobilized in support of non-reductive physicalism (contrary to Raatikainen 2010). However, I also argue that such downward causation claims might point at particularly interesting dynamic properties of causal relationships that might prove salient in characterizing causal relationships (following Woodward 2010). (shrink)

This article explores some ways in which philosophical theories of causation and empirical investigations into causal learning and judgment can mutually inform one another.

Giorgos Tsiolis and Michalis Christodoulou have written a deeply theoretical book arguing that we should see reconstructive biographical research as a method for constructing causal accounts of soc...

Appraisal theories of emotion generally presuppose that emotions are “directed at” various items. They also hold that emotions have motivational properties. However, although it coheres well with their views, they have yet to seriously develop the idea that the function of emotional direction is to guide those properties. I argue that this “guidance hypothesis” can open up a promising new field of research in emotion theory. But I also argue that before appraisal theorists can take full advantage of it, (...) they must drop their further assumption that to determine an emotion's direction, one need only retrace the process that caused it. Contrary to this “retracing view,” I argue for an “independence thesis”: directed emotions are produced by two functionally independent sub-processes. The first, “affect-causation,” functions in part to produce a state with certain motivational properties given certain representations. The second, “affect-direction,” has the function of optimally guiding those motivational properties by associating them with representations that may properly be quite dissimilar from the causal ones. By provisionally adopting the independence thesis and empirically testing the guidance hypothesis, I argue that appraisal theorists stand a good chance of significantly increasing the explanatory power of their theories. (shrink)

A fundamental goal of research in neuroscience is to uncover the causal structure of the brain. This focus on causation makes sense, because causal information can provide explanations of brain function and identify reliable targets with which to understand cognitive function and prevent or change neurological conditions and psychiatric disorders. In this research, one of the most frequently used causal concepts is ‘mechanism’ — this is seen in the literature and language of the field, in grant and (...) funding inquiries that specify what research is supported, and in journal guidelines on which contributions are considered for publication. In these contexts, mechanisms are commonly tied to expressions of the main aims of the field and cited as the ‘fundamental’, ‘foundational’ and/or ‘basic’ unit for understanding the brain. Despite its common usage and perceived importance, mechanism is used in different ways that are rarely distinguished. Given that this concept is defined in different ways throughout the field — and that there is often no clarification of which definition is intended — there remains a marked ambiguity about the fundamental goals, orientation and principles of the field. Here we provide an overview of causation and mechanism from the perspectives of neuroscience and philosophy of science, in order to address these challenges. (shrink)

The problem of mental causation in contemporary philosophy of mind concerns the possibility of holding two different views that are in apparent tension. The first is physicalism, the view that there is nothing more to the world than the physical. The second is that the mental has genuine causal efficacy in a way that does not reduce to pure physical particle-bumping. This article provides a historical background to this question, with focus on Davidson’s anomalous monism and Kim’s causal exclusion (...) problem. Responses to causal exclusion are categorized in terms of six different argumentative strategies. In conclusion, caution is advised regarding the inclination to reduce the mental to the physical and sketch a positive direction for substantively characterizing mental causation by recourse to well-confirmed accounts of causation coupled with empirical research. (shrink)

We claim that if a complete philosophy of evidence-based practice is intended, then attention to the nature of causation in health science is necessary. We identify how health science currently conceptualises causation by the way it prioritises some research methods over others. We then show how the current understanding of what causation is serves to constrain scientific progress. An alternative account of causation is offered. This is one of dispositionalism. We claim that by understanding (...) class='Hi'>causation from a dispositionalist stance, many of the processes within an evidence-based practice framework are better accounted for. Further, some of the problems associated with the health research, e.g. external validity of causal findings, dissolve. (shrink)

Sometimes you make a choice. Whether or not you made it was up to you. The choice was free. But how can this be? A scientific view of the world may leave no room for free choice. Free will literature continually explodes. Yet experts still focus on control or on a power to do otherwise. Sadly, they neglect another intuitive feature of free will: being an underived source or ultimate originator. When acting freely, one is a self-determined, self-directed, sole author (...) of change. Surprisingly, though the literature is replete with this pre-theoretic feature of free will, virtually no one makes rigorous use of it when constructing arguments. Equipped with fresh research, this book contends that agent-causation—currently an unpopular theory—deserves serious reconsideration. Only agent-causation accounts for ultimate origination, and popular objections fail under rigorous scrutiny. This book is tightly argued. It challenges and deepens recent advances in free will scholarship made by Peter van Inwagen, Robert Kane, Carl Ginet, Randy Clarke, Stewart Goetz, Tim O’Connor, and others. (shrink)

