Mechanistic accounts of explanation have recently found popularity within philosophy of science. Presently, we introduce the idea of an extended mechanistic explanation, which makes explicit room for the role of environment in explanation. After delineating Craver and Bechtel’s account, we argue this suggestion is not sufficiently robust when we take seriously the mechanistic environment and modeling practices involved in studying contemporary complex biological systems. Our goal is to extend the already profitable mechanistic picture by pointing out the importance of the (...) mechanistic environment. It is our belief that extended mechanistic explanations, or mechanisms that take into consideration the temporal sequencing of the interplay between the mechanism and the environment, allow for mechanistic explanations regarding a broader group of scientific phenomena. (shrink)

Jaegwon Kim’s influential exclusion argument attempts to demonstrate the inconsistency of nonreductive materialism in the philosophy of mind. Kim’s argument begins by showing that the three main theses of nonreductive materialism, plus two additional considerations, lead to a specific and familiar picture of mental causation. The exclusion argument can succeed only if, as Kim claims, this picture is not one of genuine causal overdetermination. Accordingly, one can resist Kim’s conclusion by denying this claim, maintaining instead that the effects of the (...) mental are always causally overdetermined. I call this strategy the ‘ overdetermination challenge’. One of the main aims of this paper is to show that the overdetermination challenge is the most appropriate response to Kim’s exclusion argument, at least in its latest form. I argue that Kim fails to adequately respond to the overdetermination challenge, thus failing to prevent his opponents from reasonably maintaining that the effects of the mental are always causally overdetermined. Interestingly, this discussion reveals a curious dialectical feature of Kim’s latest response to the overdetermination challenge: if it succeeds, then a new, simpler and more compact version of the exclusion argument is available. While I argue against the consequent of this conditional, thereby also rejecting the antecedent, this dialectical feature should be of interest to philosophers on either side of this debate. (shrink)

Many philosophers worry that the classical computational theory of mind (CTM) engenders epiphenomenalism. Building on Block’s (1990) discussion, I formulate a particularly troubling version of this worry. I then present a novel solution to CTM’s epiphenomenalist conundrum. I develop my solution within an interventionist theory of causal relevance. My solution departs substantially from orthodox versions of CTM. In particular, I reject the widespread picture of digital computation as formal syntactic manipulation.1.

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)

Jaegwon Kim’s views on mental causation and the exclusion argument are evaluated systematically. Particular attention is paid to different theories of causation. It is argued that the exclusion argument and its premises do not cohere well with any systematic view of causation.

In this paper, we address the question whether a mechanistic approach can account for evolutionary causes. The last decade has seen a major attempt to account for natural selection as a mechanism. Nevertheless, we stress the relevance of broadening the debate by including the other evolutionary causes inside the mechanistic approach, in order to be a legitimate conceptual framework on the same footing as other approaches to evolutionary theory. We analyse the current debate on natural selection as a mechanism, and (...) extend it to the rest of the evolutionary causes. We focus on three approaches that we call the stochastic view, the functional view, and the minimalist view. We argue that all of them are unable to account for evolutionary causes as mechanisms. It is concluded that the current mechanistic proposals cannot be accepted as a common framework for evolutionary causes. Finally, we outline some guidelines and requirements that any mechanistic proposal should meet in order to be applied to evolutionary theory. (shrink)

