The increasing availability of large‐scale, complex data has made research into how human genomes determine physiology in health and disease, as well as its application to drug development and medicine, an attractive field for artificial intelligence (AI) approaches. Looking at recent developments, we explore how such approaches interconnect and may conflict with needs for and notions of causal knowledge in molecular genetics and genomic medicine. We provide reasons to suggest that—while capable of generating predictive knowledge at unprecedented pace and scale—if (...) and how these approaches will be integrated with prevailing causal concepts will not only determine the future of scientific understanding and self‐conceptions in these fields. But these questions will also be key to develop differentiated policies, such as for education and regulation, in order to harness societal benefits of AI for genomic research and medicine. (shrink)

Mario Bunge vient tout juste de prendre sa retraite universitaire à l’âge vénérable de 90 ans. Après plus de soixante ans d’enseignement de la physique et de la philosophie, il laisse une oeuvre foisonnante et riche. Son style unique allie des arguments incisifs à la clarté du propos. Sa méthode puise dans le vaste arsenal des sciences, de la physique à la sociologie. Bunge suit en cela l’héritage des Lumières, qui prônait la foi en la raison ainsi qu’un certain réalisme (...) et un matérialisme qu’il reprend et retravaille à la lumière des avancées théoriques contemporaines. Peu de philosophes depuis Leibniz ou Russell ont su faire preuve d’autant d’érudition scientifique. Nul doute qu’il mérite une place de choix dans les débats entourant la philosophie des sciences contemporaines.Mario Bunge has recently retired from academic life at the venerable age of 90 years old. After more than sixty years of teaching physics and philosophy, he leaves a rich and abundant work. His unique style allies quickness and precision. His method draws from the vast realm of sciences, from physics to sociology. He thus follows the Enlightenment’s heritage that advocated a faith in reason and a kind of realism and materialism, which Bunge reorganizes from the study of modern sciences. Few philosophers since Leibniz or Russell have shown this kind of scientific erudition. No doubt that he deserves a prominent role in the contemporary debates in philosophy of sciences. (shrink)

In considering the debate about the meaning of ‘disease’, the positions are generally presented as falling into two categories: naturalist, e.g., Boorse, and normativist, e.g., Engelhardt and many others. This division is too coarse, and obscures much of what is going on in this debate. I therefore propose that accounts of the meaning of ‘disease’ be assessed according to Hare’s (1997) taxonomy of evaluative terms. Such an analysis will allow us to better understand both individual positions and their inter-relationships. Most (...) importantly, it will show that it is unlikely that there is a single unique disease-concept at issue. Rather, different authors are, for the most part, considering different concepts. (shrink)

In this paper, I examine the comparatively neglected intuition of production regarding causality. I begin by examining the weaknesses of current production accounts of causality. I then distinguish between giving a good production account of causality and a good account of production. I argue that an account of production is needed to make sense of vital practices in causal inference. Finally, I offer an information transmission account of production based on John Collier’s work that solves the primary weaknesses of current (...) production accounts: applicability and absences. (shrink)

In this paper, we examine what is to be said in defence of Machamer, Darden and Craver’s (MDC) controversial dualism about activities and entities (Machamer, Darden and Craver’s in Philos Sci 67:1–25, 2000). We explain why we believe the notion of an activity to be a novel, valuable one, and set about clearing away some initial objections that can lead to its being brushed aside unexamined. We argue that substantive debate about ontology can only be effective when desiderata for an (...) ontology are explicitly articulated. We distinguish three such desiderata. The first is a more permissive descriptive ontology of science, the second a more reductive ontology prioritising understanding, and the third a more reductive ontology prioritising minimalism. We compare MDC’s entities-activities ontology to its closest rival, the entities-capacities ontology, and argue that the entities-activities ontology does better on all three desiderata. (shrink)

