Functional robustness refers to a system’s ability to maintain a function in the face of perturbations to the causal structures that support performance of that function. Modularity, a crucial element of standard methods of causal inference and difference-making accounts of causation, refers to the independent manipulability of causal relationships within a system. Functional robustness appears to be at odds with modularity. If a function is maintained despite manipulation of some causal structure that supports that function, then (...) the relationship between that structure and function fails to be manipulable independent of other causal relationships within the system. Contrary to this line of reasoning, I argue that functional robustness often attends feedback control, rather than failures of modularity. Feedback control poses its own challenges to causal explanation and inference, but those challenges do not undermine modularity—and indeed, modularity is crucial to grappling with them. (shrink)

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

In The Biopsychosocial Model of Health and Disease, Derek Bolton and Grant Gillett argue that a defensible updated version of the biopsychosocial model requires a metaphysically adequate account of disease causation that can accommodate biological, psychological, and social factors. This present paper offers a philosophical critique of their account of biopsychosocial causation. I argue that their account relies on claims about the normativity and the semantic content of biological information that are metaphysically contentious. Moreover, I suggest that these claims are (...) unnecessary for a defence of biopsychosocial causation, as the roles of multiple and diverse factors in disease causation can be readily accommodated by a more widely accepted and less metaphysically contentious account of causation. I then raise the more general concern that they are misdiagnosing the problem with the traditional version of the biopsychosocial model. The challenge when developing an explanatorily valuable version of the biopsychosocial model, I argue, is not so much providing an adequate account of biopsychosocial causation, but providing an adequate account of causal selection. Finally, I consider how this problem may be solved to arrive at a more explanatorily valuable and clinically useful version of the biopsychosocial model. (shrink)

I examine to what extent accounts of mechanisms based on formal interventionist theories of causality can adequately represent biological mechanisms with complex dynamics. Using a differential equation model for a circadian clock mechanism as an example, I first show that there exists an iterative solution that can be interpreted as a structural causal model. Thus, in principle, it is possible to integrate causal difference-making information with dynamical information. However, the differential equation model itself lacks the right modularity properties (...) for a full integration. A formal mechanistic model will therefore have to leave out either noncausal or causal explanatory relations. (shrink)

I present three reasons why philosophers of science should be more concerned about violations of causal faithfulness (CF). In complex evolved systems, mechanisms for maintaining various equilibrium states are highly likely to violate CF. Even when such systems do not precisely violate CF, they may nevertheless generate precisely the same problems for inferring causal structure from probabilistic relationships in data as do genuine CF-violations. Thus, potential CF-violations are particularly germane to experimental science when we rely on probabilistic information (...) to uncover the DAG, rather than already knowing the DAG from which we could predict the right experiments to ‘catch out’ the hidden causal relationships. (shrink)

Analyzing causation in terms of Woodward's interventionist theory and describing the structure of the world in terms of causal powers are usually regarded as quite different projects in contemporary philosophy. Interventionists aim to give an account of how causal relations can be empirically discovered and described, without committing themselves to views about what causation really is. Causal powers theorists engage in precisely the latter project, aiming to describe the metaphysical structure of the world. In this paper, (...) I argue that interventionism can benefit from incorporating considerations about causal powers. I describe a previously undiscussed problem for Woodward's definition of an intervention variable that arises when interventionist causal models include disjunctive variables. This problem is solved not by excluding disjunctive (or logically compound) variables per se, but by excluding variables whose values represent disjunctions of too different causal powers. This suggests that interventionism and causal powers theories may be less distant from each other than is often assumed. (shrink)

Most of us have a very firm belief in mental causation; that is, we firmly believe that our own distinctly mental properties are causally efficacious in the production of our behavior. This belief is dominating in contemporary philosophy of mind as a part of the causal explanatory exclusion problem for non-reductive materialists. I do not discuss the exclusion problem; rather, I assess the conception of mental causation that is presupposed in the current debate. I propose that in order (...) to make sense of our firm belief in mental causation we need to operate with a broader conception of it than is normally seen, focusing on common-sense aspects concerning the timing, awareness, control, and tracking of mental causation. However, prominent studies in social psychology and cognitive neuroscience show that mental causation is not as self-evident, robust, and pervasive as our firm belief in it would suggest. There is therefore a tension between the common-sense, broad conception of mental causation and our empirical evidence for mental causation. A full defense of mental causation is not just a matter of securing causal efficacy but also of situating our notion of mental properties in relation to difficult issues concerning awareness, control, and judgment. (shrink)

This paper articulates an account of causation as a collection of information-theoretic relationships between patterns instantiated in the causal nexus. I draw on Dennett’s account of real patterns to characterize potential causal relata as patterns with specific identification criteria and noise tolerance levels, and actual causal relata as those patterns instantiated at some spatiotemporal location in the rich causal nexus as originally developed by Salmon. I develop a representation framework using phase space to precisely characterize (...) class='Hi'>causal relata, including their degree of counterfactual robustness, causal profiles, causal connectivity, and privileged grain size. By doing so, I show how the philosophical notion of causation can be rendered in a format that is amenable for direct application of mathematical techniques from information theory such that the resulting informational measures are causal informational measures. This account provides a metaphysics of causation that supports interventionist semantics and causal modeling and discovery techniques. (shrink)