There have been two different schools of thought on the evolution of dominance. On the one hand, followers of Wright [Wright S. 1929. Am. Nat. 63: 274–279, Evolution: Selected Papers by Sewall Wright, University of Chicago Press, Chicago; 1934. Am. Nat. 68: 25–53, Evolution: Selected Papers by Sewall Wright, University of Chicago Press, Chicago; Haldane J.B.S. 1930. Am. Nat. 64: 87–90; 1939. J. Genet. 37: 365–374; Kacser H. and Burns J.A. 1981. Genetics 97: 639–666] have defended the view that dominance (...) is a product of non-linearities in gene expression. On the other hand, followers of Fisher [Fisher R.A. 1928a. Am. Nat. 62: 15–126; 1928b. Am. Nat. 62: 571–574; Bürger R. 1983a. Math. Biosci. 67: 125–143; 1983b. J. Math. Biol. 16: 269–280; Wagner G. and Burger R. 1985. J. Theor. Biol. 113: 475–500; Mayo O. and Reinhard B. 1997. Biol. Rev. 72: 97–110] have argued that dominance evolved via selection on modifier genes. Some have called these “physiological” versus “selectionist,” or more recently [Falk R. 2001. Biol. Philos. 16: 285–323], “functional,” versus “structural” explanations of dominance. This paper argues, however, that one need not treat these explanations as exclusive. While one can disagree about the most likely evolutionary explanation of dominance, as Wright and Fisher did, offering a “physiological” or developmental explanation of dominance does not render dominance “epiphenomenal,” nor show that evolutionary considerations are irrelevant to the maintenance of dominance, as some [Kacser H. and Burns J.A. 1981. Genetics 97: 639–666] have argued. Recent work [Gilchrist M.A. and Nijhout H.F. 2001. Genetics 159: 423–432] illustrates how biological explanation is a multi-level task, requiring both a “top-down” approach to understanding how a pattern of inheritance or trait might be maintained in populations, as well as “bottom-up” modeling of the dynamics of gene expression. (shrink)

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

Two strains of interventionist responses to the causal exclusion argument are reviewed and critically assessed. On the one hand, one can argue that manipulating supervenient mental states is an effective strategy for manipulating the subvenient physical states, and hence should count as genuine causes to the subvenient physical states. But unless the supervenient and subvenient states manifest some difference in their manipulability conditions, there is no reason to treat them as distinct, which in turn goes against the basic assumption of (...) nonreductive physicalism. On the other hand, one can preserve the distinction between the two by introducing asymmetric manipulability conditions that the supervenience thesis entails. But this response can be used to argue that mental causes never have physical effects. However, this argumentation can also be used to show that mental causes can have mental effects. (shrink)

This article reviews the causal exclusion argument and confronts it with some recently proposed refutations based on the interventionist account of causation. I first show that there are several technical and interpretative difficulties in applying the interventionist account to the exclusion issue. Different ways of accommodating the two to one another are considered and all are shown to leave the issue without a fully satisfactory resolution. Lastly, I argue that, on the most consistent construal, the interventionist approach can provide grounds (...) for thinking that higher-level causal notions are as legitimate as lower-level causal notions, but it does not provide grounds for postulating inter-level causal interactions. (shrink)

A recent debate over the causal foundations of evolutionary theory pits those who believe that natural selection causally explains long-term, adaptive population change against those who do not. In this paper, I argue that this debate – far from being an invention of several articles in 2002 – dates from our very first engagements with evolution as a quantified, statistical science. Further, when we analyze that history, we see that a pivotal figure in the early use of statistical methodology in (...) evolutionary theory, W.F.R. Weldon, changes his mind about precisely the central claim at issue. I close by drawing some morals which I think the case can offer for the contemporary debate going forward. (shrink)

One hotly debated philosophical question in the analysis of evolutionary theory concerns whether or not evolution and the various factors which constitute it may profitably be considered as analogous to “forces” in the traditional, Newtonian sense. Several compelling arguments assert that the force picture is incoherent, due to the peculiar nature of genetic drift. I consider two of those arguments here – that drift lacks a predictable direction, and that drift is constitutive of evolutionary systems – and show that they (...) both fail to demonstrate that a view of genetic drift as a force is untenable. I go on to diagnose the reasons for the stubborn persistence of this problem, considering two open philosophical issues and offering some preliminary arguments in support of the force metaphor. (shrink)

This article considers interventionist arguments for downward causation and non-fundamental level causal explanation from the point of view of inferring causation from experiments. Several authors have utilised the interventionist theory of causal explanation to argue that the causal exclusion argument is moot and that higher-level as well as downward causation is real. I show that this argument can be made when levels are understood as levels of grain, leaving us with a choice between causal explanations pitched at different levels. Causal (...) proportionality has been suggested as a principle for choosing the correct level of description for causal explanations, but this suggestion has serious problems. I offer an alternative principle, based on the idea that explanations should track actual difference-makers. I then consider claims about systems causally influencing their own parts. Such claims risk conceptual confusion for the same reason as the exclusion argument, by conflating causal and constitutive dependencies. The distinction between causation and constitution is used to give criteria for the correct use of the idea of downward causation. (shrink)