This book covers the overlap between informatics, computer science, philosophy of causation, and causal inference in epidemiology and population health research. Key concepts covered include how data are generated and interpreted, and how and why concepts in health informatics and the philosophy of science should be integrated in a systems-thinking approach. Furthermore, a formal epistemology for the health sciences and public health is suggested. -/- Causation in Population Health Informatics and Data Science provides a detailed guide of (...) the latest thinking on causal inference in population health informatics. It is therefore a critical resource for all informaticians and epidemiologists interested in the potential benefits of utilising a systems-based approach to causal inference in health informatics. (shrink)

Ehring shows the inadequacy of received theories of causation, and, introducing conceptual devices of his own, provides a wholly new account of causation as the persistence over time of individual properties, or "tropes.".

Theory of illness causation is an important issue in all biomedical sciences, and solid etiological explanations are needed in order to develop therapeutic approaches in medicine and preventive interventions in public health. Until now, the literature about the theoretical underpinnings of illness causation research has been scarce and fragmented, and lacking a convenient summary. This interdisciplinary book provides a convenient and accessible distillation of the current status of research into this developing field, and adds a personal (...) flavor to the discussion by proposing the etiological stance as a comprehensive approach to identify modifiable causes of illness. (shrink)

This volume brings together a collection of new essays by leading scholars on the subject of causation in the early modern period, from Descartes to Lady Mary Shepherd. Aimed at researchers, graduate students and advanced undergraduates, the volume advances the understanding of early modern discussions of causation, and situates these discussions in the wider context of early modern philosophy and science. Specifically, the volume contains essays on key early modern thinkers, such as Descartes, Hobbes, Spinoza, Leibniz, Hume, Kant. (...) It also contains essays that examine the important contributions to the causation debate of less widely discussed figures, including Louis la Forge, Thomas Brown and Lady Mary Shepherd. (shrink)

Empirical research has recently emerged as a key method for understanding the nature of causation, and our concept of causation. One thread of research aims to test intuitions about the nature of causation in a variety of classic cases. These experiments have principally been used to try to resolve certain debates within analytic philosophy, most notably that between proponents of transference and dependence views of causation. The other major thread of empirical research on (...) our concept of causation has investigated the role that normative considerations play in causal judgments. These experimental results suggest that philosophical accounts of our concept of causation should take a broader view of what might be relevant. For both lines of research, we describe some of the significant experiments and outline key philosophical morals that have been drawn, all while pointing out various limitations. We conclude by considering other kinds of empirical research that should be philosophically interesting for those studying the nature of causation and our concept of causation. In particular, we point towards the need for philosophical research about causal perception, causal reasoning, and causal learning, as well as ways in which this research could play a role in prescriptive metaphysics. (shrink)

The past few decades have seen an explosion of research on causal reasoning in philosophy, computer science, and statistics, as well as descriptive work in psychology. In Causation with a Human Face, James Woodward integrates these lines of research and argues for an understanding of how each can inform the other: normative ideas can suggest interesting experiments, while descriptive results can suggest important normative concepts. Woodward's overall framework builds on the interventionist treatment of causation that he (...) developed in Making Things Happen. Normative ideas discussed include proposals about the role of invariant or stable relationships in successful causal reasoning and the notion of proportionality. He argues that these normative ideas are reflected in the causal judgments that people actually make as a descriptive matter. Woodward also discusses the common philosophical practice-particularly salient in philosophical accounts of causation--of appealing to intuitions or judgments about cases in support of philosophical theses. He explores how, properly understood, such appeals are not different in principle from appeals to results from empirical research, and demonstrates how they may serve as a useful source of information about causal cognition. (shrink)