Applied Evolutionary Epistemology is a scientific-philosophical theory that defines evolution as the set of phenomena whereby units evolve at levels of ontological hierarchies by mechanisms and processes. This theory also provides a methodology to study evolution, namely, studying evolution involves identifying the units that evolve, the levels at which they evolve, and the mechanisms and processes whereby they evolve. Identifying units and levels of evolution in turn requires the development of ontological hierarchy theories, and examining mechanisms and processes necessitates theorizing (...) about causality. Together, hierarchy and causality theories explain how biorealities form and diversify with time. This paper analyzes how Applied EE redefines both hierarchy and causality theories in the light of the recent explosion of network approaches to causal reasoning associated with studies on reticulate and macroevolution. Causality theories have often been framed from within a rigid, ladder-like hierarchy theory where the rungs of the ladder represent the different levels, and the elements on the rungs represent the evolving units. Causality then is either defined reductionistically as an upward movement along the strands of a singular hierarchy, or holistically as a downward movement along that same hierarchy. Upward causation theories thereby analyze causal processes in time, i.e. over the course of natural history or phylogenetically, as Darwin and the founders of the Modern Synthesis intended. Downward causation theories analyze causal processes in space, ontogenetically or ecologically, as the current eco-evo-devo schools are evidencing. This work demonstrates how macroevolution and reticulate evolution theories add to the complexity by examining reticulate causal processes in space–time, and the interactional hierarchies that such studies bring forth introduce a new form of causation that is here called reticulate causation. Reticulate causation occurs between units and levels belonging to different as well as to the same ontological hierarchies. This article concludes that beyond recognizing the existence of multiple units, levels, and mechanisms or processes of evolution, also the existence of multiple kinds of evolutionary causation as well as the existence of multiple evolutionary hierarchies needs to be acknowledged. This furthermore implies that evolution is a pluralistic process divisible into different kinds. (shrink)

Some philosophers of physics recently expressed their skepticism about causation (Norton 2003b, 2007). However, this is not new. The view that causation does not refer to any ontological category perhaps can be attributed to Hume, Kant and Russell. On the other hand, some philosophers (Wesley Salmon and Phil Dowe) view causation as a physical process and some others (Cartwright) view causation as making claims about capacities possessed by objects. The issue about the ontological status of causal claims involves issues concerning (...) the ontological status of capacity, modality and dispositional claims. In this paper, my goal is to show that without engaging metaphysical debates about the ontological status of causal claims, it can be shown that we can objectively assign truth values to these statements. I argue that for causal claims to be objective we don't need to postulate the existence of special facts (specific to causal claims) in addition to ordinary physical facts described by physical theories. This, I think, is enough to justify the usefulness of this concept in certain branches (may be all) of science. Once this is achieved, there is no need to engage in unnecessary metaphysical debates. So, even if advanced physical theories don't mention this notion, causal reasoning can still be important in understanding the world not in the sense that science discovers special ontological category called causation but in the sense that we come to know certain facts about the world. (shrink)

This paper argues that challenges that are grand in scope such as "lifelong health and wellbeing", "climate action", or "food security" cannot be addressed through scientific research only. Indeed scientific research could inhibit addressing such challenges if scientific analysis constrains the multiple possible understandings of these challenges into already available scientific categories and concepts without translating between these and everyday concerns. This argument builds on work in philosophy of science and race to postulate a process through which non-scientific notions become (...) part of science. My aim is to make this process available to scrutiny: what I call founding everyday ideas in science is both culturally and epistemologically conditioned. Founding transforms a common idea into one or more scientifically relevant ones, which can be articulated into descriptively thicker and evaluatively deflated terms and enable operationalisation and measurement. The risk of founding however is that it can invisibilise or exclude from realms of scientific scrutiny interpretations that are deemed irrelevant, uninteresting or nonsensical in the domain in question-but which may remain salient for addressing grand-in-scope challenges. The paper considers concepts of "wellbeing" in development economics versus in gerontology to illustrate this process. (shrink)

This paper considers the applicability of standard accounts of causation to living systems. In particular it examines critically the increasing tendency to equate causal explanation with the identification of a mechanism. A range of differences between living systems and paradigm mechanisms are identified and discussed. While in principle it might be possible to accommodate an account of mechanism to these features, the attempt to do so risks reducing the idea of a mechanism to vacuity. It is proposed that the solution (...) to this problem requires the development of a philosophical account of process adequate to apply to living systems. (shrink)

This paper considers the applicability of standard accounts of causation to living systems. In particular it examines critically the increasing tendency to equate causal explanation with the identification of a mechanism. A range of differences between living systems and paradigm mechanisms are identified and discussed. While in principle it might be possible to accommodate an account of mechanism to these features, the attempt to do so risks reducing the idea of a mechanism to vacuity. It is proposed that the solution (...) to this problem requires the development of a philosophical account of process adequate to apply to living systems. (shrink)

This paper considers the applicability of standard accounts of causation to living systems. In particular it examines critically the increasing tendency to equate causal explanation with the identification of a mechanism. A range of differences between living systems and paradigm mechanisms are identified and discussed. While in principle it might be possible to accommodate an account of mechanism to these features, the attempt to do so risks reducing the idea of a mechanism to vacuity. It is proposed that the solution (...) to this problem requires the development of a philosophical account of process adequate to apply to living systems. (shrink)