Over the past decade philosophers of biology have discussed whether evolutionary theory is a causal theory or a phenomenological study of evolution based solely on the statistical features of a population. This article reviews this controversy from three aspects, respectively concerning the assumptions, applications, and explanations of evolutionary theory, with a view to arriving at a definite conclusion in each contention. In so doing I also argue that an implicit methodological assumption shared by both sides of the debate, namely the (...) overconfidence in conceptual analysis as a tool to understand the scientific theory, is the real culprit that has both generated the problem and precluded its solution for such a long time. (shrink)

Recent discussions in the philosophy of biology have brought into question some fundamental assumptions regarding evolutionary processes, natural selection in particular. Some authors argue that natural selection is nothing but a population-level, statistical consequence of lower-level events (Matthen and Ariew [2002]; Walsh et al. [2002]). On this view, natural selection itself does not involve forces. Other authors reject this purely statistical, population-level account for an individual-level, causal account of natural selection (Bouchard and Rosenberg [2004]). I argue that each of these (...) positions is right in one way, but wrong in another; natural selection indeed takes place at the level of populations, but it is a causal process nonetheless. (shrink)

Causalism is the thesis that natural selection can cause evolution. A standard argument for causalism involves showing that a hypothetical intervention on some population-level property that is identified with natural selection will result in evolution. In a pair of articles, one of which recently appeared in the pages of this journal, Jun Otsuka has put forward a quite different argument for causalism. Otsuka attempts to show that natural selection can cause evolution by considering a hypothetical intervention on an individual-level property. (...) Specifically, Otsuka identifies natural selection with the causal relationship between a trait and fitness, claims an intervention on the strength of this relationship can cause evolution, then concludes that natural selection can cause evolution. Below I describe why Otsuka’s argument for causalism is unconvincing. Central to my criticism is that Otsuka’s argument works only if one adopts an indefensible account of natural selection, according to which natural selection can occur in the absence of trait or fitness variation. I go on to explain why any attempt to demonstrate the truth of causalism via a hypothetical intervention on an individual-level property would appear to require one to adopt an account of natural selection that is inadequate for the same reason. This in turn means the plausibility of causalism does indeed depend on the plausibility of the claim that population-level properties, which supervene on the properties of the individuals in the population, can be causally efficacious. (shrink)

There are ongoing debates in philosophy of biology about what falls within natural selection's explanatory scope. These include debates about whether selection can explain individual-level traits, the extent to which selection can explain distributions of trait frequencies, and whether selection can explain the origin of novel traits. Here I'll survey these debates, suggest which views seem most plausible, and describe some useful conceptual frameworks for thinking about the issues involved.

We have argued elsewhere that: (A) Natural selection is not a cause of evolution. (B) A resolution-of-forces (or vector addition) model does not provide us with a proper understanding of how natural selection combines with other evolutionary influences. These propositions have come in for criticism recently, and here we clarify and defend them. We do so within the broad framework of our own “hierarchical realization model” of how evolutionary influences combine.

In this paper, using a multilevel approach, we defend the positive role of natural selection in the generation of organismal form. Despite the currently widespread opinion that natural selection only plays a negative role in the evolution of form, we argue, in contrast, that the Darwinian factor is a crucial (but not exclusive) factor in morphological organization. Analyzing some classic arguments, we propose incorporating the notion of ‘downward causation’ into the concept of ‘natural selection.’ In our opinion, this kind of (...) causation is fundamental to the operation of selection as a creative evolutionary process. (shrink)