We argue that current discussions of criteria for actual causation are ill-posed in several respects. (1) The methodology of current discussions is by induction from intuitions about an infinitesimal fraction of the possible examples and counterexamples; (2) cases with larger numbers of causes generate novel puzzles; (3) “neuron” and causal Bayes net diagrams are, as deployed in discussions of actual causation, almost always ambiguous; (4) actual causation is (intuitively) relative to an initial system state since state changes (...) are relevant, but most current accounts ignore state changes through time; (5) more generally, there is no reason to think that philosophical judgements about these sorts of cases are normative; but (6) there is a dearth of relevant psychological research that bears on whether various philosophical accounts are descriptive. Our skepticism is not directed towards the possibility of a correct account of actual causation; rather, we argue that standard methods will not lead to such an account. A different approach is required. Once upon a time a hungry wanderer came into a village. He filled an iron cauldron with water, built a fire under it, and dropped a stone into the water. “I do like a tasty stone soup” he announced. Soon a villager added a cabbage to the pot, another added some salt and others added potatoes, onions, carrots, mushrooms, and so on, until there was a meal for all. (shrink)

This dissertation begins by addressing the question of when a causal model is apt for deciding questions of actual causation with respect to some target situation. I first provide relevant background about causal models, explain what makes them promising as a tool for analyzing actual causation, and motivate the need for a theory of aptness as part of such an analysis (Chapter 1). I then define what it is for a model on a given interpretation to be accurate (...) of, that is, say only true things about, some target situation. This involves a systematization of various representational principles mentioned and/or discussed throughout the literature into a method of interpretation, which I propose be taken as standard (Chapter 2). Next, I explain and address two reasons for which accuracy as I’ve defined it is insufficient for aptness. The first reason – already discussed in the literature – is the problem of structural isomorphs. In response, I propose the aptness condition of Explicit Partial Mediation (Chapter 3). The second reason – which has yet to be noticed – is the problem of the indeterminacy of accuracy. As I demonstrate, a model is accurate of a target situation only relative to a set of background possibilities – what I call a modal profile. It follows that a model represents a situation only relative to some modal profile or other. I go on to discuss the ramifications of this observation for a theory of actual causation in terms of models. I argue that the relativity be taken at face value and built into our metaphysical account of causation, resulting in a view that I call causal relativism (Chapter 4). I explore one advantage of this view in detail: that the resulting account can defend the principle of strong proportionality against several objections (Chapter 5). Finally, I apply the earlier discussion of aptness to attempts to provide a semantics of counterfactuals in terms of causal models – an interventionist semantics. I show how just as a similarity semantics relies on an opaque notion of similarity, an interventionist semantics relies on an analogous notion of aptness. The challenge of articulating aptness thus undermines the claim that an interventionist semantics avoids representational problems inherent in a similarity semantics (Chapter 6). I close with a recap and suggestions for future research (Chapter 7). -/- . (shrink)

Extant research has shown that ordinary causal judgments are sensitive to normative factors. For instance, agents who violate a norm are standardly deemed more causal than norm-conforming agents in identical situations. In this paper, we explore two competing explanations for the Norm Effect: the Responsibility View and the Bias View. According to the former, the Norm Effect arises because ordinary causal judgment is intimately intertwined with moral responsibility. According to the alternative view, the Norm Effect is the result of (...) a blame-driven bias. In a series of five preregistered experiments (N = 2688), we present evidence that predominantly favours the Bias View. In particular, and against predictions made by the Responsibility View, we show that participants deem agents who violate nonpertinent or silly norms – norms that do not relate to the outcome at hand – as more causal, and that this effect cannot be explained in terms of plausible mediators such as the agent’s foreknowledge and desire, or the foreseeability of harm. We close with a discussion regarding the implications of these findings, in as regards the just assessment of proximate cause in the law. (shrink)

This Element provides an accessible introduction to the contemporary philosophy of causation. It introduces the reader to central concepts and distinctions and to key tools drawn upon in the contemporary debate. The aim is to fuel the reader's interest in causation, and to equip them with the resources to contribute to the debate themselves. The discussion is historically informed and outward-looking. 'Historically informed' in that concise accounts of key historical contributions to the understanding of causation set the (...) stage for an examination of the latest research. 'Outward looking' in that illustrations are provided of how the philosophy of causation relates to issues in the sciences, law, and elsewhere. The aim is to show why the study of causation is of critical importance, besides being fascinating in its own right. (shrink)

We argue that current discussions of criteria for actual causation are ill-posed in several respects. (1) The methodology of current discussions is by induction from intuitions about an infinitesimal fraction of the possible examples and counterexamples; (2) cases with larger numbers of causes generate novel puzzles; (3) "neuron" and causal Bayes net diagrams are, as deployed in discussions of actual causation, almost always ambiguous; (4) actual causation is (intuitively) relative to an initial system state since state changes (...) are relevant, but most current accounts ignore state changes through time; (5) more generally, there is no reason to think that philosophical judgements about these sorts of cases are normative; but (6) there is a dearth of relevant psychological research that bears on whether various philosophical accounts are descriptive. Our skepticism is not directed towards the possibility of a correct account of actual causation; rather, we argue that standard methods will not lead to such an account. A different approach is required. (shrink)