The field of the philosophy of biology is flourishing in its aim to evaluate and rethink the view inherited from the previous century ---the Modern Synthesis. Different research areas and theories have come to the fore in the last decades in order to account for different biological phenomena that, in the first instance, fall beyond the explanatory scope of the Modern Synthesis. This thesis is anchored and motivated by this revolt in the philosophy of biology. -/- (...) The central target in this context is the possibility of naturalizing teleology, a classical nightmare for the history of biology itself. This requires, principally, understanding the causes of teleological explanations without assuming an unfashioned backward causation of sorts. As the riddles of teleological explanations are about their temporal dimension, I analyze different temporal scales of biological processes: evolutionary, developmental, and physiological. -/- The first one is the one defended in the context of the Modern Synthesis. As expected, one of the aims of this thesis is to evaluate the adequacy of an evolutionary account of teleological explanation. The scrutiny is negative. Evolutionary explanations in the context of the Modern Synthesis lack the necessary causal roots to naturalize teleology. Concerning the physiological scale, a long tradition pushed up by Kant and the organicist movement in the 20th century allows us to better understand how teleological explanations can be naturalized in physiological process. The key notions in this temporal scale are self-organization and the recursive, looped character of physiological process. While the physiological scale may be suitably accounted by contemporaries views, such as Autonomous Systems Theory, different central teleological phenomena remain unexplained from a purely physiological perspective. In particular, different issues concerning the (adaptive) construction of organism ---such as plasticity, robustness, variation, novelty, inheritance--- deserve an ontogenetic analysis. -/- The principal aim of this thesis is to provide a theory of teleological development that falls beyond the Modern Synthesis' framework and is prompted by different insights from the history of biology. I call it Agential Teleosemantics. It rests on two central pillars. First, that developmental processes, beyond any gene-centered stance, can be understood in informational terms; i.e. developmental processes are about the interaction of developmental resources conveying biological information. The second ingredient is agentivity, namely the idea that development is regulated by an agentive system according to the adaptiveness of the phenotypic outcomes produced. The role of agency in Agential Teleosemantic is equivalent to the role of genes in the Modern Synthesis: it is responsible for explaining the order and the adaptive complexity in the living realm. -/- The second target of this thesis regards the possibility of naturalizing intentional explanations in cognitive science. The central project involved in such an aim is known as teleosemantics. Classical teleosemantics however is etiological: it explains the teleofunctions of representational systems in terms of evolutionary processes. The different disputes in the contemporary philosophy of biology provide two insights to analyze teleosemantics in cognitive science. First, the challenges against the Modern Synthesis must be extended to the evolutionary approach of etiological teleosemantics. Second, as Agential Teleosemantics suggests an alternative source for teleofunctions ---ontogeny, I offer an attempt to integrate Agential Teleosemantics into cognitive science in order to provide an alternative teleosemantic project to understand intentional explanations in cognitive science. (shrink)

The anti-reductionist character of the recent philosophy of biology and the dynamic development of the science of emergent properties prove that the time is ripe to reintroduce the thought of Aristotle, the first advocate of a “top-down” approach in life-sciences, back into the science/philosophy debate. His philosophy of nature provides profound insights particularly in the context of the contemporary science of evolution, which is still struggling with the questions of form, teleology, and the role of chance (...) in evolutionary processes. However, although Aristotle is referenced in the evolutionary debate, a thorough analysis of his theory of hylomorphism and the classical principle of causality which he proposes is still needed in this exchange. Such is the main concern of the first part of the present article which shows Aristotle’s metaphysics of substance as an open system, ready to incorporate new hypothesis of modern and contemporary science. The second part begins with the historical exploration of the trajectory from Darwin to Darwinism regarded as a metaphysical position. This exploration leads to an inquiry into the central topics of the present debate in the philosophy of evolutionary biology. It shows that Aristotle’s understanding of species, teleology, and chance – in the context of his fourfold notion of causality – has a considerable explanatory power which may enhance our understanding of the nature of evolutionary processes. This fact may inspire, in turn, a retrieval of the classical theology of divine action, based on Aristotelian metaphysics, in the science/theology dialogue. The aim of the present article is to prepare a philosophical ground for such project. (shrink)

In her landmark book, Language, Thought, and Other Biological Categories (Millikan1984),1 Ruth Garrett Millikan utilizes the idea of a biological function to solve philosophical problems associated with the phenomena of language, thought, and meaning. Language and thought are activities of biological organisms, according to Millikan, and we should treat them as such when trying to answer related philosophical questions. Of special interest is Millikan’s treatment of intentionality. Here Millikan employs the notion of a biological function to explain what it is (...) for one thing in nature, a bee dance (43), for example, to be about another, in this case, the location of a nectar source. My concern in this paper is to understand whether Millikan’s account of intentionality adequately explains how humans achieve reference, in language or thought, to individuals and groups in their environment. In bringing her theory of intentional content to bear on human activities, Millikan focuses largely on natural language. Thus, in what follows, I begin by laying out the biology-based principles that underlie Millikan’s theory of content, then proceed with an explanation of how the theory is to apply to natural language. As it appears, Millikan’s account of how content is determined for natural language terms and sentences rests on the determinacy of intentional content at the psychological level. This leads me to take a careful look at what Millikan says about the content of mental representations, in hopes of finding a sufficient basis there for the application of Millikan’s theory of content to natural language. Ultimately, I conclude that Millikan’s theory faces a problem of vacuity. If we approach the theory as a theory of intentional content, intended to explain the nature of reference, the theory is lacking in an extremely important respect: Millikan explains how it could be one of the biological functions of a mental or natural language term to refer, without telling us precisely what in the natural order constitutes the reference relation.. (shrink)