Elliott Sober and his defenders think of selection, drift, mutation, and migration as distinct evolutionary forces. This paper exposes an ambiguity in Sober's account of the force of selection: sometimes he appears to equate the force of selection with variation in fitness, sometimes with ‘selection for properties’. Sober's own account of fitness as a property analogous to life-expectancy shows how the two conceptions come apart. Cases where there is selection against variance in offspring number also show that selection and drift (...) cannot be distinguished in the way Sober hopes for. These issues have significance beyond the parochial matter of the coherence of Sober's system. There is no good principled answer to the question of which features of a population should count among the contributors to fitness. This means there is no non-arbitrary account of the nature of selection. (shrink)

Sober 2011 argues that, contrary to Hume, some causal statements can be known a priori to be true—notably, some ‘would promote’ statements figuring in causal models of natural selection. We find Sober's argument unconvincing. We regard the Humean thesis as denying that causal explanations contain any a priori knowable statements specifying certain features of events to be causally relevant. We argue that not every ‘would promote’ statement is genuinely causal, and we suggest that Sober has not shown that his examples (...) of ‘would promote’ statements manage to achieve a priori status without sacrificing their causal character. (shrink)

Statistical reasoning is an integral part of modern scientific practice. In The Seven Pillars of Statistical Wisdom Stephen Stigler presents seven core ideas, or pillars, of statistical thinking and the historical developments of each of these pillars, many of which were concurrent with developments in biology. Here we focus on Stigler’s fifth pillar, regression, and his discussion of how regression to the mean came to be thought of as a solution to a challenge for the theory of natural selection. Stigler (...) argues that the purely mathematical phenomenon of regression to the mean provides a resolution to a problem for Darwin’s evolutionary theory. Thus, he argues that the resolution to the problem for Darwin’s theory is purely mathematical, rather than causal. We show why this argument is problematic. (shrink)

The key idea of the interventionist account of causation is that a variable A causes a variable B if and only if B would change if A were manipulated in the appropriate way. This paper raises two problems for Woodward's (2003) version of interventionism. The first is that the conditions it imposes are not sufficient for causation, because these conditions are also satisfied by non-causal relations of nomological dependence expressed in association laws. Such laws ground a relation of mutual manipulability (...) that is incompatible with the asymmetry of causation. Several ways of defending the interventionist account are examined and found unsatisfying. The second problem is that it often seems to be impossible, in a model that contains variables linked by an association law, to satisfy the conditions imposed on interventions on such variables. Various ways to solve this second problem, most importantly the analysis of manipulability in terms of difference making, are examined. Given that none solves the problem, I conclude that the interventionist conditions are neither sufficient nor necessary for causation. It is suggested that they provide an analysis of nomological dependence, which may be supplemented with the notion of a causal process to yield an analysis of causation. (shrink)

‘Statisticalists’ argue that the individual interactions of organisms taken together constitute natural selection. On this view, natural selection is an aggregated effect of interactions rather than some added cause acting on populations. The statisticalists’ view entails that natural selection and drift are indistinguishable aggregated effects of interactions, so that it becomes impossible to make a difference between them. The present paper attempts to make sense of the difference between selection and drift, given the main insights of statisticalism; basically, it will (...) disentangle the various kinds of indistinguishability between selection and drift that happen within biology, by examining the epistemological and metaphysical nature of the distinction between selection and drift. It will be based on a ‘difference-making account’ of selection. The first section will explicate the inscrutability of selection and drift, its various types in the statisticalist writings, and its implications. The second section specifies concepts of natural selection and drift in the difference making account of selection I am using, and shows that one can derive from this the statistical signatures of selection and drift. On this basis I focus on one sort of indistinguishability issue about selection and drift, which I call epistemic opacity, and explain why it mostly affects small populations. The last section explains why epistemic opacity does not raise an genuine epistemic problem for evolutionary biology. (shrink)