The current consensus view of causation in physics, as commonly held by scientists and philosophers, has several serious problems. It fails to provide an epistemology for the causal knowledge that it claims physics to possess; it is inapplicable in a prominent area of physics (classical thermodynamics); and it is difficult to reconcile with our everyday use of causal concepts and claims. In this dissertation, I use historical examples and philosophical arguments to show that the interventionist account of causation (...) constitutes a promising alternative for a “physically respectable” account of causation. The interventionist account explicates important parts of the experimental practice of physics and important aspects of the ways in which physical theory is used and applied. Moreover, the interventionist account succeeds where the consensus view of causation in physics fails. I argue that the interventionist account provides an epistemology of causal knowledge in physics that is rooted in experiment. On the interventionist view, there is a close link between experiment and the testing of causal claims. I give several examples of experiments from the early history of thermodynamics that scientists used in interventionist-type arguments. I also argue that interventionist claims made in the context of a physical theory can be epistemically justified by reference to the experimental interventions and observations that serve as evidence for the theory. I then show that the interventionist account of causation is well-suited to the patterns of reasoning that are intrinsic to thermodynamic theory. I argue that interventionist reasoning constitutes the structural foundation of thermodynamic theory, and that thermodynamic theory can provide clear answers to meaningful questions about whether or not a certain variable is a cause of another in a given context. Finally, I argue that the interventionist account offers the prospect of a unification of “physically respectable” causation and our everyday notion of causation. I conclude the dissertation by sketching an anti-foundationalist unification of causation, according to which causal reasoning occurs in the same manner in physics as it does in other branches of life and scientific research. (shrink)

This is a collection of articles which represents current research on the metaphysics of causation and laws of nature, mostly by authors working in or active in the Australasian region. The book provides an overview of current work on the theory of causation, including counterfactual, singularist, nomological and causal process approaches. It also covers work on the nature of laws of nature, with special emphasis on the scientific essentialist theory that laws of nature are, at base, the (...) fundamental dispositions or capacities of natural kinds of things. Because the book represents a good cross-section of authors currently working on these themes in the Australasian region, it conveys something of the interest and excitement of an active philosophical debate between advocates of several different research programmes in the area. (shrink)

Causation is one of the most controversial topics in philosophy. There is a wide range of philosophical accounts of causation, for example, the regularity account, the probabilistic account, the counterfactual account, the interventionist account, which can be all classified as ‘difference-making’ accounts; and the mechanistic account. Many argue that only one of these accounts is correct as there is only one type of causal relation (causal monism), while others maintain that there are multiple types of causation (causal (...) pluralism). In addition, there are eliminativists argue that science has no need of causation at all, while primitivists maintain that causation is unanalysable. Recently, the difference-making and mechanistic approaches have dominated recent philosophical discussion of causation. Other approaches and positions have been insufficiently discussed and assessed, especially in the context of philosophy of science. This volume explores and examines alternative approaches to causation. It revisits causal primitivism and causal eliminativism in the context of recent literature. It further explores the pluralistic approach, the fictionalist approach, the inferentialist approach, and the informational approach. It also examines the application of the dispositional approach, the epistemic approach, and the powerful particulars approach to the natural and social sciences. Overall, the volume is complementary to the recent discussion on the difference-making and mechanistic approaches and sheds new light on the metaphysical, epistemological, conceptual and methodological issues on causation. As such, it provides foundations for further research and teaching of this hotly debated topic. (shrink)

By giving the proper emphasis to both radical skepticism and naturalism as two independent standpoints in Hume, I wish to propose a more satisfactory account of some of the more puzzling Humean claims on causation. I place these claims alternatively in either the philosophical standpoint of the radical skeptic or in the standpoint of everyday and scientific beliefs. I characterize Hume’s radical skeptical standpoint in relation to Hume’s perceptual model of the traditional theory of ideas, and I argue that (...) Hume‘s radical skeptical argument concerning our causal inferences is inextricably linked to his skeptical argument concerning our idea of a necessary connection between cause and effect. I discuss Hume’s naturalistic account of the origin of our idea of necessity and offer a new reading of Hume’s two “definitions” of cause. I argue along the way against central aspects of two opposing styles of interpretation---Norman Kemp Smith’s and Annette Baier’s, on the one hand, and Robert Fogelin’s, on the other---that in my view do not appreciate the mutual autonomy of radical skepticism and naturalism in Hume. (shrink)