Real causal systems are complicated. Despite this, causal learning research has traditionally emphasized how causal relations can be induced on the basis of idealized events, i.e. those that have been mapped to binary variables and abstracted from time. For example, participants may be asked to assess the efficacy of a headache-relief pill on the basis of multiple patients who take the pill (or not) and find their headache relieved (or not). In contrast, the current study examines learning via interactions with (...) continuous dynamic systems, systems that include continuous variables that interact over time (and that can be continuously observed in real time by the learner). To explore such systems, we develop a new framework that represents a causal system as a network of stationary Gauss--Markov (``\OU'') processes and show how such \textit{OU networks} can express complex dynamic phenomena such as feedback loops and oscillations. To assess adult's abilities to learn such systems, we conducted an experiment in which participants were asked to identify the causal relationships of a number of OU networks, potentially carrying out multiple, temporally-extended interventions. We compared their judgments to a normative model for learning OU networks as well as a range of alternative and heuristic learning models from the literature. We found that, although participants exhibited substantial learning of such systems, they committed certain systematic errors. These successes and failures were best accounted for by a model that describes people as focusing on pairs of variables, rather than evaluating the evidence with respect to the full space of possible structural models. We argue that our approach provides both a principled framework for exploring the space of dynamic learning environments as well as new algorithmic insights into how people interact successfully with a continuous causal world. (shrink)

Comparative psychology experiments typically test a null statistical hypothesis against an alternative. Coupled with Morgan’s canon, this is often taken to imply that the model positing the simpler psychological capacity should be treated as a ‘default’ that must be ruled out before any other model can be accepted. It has been posited that this practice neglects evidence. I argue that the problem is deeper, including the way it structures the evaluation of evidence that is considered; it frames model choice around (...) the acceptance or rejection of a default. I oppose this default framing in all its forms and develop an evidentialist alternative. Default framing fails to respect the difference between experimental statistical hypotheses and substantive hypotheses such as models. It is not actually supported by the use of null hypothesis significance testing (which I retain), it distorts the weighting of evidence, and it systematically biases practice. (shrink)

The main focus of this paper is the question as to what it is for an individual to think of her environment in terms of a concept of causation, or causal concepts, in contrast to some more primitive ways in which an individual might pick out or register what are in fact causal phenomena. I show how versions of this question arise in the context of two strands of work on causation, represented by Elizabeth Anscombe and Christopher Hitchcock, respectively. I (...) then describe a central type of reasoning that, I suggest, a subject has to be able to engage in, if we are to credit her with causal concepts. I also point out that this type of reasoning turns on the idea of a physical connection between cause and effect, as articulated in recent singularist approaches of causation. (shrink)

In considering the debate about the meaning of ‘disease’, the positions are generally presented as falling into two categories: naturalist, e.g., Boorse, and normativist, e.g., Engelhardt and many others. This division is too coarse, and obscures much of what is going on in this debate. I therefore propose that accounts of the meaning of ‘disease’ be assessed according to Hare's (1997) taxonomy of evaluative terms. Such an analysis will allow us to better understand both individual positions and their interrelationships. Most (...) importantly, it will show that it is unlikely that there is a single unique disease-concept at issue. Rather, different authors are, for the most part, considering different concepts. (shrink)

Glennan appeals to interventions to solve the ontological and explanatory regresses that threaten his mechanistic account of causality . I argue that Glennan’s manoeuvre fails. The appeal to interventions is not able to address the ontological regress, and it blocks the explanatory regress only at the cost of making the account inapplicable to non-modular mechanisms. I offer a solution to the explanatory regress that makes use of dynamic Bayesian networks. My argument is illustrated by a case study from systems biology, (...) namely, the mechanism for the irreversibility of apoptosis. I conclude by pointing out the implications of my argument for Glennan’s mechanistic account of causality and, more generally, for accounts of mechanistic explanation based on interventions. 1 Introduction2 Glennan’s Account of Causality3 Objections to Glennan’s Account4 Glennan’s Replies5 Ontological Symmetry?6 Explanatory Symmetry?7 A Solution to the Explanatory Regress8 The Prospects of Glennan’s Account. (shrink)