Recently some philosophers have emphasized a potentially irreconcilable conceptual antagonism between the statistical characterization of natural selection and the standard scientific discussion of natural selection in terms of forces and causes. Other philosophers have developed an account of the causal character of selectionist statements represented in terms of counterfactuals. I examine the compatibility between such statisticalism and counterfactually based causal accounts of natural selection by distinguishing two distinct statisticalist claims: firstly the suggested impossibility for natural selection to be a cause (...) acting upon populations and secondly the conceptualization that all evolutionary causes occur at the level of interactions between individual organisms. I argue that deriving the latter from the former involves supplementary assumptions concerning precisely what causation is. I critically examine two of these assumptions purportedly preventing natural selection being regarded as a cause: the locality claim and the modularity claim. I conclude that justifying the strongest version of statisticalism—i.e. evolutionary causation only occurs at the level of individual interactions between organisms—would require further metaphysical arguments that are likely to be deemed highly problematic. Additionally, I argue that such a metaphysical position would be considered incongruous with both our scientific and ordinary use of the concepts of causality and explanation as employed within our everyday epistemological framework. (shrink)

Whether mental properties are identical with neural properties is one of the central questions of contemporary philosophy of mind. Many philosophers agree that even if mental properties are identical with neural properties, the mind-brain identity thesis cannot be established on empirical grounds, but only be vindicated by theoretical philosophical considerations. In his paper ‘When Is a Brain Like the Planet?’, Clark Glymour proposes a causal criterion for local property identifications and claims that this criterion can be used to empirically establish (...) local identities between mental and neural properties. If successful, such an account would settle the debate on the mind-body problem. In this paper, I argue that Glymour’s approach falls short of its aims. The causal criterion which he proposes does not provide a sufficient condition for the local identification of properties. Moreover, his account does not succeed in rendering local mind-brain identities empirically testable. Therefore, the mind-body problem cannot be solved as easily as Glymour assumes. (shrink)

Several authors have recently claimed that the notorious causal exclusion problem, according to which higher-level causes are threatened with causal pre-emption by lower-level causes, can be avoided if causal relevance is understood in terms of Woodward's interventionist account of causation. They argue that if causal relevance is defined in interventionist terms, there are cases where only higher-level properties, but not the lower-level properties underlying them, qualify as causes of a certain effect. In this article, I show that the line of (...) reasoning supposed to establish this claim does not succeed and that interventionism is not better capable of dealing with higher-level causal claims than other accounts of causation. According to Woodward, higher-level causal claims are nonetheless more adequate than lower-level ones if they describe a realization-independent dependency relationship and, hence, meet the requirement that causes should be proportional to their effects. I argue, however, that combining interventionism with proportionality considerations raises difficulties and that, therefore, Woodward's account does not vindicate higher-level causation. (shrink)

ABSTRACT Causes must be distinct from their effects. If the temperature in a room is 15°F, this can cause water pipes to freeze. However, the temperature’s being 15°F is not a cause of the temperature’s being below the freezing point. In general, conceptual, logical, mathematical, and other non-causal dependence relations should not be misclassified as causal. In this paper, I discuss how interventionist theories of causation can meet the challenge of distinguishing between (direct or indirect) causal relations and dependence relations (...) that are due to non-causal factors. I survey several approaches to solving this problem, and propose a novel criterion based on the notion of supervenience. According to this criterion, variables are sufficiently distinct to qualify as the relata of a causal relation iff they do not have overlapping minimal supervenience bases. (shrink)

Carl Craver’s mutual manipulability criterion aims to pick out all and only those components of a mechanism that are constitutively relevant with respect to a given phenomenon. In devising his criterion, Craver has made heavy use of the notion of an ideal intervention, which is a tool for illuminating causal concepts in causal models. The problem is that typical mechanistic models contain non-causal relations in addition to causal ones, which is why the standard concept of an ideal intervention is not (...) appropriate in that context. In this paper, I first show how top-down interventions in mechanistic models violate the conditions for ideal interventions. Drawing from recent developments in the causal exclusion literature, I then argue for extended interventionism better suited for the purposes of the new mechanist. Finally, I show why adopting such an extended account leads to the surprising consequence that an important subset of mechanistic interlevel relations comes out as causal. (shrink)