The anti-reductionist character of the recent philosophy of biology and the dynamic development of the science of emergent properties prove that the time is ripe to reintroduce the thought of Aristotle, the first advocate of a “top-down” approach in life-sciences, back into the science/philosophy debate. His philosophy of nature provides profound insights particularly in the context of the contemporary science of evolution, which is still struggling with the questions of form species), teleology, and the role of (...) chance in evolutionary processes. However although Aristotle is referenced in the evolutionary debate, a thorough analysis of his theory of hylomorphism and the classical principle of causality which he proposes is still needed in this exchange. Such is the main concern of the first part of the present article which shows Aristotle’s metaphysics of substance as an open system, ready to incorporate new hypothesis of modern and contemporary science. The second part begins with the historical exploration of the trajectory from Darwin to Darwinism regarded as a metaphysical position. This exploration leads to an inquiry into the central topics of the present debate in the philosophy of evolutionary biology. It shows that Aristotle’s understanding of species teleology and chance – in the context of his fourfold notion of causality – has a considerable explanatory power which may enhance our understanding of the nature of evolutionary processes. This fact may inspire, in turn, a retrieval of the classical theology of divine action, based on Aristotelian metaphysics, in the science/theology dialogue. The aim of the present article is to prepare a philosophical ground for such project. (shrink)

This chapter explores the idea of one variable making a causal contribution to another variable, and how this idea applies to economics. It also explores the related concept of what-if questions in economics. In particular, it contrasts the modular theory of causal contributions and what-if questions (advocated by interventionists) with the ceteris paribus theory (advocated by Jim Heckman and others). It notes a problem with the modular theory raised by Nancy Cartwright. And it notes how, according to the (...) ceteris paribus theory, causal contributions and what-if questions are often indeterminate in economics. (shrink)

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

In the philosophy of mind, neuroscience, and psychology, the causal relationship between phenomenal consciousness, mentation, and brain states has always been a matter of debate. On the one hand, material monism posits consciousness and mind as pure brain epiphenomena. One of its most stringent lines of reasoning relies on a ‘loss-of-function lesion premise,’ according to which, since brain lesions and neurochemical modifications lead to cognitive impairment and/or altered states of consciousness, there is no reason to doubt the mind-brain (...) identity. On the other hand, dualism or idealism (in one form or another) regard consciousness and mind as something other than the sole product of cerebral activity pointing at the ineffable, undefinable, and seemingly unphysical nature of our subjective qualitative experiences and its related mental dimension. Here, several neuroscientific findings are reviewed that question the idea that posits phenomenal experience as an emergent property of brain activity, and argue that the premise of material monism is based on a logical correlation-causation fallacy. While these (mostly ignored) findings, if considered separately from each other, could, in principle, be recast into a physicalist paradigm, once viewed from an integral perspective, they substantiate equally well an ontology that posits mind and consciousness as a primal phenomenon. (shrink)

According to mainstream philosophical views causal explanation in biology and neuroscience is mechanistic. As the term ‘mechanism’ gets regular use in these fields it is unsurprising that philosophers consider it important to scientific explanation. What is surprising is that they consider it the only causal term of importance. This paper provides an analysis of a new causal concept—it examines the cascade concept in science and the causal structure it refers to. I argue that this concept (...) is importantly different from the notion of mechanism and that this difference matters for our understanding of causation and explanation in science. (shrink)

Advances in the empirical sectors of biology are beginning to reveal evolvability as a major evolutionary process. Yet evolvability’s theoretical role is still intensely debated. Since its inception nearly thirty years ago, the evolvability research front has put a strong emphasis on the non-genetic mechanisms that influence the short-term evolvability of individuals within populations by causing phenotypic heterogeneity, such as developmental trait plasticity, phenotypic plasticity, modularity, the G-P map, robustness, and/or epigenetic variation. However, genetic evolvability mechanisms such as mutation (...) or recombination have a deeper history in evolutionary thought that is often overlooked by those in the evolvability research front, with recent evidence suggesting that species switch to genetic evolvability mechanisms when short-term evolvability strategies fail to relieve selective pressures. For this reason, a causal distinction must be made between genetic evolvability and the more recently emphasized non-genetic (or evo-devo) evolvability to allow for its maturation as a central explanatory concept. I conclude by arguing that the anachronisms of the scientific process are the main culprit behind recent divisions in biology and likely beyond. To streamline theoretical progress, we need to build a new science with new underlying philosophies like restricted pluralism. (shrink)