How many notions of cause are there? The causality literature is witnessing a flourishing of pluralist positions. Here I focus on a recent debate on whether interpreting causality in terms of inferential relations commits one to semantic pluralism (Reiss 2011) or not (Williamson 2006). I argue that inferentialism is compatible with a ‘weak’ form of monism, where causality is envisaged as one, vague cluster concept. I offer two arguments for this, one for vagueness, one for uniqueness. Finally, I qualify in (...) what sense the resulting form of monism is ‘weak’.¿Cuántas nociones de causa hay? Hay un resurgir de posiciones pluralistas en la bibliografía sobre causalidad. Me ocuparé aquí de un debate reciente sobre si la interpretación de la causalidad en términos de relaciones inferenciales nos compromete con el pluralismo semántico (Reiss 2011) o no (Williamson 2006). Defiendo que el inferencialismo es compatible con una forma ’debil’ de monismo, donde la causalidad se presenta como un único concepto vago y de agrupación (cluster). Ofrezco para ello dos argumentos, uno sobre vaguedad y otro sobre unicidad. Finalmente, matizaré en qué sentido esta forma demonismo es ’débil’. (shrink)

Ever since Wesley Salmon’s theory, the mechanical approach to causality has found an increasing number of supporters who have developed it in different directions. Mechanical views such as those advanced by Stuart Glennan, Jim Bogen and Peter Machamer, Lindley Darden and Carl Craver have met with broad consensus in recent years. This paper analyses the main features of these mechanical positions and some of the major problems they still face, referring to the latest debate on mechanisms, causal explanation and the (...) relationship between mechanisms and counterfactuals. I shall claim that the mechanical approach can be recognised as having a fundamental explanatory power, whereas the counterfactual approach, recently developed mainly by Jim Woodward and essentially linked to the notion of intervention, has an important heuristic role. Claiming that mechanisms are by no means to be seen as parasitic on counterfactuals or less fundamental than them – as it has been recently suggested –, and that yet counterfactuals can play a part in a conceptual analysis of causation, I shall look for hints in support of the peaceful coexistence of the two. (shrink)

The counterfactual and regularity theories are universal accounts of causation. I argue that these should be generalized to produce local accounts of causation. A hallmark of universal accounts of causation is the assumption that apparent variation in causation between locations must be explained by differences in background causal conditions, by features of the causal-nexus or causing-complex. The local account of causation presented here rejects this assumption, allowing for genuine variation in causation to be explained by differences in location. I argue (...) that local accounts of causation are plausible, and have pragmatic, empirical and theoretical advantages over universal accounts. I then report on the use of presheaves as models of local causation. The use of presheaves as models of local variation has precedents in algebraic geometry, category theory and physics; they are here used as models of local causal variation. The paper presents this idea as stemming from an approach using presheaves as models of local truth. Finally, I argue that a proper balance between universal and local causation can be assuaged by moving from presheaves to fully-fledged sheaf models. (shrink)

The paper takes a novel approach to a classic problem—Hempel’s Raven Paradox. A standard approach to it supposes the solution to consist in bringing our inductive logic into “reflective equilibrium” with our intuitive judgements about which inductive inferences we should license. This approach leaves the intuitions as a kind of black box and takes it on faith that, whatever the structure of the intuitions inside that box might be, it is one for which we can construct an isomorphic formal edifice, (...) a system of inductive logic. By popping open the box we can see whether that faith is misplaced. I aim, therefore, to characterize our pre-theoretical, intuitive understanding of generalizations like “ravens are black” and argue that, intuitively, we take them to mean, for instance: “ravens are black by some indeterminate yet characteristic means.” I motivate and explicate this formulation and bring it to bear on Hempel’s Problem. (shrink)

Philosophers of physics have long debated whether the Past State of low entropy of our universe calls for explanation. What is meant by “calls for explanation”? In this article we analyze this notion, distinguishing between several possible meanings that may be attached to it. Taking the debate around the Past State as a case study, we show how our analysis of what “calling for explanation” might mean can contribute to clarifying the debate and perhaps to settling it, thus demonstrating the (...) fruitfulness of this analysis. Applying our analysis, we show that two main opponents in this debate, Huw Price and Craig Callender, are, for the most part, talking past each other rather than disagreeing, as they employ different notions of “calling for explanation”. We then proceed to show how answering the different questions that arise out of the different meanings of “calling for explanation” can result in clarifying the problems at hand and thus, hopefully, to solving them. (shrink)