While it is generally agreed that the concept of homology refers to individuated traits that have been inherited from common ancestry, we still lack an adequate account of trait individuation or inheritance. Here I propose that we utilize a counterfactual criterion of causation to link each trait with a developmental-causal (DC) gene. A DC gene is made up of the genetic information (which might or might not be physically contiguous in the genome) that is needed for the production of (...) the organismic attributes that comprise the trait. I argue that individuated traits—phenes—correspond to organismic features that are caused by DC genes. Using such an approach, we can define a DC map, which shows the relations between each pair of phenes and provides a succinct summary of genotype-phenotype relationships and phenotypic complexity. Phenes in parents and offspring are judged to be homologous if their DC genes are composed of orthologous genetic factors. When comparing more distantly related organisms, traits are homologous when linked by a chain of parent-offspring homologs along the path of ancestry that links the two organisms. There are three possible ways to deal with the potential for multiple equivalent DC genes: maximal, minimal, and consensus homology. Whereas maximal homology has limited utility, the other two approaches have value and can help to guide research at the intersection of evolution and development. (shrink)

This book brings together research on the topic of causation from experts in the fields of linguistics, philosophy, and psychology. It draws on data from a wide range of languages and seeks to arrive at a more sophisticated understanding of how causal concepts are expressed in causal meanings, and how those meanings are organized into structures.

Some recent arguments defending the genuine causal efficacy of the mental have been relying on empirical research on neuroprosthetics. This essay presents a critical analysis of these arguments. The problem of mental causation, and the basic idea and results of neuroprosthetics are reviewed. It is shown how appealing to the research on neuroprosthetics can be interpreted to give support to the idea of mental causation. However, it does so only in a rather deflationary sense: by holding (...) the mental identical with the neural. So contrary to what the arguments have been assuming, neuroprosthetics cannot be used to argue for nonreductive physicalism. It can rather be taken to illustrate just the opposite: how the mental and the physical are identical. (shrink)

The fact that causal laws in the social sciences are most realistically expressed as both multivariate and stochastic has a number of very important implications for indirect measurement and generalizability. It becomes difficult to link theoretical definitions of general constructs in a one-to-one relationship to research operations, with the result that there is conceptual slippage in both experimental and nonexperimental research. It is argued that problems of this nature can be approached by developing specific multivariate causal models that (...) incorporate sources of measurement bias, along with the theoretical variables of interest. Many general concepts are defined in such a way that causal assumptions are built into the definitions themselves. Additionally, in any given piece of research it is necessary to omit many variables from consideration, and this is often done without careful consideration of the assumptions required to justify such omissions. Finally, generalization to more inclusive populations or a diversity of settings ordinarily requires one to replace constants by variables. It is concluded that the criteria of parsimony, generalizability, and precision are incompatible, given the multivariate nature of social causation, and the author expresses his own preference for sacrificing parsimony in favor of the objectives of achieving increased precision and generalizability of social science laws. (shrink)

In recent years, biologists and philosophers of science have argued that evolutionary theory should incorporate more seriously the idea of ‘reciprocal causation.’ This notion refers to feedback loops whereby organisms change their experiences of the environment or alter the physical properties of their surroundings. In these loops, in particular niche constructing activities are central, since they may alter selection pressures acting on organisms, and thus affect their evolutionary trajectories. This paper discusses long-standing problems that emerge when studying such reciprocal (...) causal processes between organisms and environments. By comparing past approaches to reciprocal causation from the early twentieth century with contemporary ones in niche construction theory, we identify two central reoccurring problems: All of these approaches have not been able to provide a conceptual framework that allows maintaining meaningful boundaries between organisms and environments, instead of merging the two, and integrating experiential and physical kinds of reciprocal causation. By building on case studies of niche construction research, we provide a model that is able to solve these two problems. It allows distinguishing between mutually interacting organisms and environments in complex scenarios, as well as integrating various forms of experiential and physical niche construction. (shrink)