This paper is concerned with the content of the causal proportionality constraint. It investigates two general versions of the constraint, namely “horizontal” and “vertical” proportionality. Moreover, it discusses whether proportionality is considered an ontic or an epistemic, i.e. explanatory, constraint on causation in the context of some of the most prominent theories of causation. The following main claims are defended: (1) The horizontal (HP) and the vertical version (VP) of the proportionality constraint are logically independent. (2) HP is implied by (...) some prominent theories of causation, not by others. (3) None of the discussed popular theories of causation contradicts either HP or VP. (4) HP and VP are not ontic or epistemic principles as such; rather, whether they are ontic or epistemic depends on the theories chosen plus background assumptions about the existence of higher-level causes and their non-identity to lower-level ones. (shrink)

Counterfactual conditionals have been appealed to in various ways to show how the mind can be causally efficacious. However, it has often been overestimated what the truth of certain counterfactuals actually indicates about causation. The paper first identifies four approaches that seem to commit precisely this mistake. The arguments discussed involve erroneous assumptions about the connection of counterfactual dependence and genuine causation, as well as a disregard of the requisite evaluation conditions of counterfactuals. In a second step, the paper uses (...) the insights of the foregoing analyses to formulate a set of counterfactuals-based conditions that are characterized as sufficient to establish singular causal claims. The paper concludes that there are ample reasons to believe that some mental events satisfy all these conditions with respect to certain further events and, hence, that mental events sometimes are causes. (shrink)

Recent papers by a number of philosophers have been concerned with the question of whether natural selection is a causal process, and if it is, whether the causes of selection are properties of individuals or properties of populations. I shall argue that much confusion in this debate arises because of a failure to distinguish between causal productivity and causal relevance. Causal productivity is a relation that holds between events connected via continuous causal processes, while causal relevance is a relationship that (...) can hold between a variety of different kinds of facts and the events that counterfactually depend upon them. I shall argue that the productive character of natural selection derives from the aggregation of individual processes in which organisms live, reproduce and die. At the same time, a causal explanation of the distribution of traits will necessarily appeal both to causally relevant properties of individuals and to causally relevant properties that exist only at the level of the population. (shrink)

I criticize some arguments against the causal interpretability of population genetics put forward by Denis Walsh ([2007], [2010]). In particular, I seek to undermine the contention that population genetics exhibits frame of reference relativity or subjectivity with respect to its formal representations. I also show that classical population genetics does not fall foul of some criteria for causal representation put forward by James Woodward ([2003]), although those criteria do undermine some causalist stances. 1 Introduction2 Modularity3 The Crucially Important Point4 The (...) Gillespie Case: Density-Dependent Selection5 Conclusion. (shrink)

In this paper I reconstruct and evaluate the validity of two versions of causal exclusion arguments within the theory of causal Bayes nets. I argue that supervenience relations formally behave like causal relations. If this is correct, then it turns out that both versions of the exclusion argument are valid when assuming the causal Markov condition and the causal minimality condition. I also investigate some consequences for the recent discussion of causal exclusion arguments in the light of an interventionist theory (...) of causation such as Woodward's (2003) and discuss a possible objection to my causal Bayes net reconstruction. (shrink)

Do evolutionary processes such as selection and random drift cause evolutionary change, or are they merely convenient ways of describing or summarizing it? Philosophers have lined up on both sides of this question. One recent defense (Reisman and Forber 2005) of the causal status of selection and drift appeals to a manipulability theory of causation. Yet, even if one accepts manipulability, there are still reasons to doubt that genetic drift, in particular, is genuinely causal. We will address two challenges to (...) treating drift as causal within a manipulation framework. We will argue that both challenges ultimately fail, but that they raise interesting and subtle issues about the nature of causation and the differences between selection and drift. ‡Thanks to audiences at the ‘PBDB1' Conference and the 2006 PSA Meeting for valuable feedback. †To contact the authors, please write to: Patrick Forber, Tufts University, Philosophy Department, Miner Hall, Medford, MA 02155; e-mail: [email protected]. (shrink)

There has recently been a renewed interest in the “force” interpretation of evolutionary biology. In this article, I present the general structure of the arguments for the force interpretation and identify a problem in its overly permissive conditions for being a Newtonian force. I then attempt a solution that (1) helps to illuminate the difference between forces and other types of causes and (2) makes room for random genetic drift as a force. In particular, I argue that forces are not (...) different in kind from other types of causes but rather that forces are situated on a continuum of causes distinguished by their unifying power. †To contact the author, please write to: Department of Philosophy, University of Wisconsin–Madison, 5185 Helen C. White Hall, Madison, WI 53706; e‐mail: [email protected]. (shrink)