Pharmacogenetics and pharmacogenomics are related facets of cutting edge therapeutic research in a field that relates pharmacological properties to the genetic characteristics of human beings. An optimistic interpretation suggests that “One-Size-Fits-All” therapeutics, whose effects can only be predicted in probabilistic terms, will give way eventually to individual tailor-made therapies with entirely predictable properties in each patient. Yet the concept of anticipating individual pharmacotherapeutic response appears to disregard some of the fundamental limitations of causal understanding in the biological world of structure–action (...) relationships. It is not simply a problem of confronting complexity – which might be overcome in time with advances in biotechnology and computing power – but the inescapable paradox of the genetic characteristics of individuals within the human species. The aleatory process of evolution ensures that with the exception of monozygotic twins, every human being is genetically unique. At the same time there appears to be more in common than divides. Pharmacogenomics provides a climate in which to explore and better understand the variable causal relationships between genetic element, protein and therapeutic or toxic actions, but can only do so in abstraction. Thus␣predictive power may be enhanced but is ultimately constrained by insuperable probabilistic considerations. (shrink)

There are several different ways in which chance affects evolutionary change. That all of these processes are called “random genetic drift” is in part a due to common elements across these different processes, but is also a product of historical borrowing of models and language across different levels of organization in the biological hierarchy. A history of the concept of drift will reveal the variety of contexts in which drift has played an explanatory role in biology, and will shed light (...) on some of the philosophical controversy surrounding whether drift is a cause of evolutionary change. (shrink)

The emphasis on the organization of entities and their activities and interactions has been labeled one of the most distinct contributions of mechanistic philosophy. In this paper I discuss the manner in which the organization of entities and their activities and interactions participates in bringing about phenomena. I present a well-known example from molecular biology—the functioning of the genetic switch in phage lambda—and discuss Marco J. Nathan’s notion of causation by concentration. Nathan introduces causation by concentration to account for the (...) irreducible causal role that the concentration ratio between two kinds of proteins possesses in the genetic switch mechanism in phage lambda. I discuss what the irreducibility of this causal role amounts to and provide a mechanistic interpretation of Nathan’s causation by concentration; that is, I explain this irreducible causal role as one organizational feature of this mechanism. The paper concludes that biological mechanisms need a causal pluralist framework [similar to Glennan’s account in, and but slightly modified] where organizational features such as the concentration ratio have a causally relevant role, yet all the causally productive relations occur at the level of entities or individuals. (shrink)

It is argued that causal understanding originates in experiences of acting on objects. Such experiences have consistent features that can be used as clues to causal identification and judgment. These are singular clues, meaning that they can be detected in single instances. A catalog of 14 singular clues is proposed. The clues function as heuristics for generating causal judgments under uncertainty and are a pervasive source of bias in causal judgment. More sophisticated clues such as mechanism clues and repeated interventions (...) are derived from the 14. Research on the use of empirical information and conditional probabilities to identify causes has used scenarios in which several of the clues are present, and the use of empirical association information for causal judgment depends on the presence of singular clues. It is the singular clues and their origin that are basic to causal understanding, not multiple instance clues such as empirical association, contingency, and conditional probabilities. (shrink)

This dissertation argues that cognition is a kind of natural agency. Natural agency is the capacity that certain systems have to act in accordance with their own norms. Natural agents are systems that bias their repertoires in response to affordances in the pursuit of their goals. Cognition is a special mode of this general phenomenon. Cognitive systems are agents that have the additional capacity to actively take their worlds to be certain ways, regardless of whether the world is really that (...) way. In this way, cognitive systems are desituated. Desituatedness is the root of specifically cognitive capacities for representation and abstraction. There are two main reasons why this view needs defending. First, natural agency is typically viewed as incompatible with natural science because it is committed to a teleological mode of explanation. Second, cognition is typically held to be categorically distinct from natural agency. This dissertation argues against both of these views. It argues against the incompatibility of agency and natural science by demonstrating that systems biology, general systems theory, and sciences that deal with complex systems have typically underappreciated conceptual and theoretical resources for grounding agency in the causal structure of the world. These conceptual resources do not, however, reduce agency to systems theory because the normativity inherent in agency demands descriptive resources beyond those of even the most sophisticated systems theory. It argues against the categorical difference between natural agency and cognition by pointing out that separating cognition from a richer web of situated, ecologically embedded relations between the agent and the world generates the frame problem, which is an insuperable obstacle to making cognition that is sufficiently responsive to the complexity of the world. Rooting cognition in natural agency is a more robust empirical bet for theorizing cognition and artificial intelligence. (shrink)

Philosophical analyses of causation have been centred on the question of what causation is. More precisely speaking, philosophers tend to address four different issues: metaphysical (what is causation out there?), epistemological (how can a causal claim be established and assessed?), conceptual (what does the word ‘cause’ mean?), and methodological (what methods ought one to use in order to establish and assess causal claims?). This chapter argues that the practical issue of causation (what is a causal claim for in practice?) is (...) highly relevant to the metaphysical, epistemological, conceptual, and methodological issues of causation. Any philosophical enquiry into causation without an examination of this practical issue is incomplete. In other words, a promising approach to causation ought to take all of the metaphysical, epistemological, conceptual, methodological, and practical issues into account. (shrink)