If a woman in the audience at a presentation raises her hand, we would take this as evidence that she intends to ask a question. In normal circumstances, we would be right to say that she raises her hand because she intends to ask a question. We also expect that there could, in principle, be a causal explanation of her hand’s rising in purely physiological terms. Ordinarily, we take the existence and compatibility of both kinds of causes for granted. But (...) this can come to seem strange. When we imagine tracking the physiological process that culminates in her hand’s rising, it is hard to find a purchase for her intention. The physiological process seems not to need assistance from her intention in order to get where it’s going, chugging along as it does according to principles that appear to have very little in common with ordinary psychological ones. The presumed self-sufficiency of physiological processes can, in a similar fashion, appear to muscle psychological states quite generally out of the causal picture. (shrink)

Common sense supposes thoughts can cause bodily movements and thereby bring about changes in where the agent is or how his surroundings are. Many philosophers suppose that any such outcome is realized in a complex state of affairs involving only microparticles; that previous microphysical developments were sufficient to cause that state of affairs; hence that, barring overdetermination, causation by the mental is excluded. This paper argues that the microphysical swarm that realizes the outcome is an accident (Aristotle) or a (...) coincidence (David Owens) and has no cause, though each component movement in it has one. Mental causation faces no competition “from below”. (shrink)

A standard platitude about the function of causal knowledge or theories is that they are valuable because they support prediction, explanation, and control. Knowledge of predator-prey relations enables us to predict future animal populations, as well as design policies or interventions that help influence those populations. If we understand the underlying biochemical mechanisms of some disease, then we can predict who is at risk for it, explain why it produces particular symptoms, and develop interventions to try to reduce its prevalence (...) or the symptom severity. Of course, there are many situations in which one has, for practical reasons, only some of these desiderata; for example, control might be infeasible for technical or ethical reasons. But these remain, for many researchers, the ideal for why causal knowledge is a valuable end of scientific inquiry, including biological inquiry. There are, however, certain types of systems—in particular, chaotic systems—in which it appears that these ends are unattainable, and these systems appear to be widespread in the biological domain, broadly construed. In this paper, we will show why it is natural to think that causal models of chaotic systems cannot satisfy any of the three functions. But we will also show why this natural thought is wrong: we can have usable causal knowledge about even chaotic systems. Moreover, the ways in which we can have such knowledge lead us naturally to rethink a standard understanding of how causal learning and modeling proceed. In particular, just as we often must find the appropriate variables for a causal system, we also must determine the proper level or granularity of description for the dynamics of that system. (shrink)

James decides that the best price today on pork chops is at Supermarket S, then James makes driving motions for twenty minutes, then James’ car enters the parking lot at Supermarket S. Common sense supposes that the stages in this sequence may be causally connected, and that the pattern is commonplace: James’ belief (together with his desire for pork chops) causes bodily behavior, and the behavior causes a change in James’ whereabouts. Anyone committed to the idea that beliefs and desires (...) are states installed by evolution must, it seems, think something similar. For how can one see beliefs and desires as conferring selective advantage if not by supposing that, by causing bodily behavior in their subjects, they brought about changes in their subjects’ surroundings? Yet many, many philosophers currently think or worry that mental causation is illusory (see, e.g., Heil and Mele 1993, or Macdonald and Macdonald 1995). Any physical changes which a mental state appears to cause can be viewed as a complex event involving microparticles, and for any such complex event, many philosophers suppose, there will have been previous microphysical occurrences sufficient to cause it. Barring routine overdetermination of such complex events, the apparent causation of mental events seems to be excluded. Nor does it help to say that some salient segment of the previous microphysical event just is the mental event, differently described (Davidson 1970). For describing the previous events as microphysical seems to spotlight the very features in virtue of which they did their causal work; the mental features seem epiphenomenal (Yablo 1992b: pp. 425-36; Yablo 1992a). This paper argues that the complex physical events, which mental events seem excluded from causing, are not caused at all. For they are either accidents, in something like Aristotle’s sense (Sorabji 1980: pp. 3-25), or coincidences, in a sense which David Owens has recently sharpened (Owens 1992). (shrink)