Causation has always been a philosophically controversial subject matter. While David Hume’s empiricist account of causation has been the dominant influence in analytic philosophy and science during modern times, a minority view has instead connected causation essentially to agency and manipulation. A related approach has for the first time gained widespread popularity in recent years, due to new powerful theories of causal inference in science that are based in a technical notion of intervention, and James Woodward’s closely connected (...) interventionist theory of causation in philosophy. This monograph assesses five manipulationist or interventionist theories of causation, viewed as theories that purport to tell us what causation is by providing us with the meaning of causal claims. It is shown that they cannot do this, as the conditions on causation that they impose are too weak, mainly due to ineliminable circularities in their definitions of causal terms. It is then argued that a subset of Woodward’s theory can nevertheless contribute crucially to an explanation of the unique role that manipulation has in our acquisition of causal knowledge. This explanation differs from the common regularist explanation of the epistemic utility of manipulation and experiment, and it is taken to confirm several important manipulationist intuitions. However, the success of the explanation depends on (this subset of) interventionism not itself being understood as a theory of causation, but as a theory of intervention. (shrink)

In this paper, I defend the agent/patient distinction against critics who argue that causal interactions are symmetrical. Specifically, I argue that there is a widespread type of causal interaction between distinct entities, resulting in a type of ontological asymmetry that provides principled grounds for distinguishing agents from patients. The type of interaction where the asymmetry is found is when one of the entities undergoes a change in kind, structure, powers, or intrinsic properties as a result of the interaction (...) while the other does not. Interactions of this type are widespread in molecular biology and chemistry. I focus specifically on (i) the actions of enzymes on substrates and (ii) water molecules breaking the bonds of polarized molecules. Finally, I respond to objections by laying out and to a limited extent defending three commitments of my account: emergent entities and powers, realism about chemical kinds or structures, and the assumption of the agent/patient distinction in functional attributions in biology. (shrink)

In its classical form, epiphenomenalism is the view that conscious mental events have no physical effects: while physical events cause mental events, the opposite is never true. Unlike classical epiphenomenalism, contemporary forms do not hold that conscious men­ tal states always lack causal efficacy, only that they are epiphenomenal relative to certain kinds of action, ones we pre-theoretically would have thought consciousness to causally contribute to. Two of these contemporary, empirically based challenges to the efficacy of the mental are (...) the focus of this chapter. The first, originating in research by Libet, has been interpreted as showing that the neural events initiating voluntary actions precede our conscious willing of them, meaning the conscious will cannot be what causes them. The second challenge, originating in studies by Milner and Goodale, consist of instances in which the content of visual consciousness and motor action dissociate, casting doubt on the intuitive view that visual consciousness guides visually based motor action. (shrink)

In this chapter we examine the relationship between biological information, the key biological concept of specificity, and recent philosophical work on causation. We begin by showing how talk of information in the molecular biosciences grew out of efforts to understand the sources of biological specificity. We then introduce the idea of ‘causal specificity’ from recent work on causation in philosophy, and our own, information theoretic measure of causal specificity. Biological specificity, we argue, is simple the causal (...) specificity of certain biological processes. This, we suggest, means that causal relationships in biology are ‘informational’ relationships simply when they are highly specific relationships. Biological information can be identified with the storage, transmission and exercise of biological specificity. It has been argued that causal relationships should not be regarded as informational relationship unless they are ‘arbitrary’. We argue that, whilst arbitrariness is an important feature of many causal relationships in living systems, it should not be used in this way to delimit biological information. Finally, we argue that biological specificity, and hence biological information, is not confined to nucleic acids but distributed among a wide range of entities and processes. (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)

In biomedical measurement, biomarkers are used to achieve reliable prediction of, and useful causal information about patient outcomes while minimizing complexity of measurement, resources, and invasiveness. A biomarker is an assayable metric that discloses the status of a biological process of interest, be it normative, pathophysiological, or in response to intervention. The greatest utility from biomarkers comes from their ability to help clinicians (and researchers) make and evaluate clinical decisions. In this paper we discuss a specific methodological use of (...) clinical biomarkers in pharmacological measurement: Some biomarkers, called ‘surrogate markers’, are used to substitute for a clinically meaningful endpoint corresponding to events and their penultimate risk factors. We confront the reliability of clinical biomarkers that are used to gather information about clinically meaningful endpoints. Our aim is to present a systematic methodology for assessing the reliability of multiple surrogate markers (and biomarkers in general). To do this we draw upon the robustness analysis literature in the philosophy of science and the empirical use of clinical biomarkers. After introducing robustness analysis we present two problems with biomarkers in relation to reliability. Next, we propose an intervention-based robustness methodology for organizing the reliability of biomarkers in general. We propose three relevant conditions for a robust methodology for biomarkers: (R1) Intervention-based demonstration of partial independence of modes: In biomarkers partial independence can be demonstrated through exogenous interventions that modify a process some number of “steps” removed from each of the markers. (R2) Comparison of diverging and converging results across biomarkers: By systematically comparing partially-independent biomarkers we can track under what conditions markers fail to converge in results, and under which conditions they successfully converge. (R3) Information within the context of theory: Through a systematic cross-comparison of the markers we can make causal conclusions as well as eliminate competing theories. We apply our robust methodology to currently developing Alzheimer’s research to show its usefulness for making causal conclusions. (shrink)