Many approaches to quantum gravity -the theory that should account for quantum and gravitational phenomena under the same theoretical umbrella- seem to point at some form of spacetime emergence, i.e., the fact that spacetime is not a fundamental entity of our physical world. This tenet has sparked many philosophical discussions: from the so-called empirical incoherence problem to different accounts of emergence and mechanisms thereof. In this contribution, I focus on the partial order relation of causal set theory and argue that (...) causation can be characterized as an a-temporal constraint over the kinematic space defined by the theory. The relation constrains the growth of a new element/event with respect to the other elements/events of a given set. Therefrom, the flow of time emerges from the collection of the possible growths of the given set, where each possibility is characterized by a classical probability assigned by the dynamics of the theory. (shrink)

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 editorial offers new ways to ethically practice, evaluate, and use quantitative research. Our central claim is that ready-made formulas for QR, including ‘best practices’ and common notions of ‘validity’ or ‘objectivity,’ are often divorced from the ethical and practical implications of doing, evaluating, and using QR for specific purposes. To focus on these implications, we critique common theoretical foundations for QR and then recommend approaches to QR that are ‘built for purpose,’ by which we mean designed to ethically address (...) specific problems or situations on terms that are contextually relevant. For this, we propose a new tool for evaluating the quality of QR, which we call ‘relational validity.’ Studies, including their methods and results, are relationally valid when they ethically connect researchers’ purposes with the way that QR is oriented and the ways that it is done—including the concepts and units of analysis invoked, as well as what its ‘methods’ imply more generally. This new way of doing QR can provide the liberty required to address serious worldly problems on terms that are both practical and ethically informed in relation to the problems themselves rather than the confines of existing QR logics and practices. (shrink)

The essay discusses Donald Davidson’s concept of anomalous monism in the framework of Husserlian phenomenology. It develops in four stages. Section 1 is devoted to a critical presentation of the argument for anomalous monism. Section 2 succinctly examines those Husserlian notions that best provide the ground for a discussion parallel to Davidson’s. In Sect. 3, the aporetic status of “mental causation” is analyzed by providing a genetic-phenomenological account of efficient causation. Section 4 draws some general conclusions concerning the kind of (...) efficaciousness that must be attributed to consciousness and discusses the sense in which anomalous monism can be defended in a phenomenological framework, but not in a naturalistic one. (shrink)

This paper is a realist argument for the existence of “social objects”. Social objects, I argue, are the outcome states of a contingent causal process and in turn posses causal properties. This argument has consequences for what we can mean by realism and consequences for the development of a realist methodology. Realism should abandon the notion of natural necessity in favour of a view that the “real” nature of the social world is contingent and necessity is only revealed in outcome (...) states. This, I argue, has both theoretical and methodological implications and I develop my argument through two case studies, of homelessness and ethnicity. (shrink)

There is a systematic and suggestive analogy between grounding and causation. In my view, this analogy is no coincidence. Grounding and causation are alike because grounding is a type of causation: metaphysical causation. In this paper I defend the identification of grounding with metaphysical causation, drawing on the causation literature to explore systematic connections between grounding and metaphysical dependence counterfactuals, and I outline a non-reductive counterfactual theory of grounding along interventionist lines.

The mechanistic and causal accounts of explanation are often conflated to yield a ‘causal-mechanical’ account. This paper prizes them apart and asks: if the mechanistic account is correct, how can causal explanations be explanatory? The answer to this question varies according to how causality itself is understood. It is argued that difference-making, mechanistic, dualist and inferentialist accounts of causality all struggle to yield explanatory causal explanations, but that an epistemic account of causality is more promising in this regard.

It is tempting to analyse causality in terms of just one of the indicators of causal relationships, e.g., mechanisms, probabilistic dependencies or independencies, counterfactual conditionals or agency considerations. While such an analysis will surely shed light on some aspect of our concept of cause, it will fail to capture the whole, rather multifarious, notion. So one might instead plump for pluralism: a different analysis for a different occasion. But we do not seem to have lots of different concepts of cause (...) – just one eclectic notion. The resolution of this conundrum, I think, requires us to accept that our causal beliefs are generated by a wide variety of indicators, but to deny that this variety of indicators yields a variety of concepts of cause. This focus on the relation between evidence and causal beliefs leads to what I call epistemic causality. Under this view, certain causal beliefs are appropriate or rational on the basis of observed evidence; our notion of cause can be understood purely in terms of these rational beliefs. Causality, then, is a feature of our epistemic representation of the world, rather than of the world itself. This yields one, multifaceted notion of cause. (shrink)