Arguments for an extended evolutionary synthesis often center on the concept of “reciprocal causation.” Proponents argue that reciprocal causation is superior to standard models of evolutionary causation for at least two reasons. First, it leads to better scientific models with more predictive power. Second, it more accurately represents the causal structure of the biological world. Simply put, proponents of an extended evolutionary synthesis argue that reciprocal causation is empirically and explanatorily apt relative to competing causal frameworks. (...) In this paper, I present quantitative survey data from faculty members in biology departments at universities across the United States to evaluate this claim. The survey data indicate that a majority of the participants do not agree (i.e., most either disagree or neither agree nor disagree) that the concept of reciprocal causation confers a larger advantage on research practices. However, a majority of the participants agree that the causal framework of the extended evolutionary synthesis more accurately represents the structure of the biological world. These results demonstrate that the explanatory merits of a conceptual framework and its practical utility can come apart in interesting and informative ways. (shrink)

Epidemiologists’ discussions on causation are not always very enlightening with regard to the notion of ‘cause’ in epidemiology. Epidemiologists rightly work from a science-based approach to causation in epidemiology, but largely disagree about the matter. Disagreement may be partly due to confusion of the question of useful concepts for causal inference in epidemiological practice with the question of the metaphysical presuppositions of causal concepts used in epidemiology. In other words, epidemiologists seem to confuse the practical results of epidemiological (...) research at the population level with the metaphysical views about the reality of disease causation at the individual level in their writings on causation. (shrink)

By giving the proper emphasis to both radical skepticism and naturalism as two independent standpoints in Hume, I wish to propose a more satisfactory account of some of the more puzzling Humean claims on causation. I place these claims alternatively in either the philosophical standpoint of the radical skeptic or in the standpoint of everyday and scientific beliefs. I characterize Hume’s radical skeptical standpoint in relation to Hume’s perceptual model of the traditional theory of ideas, and I argue that (...) Hume‘s radical skeptical argument concerning our causal inferences is inextricably linked to his skeptical argument concerning our idea of a necessary connection between cause and effect. I discuss Hume’s naturalistic account of the origin of our idea of necessity and offer a new reading of Hume’s two “definitions” of cause. I argue along the way against central aspects of two opposing styles of interpretation---Norman Kemp Smith’s and Annette Baier’s, on the one hand, and Robert Fogelin’s, on the other---that in my view do not appreciate the mutual autonomy of radical skepticism and naturalism in Hume. (shrink)

Defining experiment was particularly vexed in the realm of anatomical dissection and vivisection. Was dissection merely descriptive, or something more? Harvey's discovery of the circulation of the blood and Aselli's discovery of the so-called lacteal veins shaped much anatomical research between the late 1620s and the 1650s. While the techniques of dissection and vivisection gained wide use, there was much debate on the validity of the circulation in particular, and its relationship to the lacteal veins. Critics, particularly the French (...) anatomist Jean Riolan, but also the natural philosopher Pierre Gassendi, focused on the lack of causation in Harvey's method and the lack of medical use and not on his use of vivisection. Jean Pecquet's discovery of the thoracic duct in 1651 changed the terms of the debate by definitively connecting the circulation with the lacteals. Riolan's critiques of Pecquet in the 1650s show profoundly differing notions of the purpose of dissection. While Gassendi eventually accepted Harvey's concept of the circulation, Riolan never did. (shrink)

Made famous by Ernst Mayr (1961), the distinction between proximate and ultimate causation in biological explanation is widely seen as a key tenet of evolutionary theory and a central organizing principle for evolutionary research. The study of immediate, individual-level mechanistic causes of development or physiology (“proximate causation”) is distinguished from the study of historical, population-level statistical causes in evolutionary biology (“ultimate causation”). Since evolutionary developmental biology (evo-devo) is a field that explicitly uses so-called “proximate” sciences such (...) as developmental biology, morphology, and embryology in the study of evolution, it challenges the standard construal of the proximate-ultimate distinction and its associated account of causation. The exact nature of the challenge and its ramifications for the viability of the distinction more broadly are contested, but these conceptual questions are central to the status and significance of evo-devo in contemporary evolutionary biology. (shrink)

But if there aren’t, then ‘they’ are not caused by anything and do not cause anything. That certainly appears to be false, however. John’s absence from our party might have been caused by his having fallen ill, and might cause a commotion. Dick’s not eating his soup might have been caused by his having fallen ill, and might cause a commotion.

This essay introduces Philosophia Christi’s symposium on the book, Philosophical Essays on Divine Causation, edited by Greg Ganssle. A short review of each essay in the symposium follows. A call is given for Christian philosophers to take divine causation into account while doing research in their primary area of philosophy. These updated and expanded essays were first presented in a more limited form at the 2023 Pacific Division Meeting of the American Philosophical Association.