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

This paper examines the adequacy of causal graph theory as a tool for modeling biological phenomena and formalizing biological explanations. I point out that the causal graph approach reaches it limits when it comes to modeling biological phenomena that involve complex spatial and structural relations. Using a case study from molecular biology, DNA-binding and -recognition of proteins, I argue that causal graph models fail to adequately represent and explain causal phenomena in this field. The inadequacy (...) of these models is due to their failure to include relevant spatial and structural information in a way that does not render the model non-explanatory, unmanageable, or inconsistent with basic assumptions of causal graph theory. (shrink)

The issue of downward causation (and mental causation in particular), and the exclusion problem is discussed by taking into account some recent advances in the philosophy of science. The problem is viewed from the perspective of the new interventionist theory of causation developed by Woodward. It is argued that from this viewpoint, a higher-level (e.g., mental) state can sometimes truly be causally relevant, and moreover, that the underlying physical state which realizes it may fail to be such.

Kim’s causal exclusion argument purports to demonstrate that the non-reductive physicalist must treat mental properties (and macro-level properties in general) as causally inert. A number of authors have attempted to resist Kim’s conclusion by utilizing the conceptual resources of Woodward’s interventionist conception of causation. The viability of these responses has been challenged by Gebharter, who argues that the causal exclusion argument is vindicated by the theory of causal Bayesian networks (CBNs). Since the interventionist conception of causation relies (...) crucially on CBNs for its foundations, Gebharter’s argument appears to cast significant doubt on interventionism’s anti-reductionist credentials. In the present article, we both (1) demonstrate that Gebharter’s CBN-theoretic formulation of the exclusion argument relies on some unmotivated and philosophically significant assumptions (especially regarding the relationship between CBNs and the metaphysics of causal relevance), and (2) use Bayesian networks to develop a general theory of causal inference for multi-level systems that can serve as the foundation for an anti-reductionist interventionist account of causation.1. (shrink)

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

The relationship between psychological states and the brain remains an unresolved issue in philosophy of psychology. One appealing solution that has been influential both in science and in philosophy is Dennett’s concept of the intentional stance, according to which beliefs and desires are real and objective phenomena, but not necessarily states of the brain. A fundamental shortcoming of this approach is that it does not seem to leave any causal role for beliefs and desires in influencing behavior. (...) In this paper, I show that intentional states ascribed from the intentional stance should be seen as real causes, develop this to an independently plausible ontological position, and present a response to the latest interventionist causal exclusion worries. (shrink)

The explanatory role of natural selection is one of the long-term debates in evolutionary biology. Nevertheless, the consensus has been slippery because conceptual confusions and the absence of a unified, formal causal model that integrates different explanatory scopes of natural selection. In this study we attempt to examine two questions: (i) What can the theory of natural selection explain? and (ii) Is there a causal or explanatory model that integrates all natural selection explananda? For the first question, (...) we argue that five explananda have been assigned to the theory of natural selection and that four of them may be actually considered explananda of natural selection. For the second question, we claim that a probabilistic conception of causality and the statistical relevance concept of explanation are both good models for understanding the explanatory role of natural selection. We review the biological and philosophical disputes about the explanatory role of natural selection and formalize some explananda in probabilistic terms using classical results from population genetics. Most of these explananda have been discussed in philosophical terms but some of them have been mixed up and confused. We analyze and set the limits of these problems. (shrink)

The methodological nonreductionism of contemporary biology opens an interesting discussion on the level of ontology and the philosophy of nature. The theory of emergence (EM), and downward causation (DC) in particular, bring a new set of arguments challenging not only methodological, but also ontological and causal reductionism. This argumentation provides a crucial philosophical foundation for the science/theology dialogue. However, a closer examination shows that proponents of EM do not present a unified and consistent definition of DC. Moreover, (...) they find it difficult to prove that higher-order properties can be causally significant without violating the causal laws that operate at lower physical levels. They also face the problem of circularity and incoherence in their explanation. In our article we show that these problems can be overcome only if DC is understood in terms of formal rather than physical (efficient) causality. This breakdown of causal monism in science opens a way to the retrieval of the fourfold Aristotelian notion of causality. (shrink)

The problem of mental causation is discussed by taking into account some recent developments in the philosophy of science. The problem is viewed from the perspective of the new interventionist theory of causation developed by Woodward. The import of the idea that causal claims involve contrastive classes in mental causation is also discussed. It is argued that mental causation is much less a problem than it has appeared to be.