The epistemic theory of causality is analogous to epistemic theories of probability. Most proponents of epistemic probability would argue that one's degrees of belief should be calibrated to chances, insofar as one has evidence of chances. The question arises as to whether causal beliefs should satisfy an analogous calibration norm. In this paper, I formulate a particular version of a norm requiring calibration to chances and argue that this norm is the most fundamental evidential norm for epistemic probability. I then (...) develop an analogous calibration norm for epistemic causality, argue that it is the *only* evidential norm required for epistemic causality, and show how an epistemic account of causality that incorporates this norm can be used to analyse objective causal relationships. (shrink)

The most compelling extant accounts of explanation casts all explanations as causal. Yet there are sciences, theoretical population biology in particular, that explain their phenomena by appeal to statistical, non-causal properties of ensembles. I develop a generalised account of explanation. An explanation serves two functions: metaphysical and cognitive. The metaphysical function is discharged by identifying a counterfactually robust invariance relation between explanans event and explanandum. The cognitive function is discharged by providing an appropriate description of this relation. I offer examples (...) of explanations from portfolio theory and population genetics that meet this characterisation. In each case the invariance relation holds between a statistical property of an ensemble and a change in structure of the ensemble. In neither case, however, does the statistical property cause the outcome it explains. There are genuine statistical, non-causal scientific explanations. (shrink)

In everyday life, people typically observe fragments of causal networks. From this knowledge, people infer how novel combinations of causes they may never have observed together might behave. I report on 4 experiments that address the question of how people intuitively integrate multiple causes to predict a continuously varying effect. Most theories of causal induction in psychology and statistics assume a bias toward linearity and additivity. In contrast, these experiments show that people are sensitive to cues biasing various integration rules. (...) Causes that refer to intensive quantities (e.g., taste) or to preferences (e.g., liking) bias people toward averaging the causal influences, whereas extensive quantities (e.g., strength of a drug) lead to a tendency to add. However, the knowledge underlying these processes is fallible and unstable. Therefore, people are easily influenced by additional task‐related context factors. These additional factors include the way data are presented, the difficulty of the inference task, and transfer from previous tasks. The results of the experiments provide evidence for causal model and related theories, which postulate that domain‐general representations of causal knowledge are influenced by abstract domain knowledge, data‐driven task factors, and processing difficulty. (shrink)

In “Modern Moral Philosophy,” Elizabeth Anscombe charged that Sidgwick's failure to distinguish intended from merely foreseen consequences of an action counted as a very bad degeneration of thought. Sidgwick's failure is endemic to contemporary normative models of decision and choice. There are three components to rational decision making on these models: what the agent wants the prospective actions or policies under consideration and what the agent expects will happen as a result of taking specific action or adopting specific policy measures. (...) The prospective actions are often modeled as lotteries across possible outcomes. Choice on any lottery-based model or representation is choice among probability distributions. Participants in contemporary risk assessment studies do not make decisions in the way suggested by these models. Instead, the participants deploy a distinctive form of estimating the future. I advance a series of considerations meant to motivate the claim that the form of estimating the future at issue for participants of risk assessment studies may be sound, even when the content of their practical judgment is dubious. The form belongs equally to ethics and to practical reason and tracks Anscombe's remarks about moral responsibility. (shrink)

Using a unique data set of causal usage drawn from research articles published between 2006–2008 in the American Journal of Sociology and American Sociological Review, this article offers an empirical assessment of causality in American sociology. Testing various aspects of what we consider the conventional wisdom on causality in the discipline, we find that “variablistic” or “covering law” models are not the dominant way of making causal claims, research methods affect but do not determine causal usage, and the use of (...) explicit causal language and the concept of “mechanisms” to make causal claims is limited. Instead, we find that metaphors and metaphoric reasoning are fundamental for causal claims-making in the discipline. On this basis, we define three dominant causal types used in sociology today, which we label the Probabilistic, Initiating and Conditioning types. We theorize this outcome as demonstrating the primary role that cognitive models play in providing inference-rich metaphors that allow sociologists to map causal relationships on to empirical processes. (shrink)