The interventionist account of causal explanation, in the version presented by Jim Woodward, has been recently claimed capable of buttressing the widely felt—though poorly understood—hunch that high-level, relatively abstract explanations, of the sort provided by sciences like biology, psychology and economics, are in some cases explanatorily optimal. It is the aim of this paper to show that this is mistaken. Due to a lack of effective constraints on the causal variables at the heart of the interventionist (...) class='Hi'>causal-explanatory scheme, as presently formulated it is either unable to prefer high-level explanations to low, or systematically overshoots, recommending explanations at so high of a level as to be virtually vacuous. (shrink)

Childhood looms large in our understanding of human life as it is a phase through which all adults have passed. Childhood is foundational to the development of selfhood, the formation of interests, values and skills and to the lifespan as a whole. Understanding what it is like to be a child, and what differences childhood makes, are essential for any broader understanding of the human condition. The Routledge Handbook of the Philosophy of Childhood and Children is an outstanding reference (...) source to the key topics, problems and debates in this exciting subject and is the first collection of its kind. Comprising over thirty chapters by a team of international contributors the Handbook is divided into five parts: ¿ Being a child ¿ Childhood and moral status ¿ Parents and children ¿ Children in society ¿ Children and the state. Questions covered include: What is a child? Is childhood a uniquely valuable state, and if so why? Can we generalize about the goods of childhood? What rights do children have, and are they different from adults¿ rights? What gives people a right to parent? What role, if any, ought biology to play in determining who has the right to parent a particular child? What kind of rights can parents legitimately exercise over their children? What roles do relationships with siblings and friends play in the shaping of childhoods? How should we think about sexuality and disabilility in childhood, and about racialised children? How should society manage the education of children, and what values should inform such practices? What is a good school? How are children¿s lives affected by being taken into social care? The Routledge Handbook of the Philosophy of Childhood and Children is essential reading for students and researchers in philosophy of childhood, political philosophy and ethics as well as those in related disciplines such as education, psychology, sociology, social policy, law, social work, youth work, neuroscience and anthropology. (shrink)

The Australian philosopher Philip Gerrans ambitiously tries to provide a general theory about the formation of delusions that should enclose neuronal, cognitive and phenomenological levels of description. His theory is defined as narrative and it is grounded on the so called “default thoughts”, that consist in simulations, autobiographical narrative fragments produced by the Default Mode Network (DMN). The DMN is a powerful simulation system that evolved to allow humans to simulate and imagine experiences in the absence of an eliciting stimulus. (...) Such imaginative/simulative process is precariously disciplined by the Self’s demands of narrative coherence. The Author’s aim is to waive the notion of belief and the causal role played by the impairments of fixation-beliefs system in the onset of delusions, as predicted by the principle doxastic theories. (shrink)

Much contemporary debate on the nature of mechanisms centers on the issue of modulating negative causes. One type of negative causability, which I refer to as “causation by absence,” appears difficult to incorporate into modern accounts of mechanistic explanation. This paper argues that a recent attempt to resolve this problem, proposed by Benjamin Barros, requires improvement as it overlooks the fact that not all absences qualify as sources of mechanism failure. I suggest that there are a number of additional types (...) of effects caused by absences that need to be incorporated to account for the diversity of causal connections in the biological sciences. Furthermore, it is argued that recognizing natural variability in mechanisms, such as attenuation, leads to some interesting line-drawing issues for contemporary philosophy of mechanisms. (shrink)

Disputes about the causal structure of natural selection have implications for teleosemantics. Etiological, mainstream teleosemantics is based on a causalist view of natural selection. The core of its solution to Brentano’s Problem lies in the solution to Kant’s Puzzle provided by the Modern Synthesis concerning populational causation. In this paper, I suggest that if we adopt an alternative, statisticalist view on natural selection, the door is open for two reflections. First, it allows for setting different challenges to etiological teleosemantics (...) that arise if a statisticalist reading of natural selection is right. Second, by providing a different solution to Kant’s Puzzle based on individual causes of evolution, statisticalism promotes a different answer to Brentano’s Problem, what I label as Agential Teleosemantics. (shrink)

Thomas Reid thinks of natural philosophy as a purely nomothetic enterprise but he maintains that it is proper for natural philosophers to employ causal terminology in formulating their explanatory claims. In this paper, I analyze this puzzle in light of Reid's distinction between efficient and physical causation – a distinction he grounds in his strict understanding of active powers. I consider several possible reasons that Reid may have for maintaining that natural philosophers ought to employ causal terminology (...) and suggest that the underlying rationale for his views is his understanding of the aims of explanation and their connection to the interests of human agents. The ultimate aim of knowing the causes of phenomena is to mollify the natural intellectual curiosity of human inquirers and provide guidance that insures successful action. The discovery of laws governing phenomena fulfills this aim and, as such, it is appropriate for natural philosophers to employ causal terminology. (shrink)

I show that the recent account of levels in neuroscience proposed by Craver and Bechtel is unsatisfactory since it fails to provide a plausible criterion for being at the same level and is incompatible with Craver and Bechtel’s account of downward causation. Furthermore, I argue that no distinct notion of levels is needed for analyzing explanations and causal issues in neuroscience: it is better to rely on more well-defined notions such as composition and scale. One outcome of this is (...) that apparent cases of downward causation can be analyzed away. (shrink)

The biological sciences have always proven a fertile ground for philosophical analysis, one from which has grown a rich tradition stemming from Aristotle and flowering with Darwin. And although contemporary philosophy is increasingly becoming conceptually entwined with the study of the empirical sciences with the data of the latter now being regularly utilised in the establishment and defence of the frameworks of the former, a practice especially prominent in the philosophy of physics, the development of that tradition hasn’t (...) received the wider attention it so thoroughly deserves. This review will briefly introduce some recent significant topics of debate within the philosophy of biology, focusing on those whose metaphysical themes (in everything from composition to causation) are likely to be of wide-reaching, cross-disciplinary interest. (shrink)

The problem causation poses is: how can we ever know more than a Humean regularity. The problem consciousness poses is: how can subjective phenomenal experience arise from something lacking experience. A recent turn in the consciousness debates suggest that the hard problem of consciousness is nothing more than the Humean problem of explaining any causal nexus in an intelligible way. This involution of the problems invites comparison with the theories of Alfred North Whitehead, who also saw them related in (...) this way. According to Whitehead, a tempting but false phenomenology of consciousness obscures temporality and leads to the causation problem, which then makes consciousness itself seem causally inexplicable. Bringing the processual nature of consciousness back into view discloses causation at work in the moment-to-moment emergence of consciousness, and it reveals that causation operates in a logically fuzzy domain where the skeptical critique of causality finds no foothold. (shrink)

Many philosophers believe that there is a causal condition on perception, and that this condition is a conceptual truth about perception. A highly influential argument for this claim is based on intuitive responses to Gricean-style thought experiments. Do the folk share the intuitions of philosophers? Roberts et al. (2016) presented participants with two kinds of cases: Blocker cases (similar to Grice’s case involving a mirror and a pillar) and Non-Blocker cases (similar to Grice’s case involving a clock and brain (...) stimulation). They found that a substantial minority agreed that seeing occurs in the Non-Blocker cases, and that in the Blocker cases significantly less agreed that seeing occurs. They thus hypothesized that folk intuitions better align with a no blocker condition than with a causal condition. This paper continues this line of enquiry with two new experiments. The paper investigates the generality and robustness of Roberts et al.’s findings by expanding the sense modalities tested from only vision to audition and olfaction as well. The paper also uses Gricean-style thought experiments as a case study for investigating the “reflection defense” against the negative project in experimental philosophy. Our results replicate and extend Roberts et al.’s study and support their hypothesis that folk intuitions better align with a no blocker condition. They also provide an empirical reason to doubt the reflection defense. (shrink)

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

Biology seems to present local and transitory regularities rather than immutable laws. To account for these historically constituted regularities and to distinguish them from mathematical invariants, Montévil and Mossio (Journal of Theoretical Biology 372:179–191, 2015) have proposed to speak of constraints. In this article we analyse the causal power of these constraints in the evolution of biodiversity, i.e., their positivity, but also the modality of their action on the directions taken by evolution. We argue that to fully (...) account for the causal power of these constraints on evolution, they must be thought of in terms of normativity. In this way, we want to highlight two characteristics of the evolutionary constraints. The first, already emphasised as reported by Gould (The structure of evolutionary theory, Harvard University Press, 2002), is that these constraints are both produced by and producing biological evolution and that this circular causation creates true novelties. The second is that this specific causality, which generates unpredictability in evolution, stems not only from the historicity of biological constraints, but also from their internalisation through the practices of living beings. (shrink)

When a group of processes achieves such closure that a set of states of affairs recurs continually, then the effect of that coherence on the world differs from what would occur in the absence of that closure. Such altered effectiveness is an attribute of the system as a whole, and would have consequences. This indicates that the network of processes, as a unit, has ontological significance. Whenever a network of processes generates continual return to a limited set of states of (...) affairs, the system may function as a “whole”— with respect to appropriate interaction partners. The balance achieved by the processes provides the form of definiteness of a unified agent. The causal powers of such coherent aggregates are indeed just the powers of the “constituents acting in concert”. However, the components act in concert in the specific way they do only because of their inclusion in the closed set of interactions that defines the coherence. This renders the causal powers of the coherence defined by that closure non-redundant, and hence the coherence, as a unit, is ontologically significant. The form of definiteness that provides internal coherence also grounds external efficacy of the societal aggregation. The closure is a structural feature of the coherence — possibly, but not necessarily, apparent in spatial structuring. This approach can provide a unified account that includes quantum microphysics, systems biology, and the philosophy of organism ─ without reducing any of these to another. (shrink)

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

In the last couple of years, a few seemingly independent debates on scientific explanation have emerged, with several key questions that take different forms in different areas. For example, the questions what makes an explanation distinctly mathematical and are there any non-causal explanations in sciences (i.e., explanations that don’t cite causes in the explanans) sometimes take a form of the question of what makes mathematical models explanatory, especially whether highly idealized models in science can be explanatory and in virtue (...) of what they are explanatory. These questions raise further issues about counterfactuals, modality, and explanatory asymmetries: i.e., do mathematical and non-causal explanations support counterfactuals, and how ought we to understand explanatory asymmetries in non-causal explanations? Even though these are very common issues in the philosophy of physics and mathematics, they can be found in different guises in the philosophy of biology where there is the statistical interpretation of the Modern Synthesis theory of evolution, according to which the post-Darwinian theory of natural selection explains evolutionary change by citing statistical properties of populations and not the causes of changes. These questions also arise in philosophy of ecology or neuroscience in regard to the nature of topological explanations. The question here is can the mathematical (or more precisely topological) properties in network models in biology, ecology, neuroscience, and computer science be explanatory of physical phenomena, or are they just different ways to represent causal structures. The aim of this special issue is to unify all these debates around several overlapping questions. These questions are: are there genuinely or distinctively mathematical and non-causal explanations?; are all distinctively mathematical explanations also non-causal; in virtue of what they are explanatory; does the instantiation, implementation, or in general, applicability of mathematical structures to a variety of phenomena and systems play any explanatory role? This special issue provides a platform for unifying the debates around several key issues and thus opens up avenues for better understanding of mathematical and non-causal explanations in general, but also, it will enable even better understanding of key issues within each of the debates. (shrink)