Kaplan and Craver :601–627, 2011) and Piccinini and Craver :283–311, 2011) argue that only mechanistic explanations of cognition are genuine causal explanations, because only evidence of mechanisms reveals the causal structure of cognition. I first argue that this claim is grounded in a commitment to the mechanistic account of causality, which cannot be endorsed by a defender of causal-nonmechanistic explanations. Then, I defend the epistemic theory of causality, which holds that causal explanations are not genuine to the extent that they (...) reveal mechanistic causal structure, but, rather, to the extent that they have evidential support and yield successful prediction, explanation, and control inferences. Finally, I enact an epistemic unification of causal explanation in cognitive science, according to which both mechanistic and nonmechanistic explanations of cognition can be genuine causal explanations. (shrink)

Hall has recently argued that there are two concepts of causality, picking out two different kinds of causal relation. McGrath, and Hitchcock and Knobe, have recently argued that the facts about causality depend on what counts as a “default” or “normal” state, or even on the moral facts. In the light of these claims you might be tempted to agree with Skyrms that causal relations constitute, metaphysically speaking, an “amiable jumble”, or with Cartwright that ‘causation’, though a single word, encompasses (...) many different kinds of things. This paper argues, drawing on the author’s recent work on explanation, that the evidence adduced in support of causal pluralism can be accommodated easily by a unified theory of causality—a theory according to which all singular causal claims concern the same fundamental causal network. (shrink)

Philosophers discussing causation take on, as one of their responsibilities, the task of specifying an ontology of causation. Both standard and non-standard accounts of that ontology make two assumptions: that the ontological category of causal relata admits a unique specification, and that cause and effect are of the same ontological type. These assumptions are rarely made explicit, but there is in fact little reason to think them true. It is argued here that, if the question has any interest, there are (...) some considerations in favor of rejecting Uniqueness and Uniformity, no good reasons in favor of them, but good reason to think that we are not in a position to make a decisive pronouncement, since some of the information needed to make a judgement on the matter is empirical in character. Philosophers have therefore made two mistakes about the relata of causation: one is to have accepted unwarranted restrictions on the categories pertinent to causation; the other is to have wrongly assumed that we are in a position to name them. (shrink)

This paper argues that the semantic facts about ‘because’ are best explained via a metaphorical treatment of metaphysical explanation that treats causal explanation as explanation par excellence. Along the way, it defends a commitment to a unified causal sense of ‘because’ and offers a proprietary explanation of grounding skepticism. With the causal metaphor account of metaphysical explanation on the table, an extended discussion of the relationship between conceptual structure and metaphysics ends with a suggestion that the semantic facts about ‘because’ (...) tell against grounding-causation unity. (shrink)

This paper presents evidence that ‘because’ is importantly ambiguous between two closely related senses covering what are usually called causal explanations, on the one hand, and grounding or metaphysical explanations, on the other hand. To this end, it introduces the lexical categories of monosemy, polysemy and homonymy; describes a test for polysemy; and discusses the results of the test when applied to ‘because’. It also shows how to understand so-called hybrid explanations in light of the semantic facts established by the (...) analysis. (shrink)

This paper is an essay in what Austin (_Proc Aristotel Soc_ 57: 1–30, 1956–1957) called "linguistic phenomenology". Its focus is on showing how the grammatical features of ordinary causal verbs, as revealed in the kinds of linguistic constructions they can figure in, can shed light on the nature of the processes that these verbs are used to describe. Specifically, drawing on the comprehensive classification of English verbs founds in Levin (_English verb classes and alternations: a preliminary investigation_, University of Chicago (...) Press, Chicago, 1993), I divide the forms of productive causal processes into five classes, corresponding to Aristotle's ontological categories: there are processes that cause change in location, in state, and in quantity; and that lead to the creation and destruction of substances. These broader categories are then subdivided into other ones, corresponding to different Levin classes, according to further differences in the causal processes they involve. I conclude by discussing the relevance of this argument to research in metaphysics and experimental philosophy. (shrink)

Sixteen years after Kim’s seminal paper offering a welcomed analysis of the emergence concept, I propose in this paper a needed extension of Kim’s work that does more justice to the actual diversity of emergentism. Rather than defining emergence as a monolithic third way between reductive physicalism and substance pluralism, and this through a conjunction of supervenience and irreducibility, I develop a comprehensive taxonomy of the possible varieties of emergence in which each taxon—theoretical, explanatory and causal emergence—is properly identified and (...) defined. This taxonomy has two advantages. First, it is unificatory in the sense that the taxa it contains derive from a common unity principle, which consequently constitutes the very hallmark of emergentism. Second, it can be shown that the emergence taxa it contains are able to meet the challenges that are commonly considered as being the hot topics on the emergentists’ agenda, namely the positivity, the consistency and the triviality/liberality challenges. (shrink)