1. Introduction: a look back at the reasons vs. causes debate. 2. The interventionist account of causation. 3. Four objections to interventionism. 4. The counterfactual analysis of event causation. 5. The role of free agency. 6. Causality in the human sciences. -- The reasons vs. causes debate reached its peak about 40 years ago. Hempel and Dray had debated the nature of historical explanation and the broader issue of whether explanations that cite an agent’s reasons are causal or not. (...) Melden, Peters, Winch, Kenny and Anscombe had contributed their anticausal conceptions. The neo-Wittgensteinians seemed to be winning the day when in 1963 Donald Davidson published his seminal paper “Actions, Reasons, and Causes”. Davidson’s paper devastated the Wittgensteinian camp. It contained, among other things, a powerful attack on the logical connection argument. Davidson argued that the existence of a logical or conceptual connection between descriptions can never eliminate a causal relation, which holds between events simpliciter, not between events under certain descriptions. Davidson maintained that in a way, reasons can be causes. When somebody acts for a certain reason, his intentional attitudes, or rather changes in his attitudes, cause his bodily movements. Davidson also argued that rationalization is a species of causal explanation. For the definition of action, he argued that intentional actions are bodily movements caused in the right way by beliefs and desires that rationalize them. Davidson’s paper paved the way for causal theories of action, which superseded neo-Wittgensteinian analyses in the following decades. The causal theory was rapidly adopted by Alvin Goldman, David Armstrong, Paul Churchland, Myles Brand and many others, entering the mainstream and dominating the philosophy of action to this very day. In 1971 Georg Henrik von Wright published his book "Explanation and Understanding". The second chapter did not deal with agency, but with causation. It developed a new account of causation, the interventionist or experimentalist account. Focusing on causation, von Wright remedied a major shortcoming of the reasons vs. causes debate. The concept of causality, and the nature of the causal relation, received little attention in this debate, a fact that holds true for both camps. Mostly it was simply taken for granted that, as Hempel had declared, “causal explanation is a special type of deductive-nomological explanation”. One camp then aligned intentional explanations with D-N explanations, while the other camp insisted on their disparity. So strictly speaking, the label “reasons/causes debate” was a misnomer. The controversy dealt primarily with the question as to whether intentional explanations can take the form of D-N explanations, while the notion of causation, and the metaphysics of the causal relation, were left obscured. With von Wright’s new approach, the situation changed. Von Wright was primarily concerned with causation, but his approach contained an implicit attack on the causal theory of action as well. His core idea was that the notion of causality is intimately linked with, or even derived from, the notion of intentionally making something happen. Other philosophers, even Hume, had considered such a connection before, but often just to reject this view, regarding it as a kind of myth belonging to the infancy of the human mind. Von Wright took the idea seriously. He submitted the analysis that p is the cause of q if and only if by doing p we could bring about q. The causal theory of action was also concerned with the relation between causation and agency, to which its name bears witness. The causal theory of action holds that actions are bodily movements with a certain causal history. This is why von Wright’s account constituted a momentous challenge to the causal theory: it reversed the direction of conceptual dependency between both notions. Davidson and his followers tried to define what an intentional action is by using the notion of causation. The causal condition which the causal theory sets is part of the definition of “doing something intentionally”. Von Wright claimed that the conceptual dependency is the other way round. He used the notions of doing, and bringing about, to explain what causal relations are. So, instead of a causal theory of action, he advocated an agency theory of causation, as it may be dubbed. It is remarkable how seldom this clash of opinions about conceptual primacy is reflected in the literature. There are few exceptions: Fred Stoutland noticed the conflict, and he published a number of papers in which he compared Davidson’s and von Wright’s views. Von Wright’s book "Explanation and Understanding" was widely read and discussed in the seventies, especially in Europe. But it strikes me that especially in North America, where the causal theory of action became the orthodoxy of the day, von Wright’s challenge went largely unnoticed. Even Davidson did not seem to take it seriously. He nowhere takes notice of the interventionist theory of causation, while he does discuss von Wright’s earlier book "Norm and Action". As is well-known, Davidson favoured an alternative account of causation, based on “the principle of the nomological character of causality”, as he somewhat clumsily called it, or, later and less clumsily, “the cause-law thesis”. Davidson’s firm adherence to a nomological theory of causality may explain why he did not take much interest in alternative accounts. [...] -/- . 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Life as self-organization is philosophically understood by L. Polo in terms of co-causality between matter, formal configuration and intrinsic efficiency. This characterization provides a dynamic account of life and soul, capable to explain both its identity and its continuous renovation. In this article I especially highlight in this author the metaphysical notions of finality, unity and cosmos, which may be helpful to understand the sense of biological systems in the universe.