The causal exclusion argument suggests that mental causes are excluded in favour of the underlying physical causes that do all the causal work. Recently, a debate has emerged concerning the possibility of avoiding this conclusion by adopting Woodward's interventionist theory of causation. Both proponents and opponents of the interventionist solution crucially rely on the notion of supervenience when formulating their positions. In this article, we consider the relation between interventionism and supervenience in detail and argue that importing supervenience relations into (...) the interventionist framework is deeply problematic. However, rather than reject interventionist solutions to exclusion wholesale, we wish to propose that the problem lies with the concept of supervenience. This would open the door for a moderate defence of the interventionist solution to the exclusion argument. (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)

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)

It is an ongoing controversy whether natural selection is a cause of population change, or a mere statistical description of how individual births and deaths accumulate. In this paper I restate the problem in terms of the reference class problem, and propose how the structure of stable equilibrium can provide a solution in continuity with biological practice. Insofar natural selection can be understood as a tendency towards equilibrium, key statisticalist criticisms are avoided. Further, in a modification of the Newtonian-force analogy, (...) it can be suggested that a better metaphor for natural selection is that of an emergent force, similar in nature to entropic forces: with magnitude and direction, but lacking a spatiotemporal origin or point of application. (shrink)

In this dissertation, I develop and defend a model of causation that allows for dualist mental causation in worlds where the physical domain is physically complete. In Part I, I present the dualist ontology that will be assumed throughout the thesis and identify two challenges for models of mental causation within such an ontology: the exclusion worry and the common cause worry. I also argue that a proper response to these challenges requires a thoroughly lightweight account of causation, i.e. an (...) account that allows for causes to be metaphysically distinct from the phenomena that produce or physically necessitate their effects. In Part II, I critically evaluate contemporary responses to these challenges from the philosophical literature. In particular, I discuss List and Stoljar’s criticism of exclusion worries, Kroedel’s alternative dualist ontology, concerns about the notion of causal sufficiency, and Lowe’s models of dualist mental causation. I argue that none of these proposals provide independent motivation for a thoroughly lightweight account of causation and therefore leave room for improvement. In the first four chapters of Part III, I develop a thoroughly lightweight model of causation, which builds on interventionist approaches to causation. First, I explain how so-called ‘holding fixed’-requirements in standard interventionist accounts stand in the way of dualist mental causation. I then argue that interventionist accounts should impose a robustness condition on causal correlations and that, with this condition in place, the ‘holding fixed’-requirements can be weakened such that they do allow for dualist mental causation. I dub the interventionist model with such weakened ‘holding fixed’-requirements ‘insensitive interventionism’, argue that it can counter the exclusion worry as well as the common cause worry, and explain under which circumstances it would predict there to be dualist mental causation. Importantly, these circumstances might, for all we know, hold in the actual world. In the final three chapters of Part III, I defend insensitive interventionism against some objections. I consider the objection that causation must be productive, the objection that causes must physically necessitate their effects, and the objection that insensitive interventionism is too permissive. I respond by drawing from the literature on causation by absences and on the relation between causation and fundamental physics. Overall, insensitive interventionism performs as well as standard interventionist accounts. I conclude that insensitive interventionism is a credible model of causation. (shrink)

Concrete Causation centers about theories of causation, their interpretation, and their embedding in metaphysical-ontological questions, as well as the application of such theories in the context of science and decision theory. The dissertation is divided into four chapters, that firstly undertake the historical-systematic localization of central problems (chapter 1) to then give a rendition of the concepts and the formalisms underlying David Lewis' and Judea Pearl's theories (chapter 2). After philosophically motivated conceptual deliberations Pearl's mathematical-technical framework is drawn on for (...) an epistemic interpretation and for emphasizing the knowledge-organizing aspect of causality in an extension of the interventionist Bayes net account of causation (chapter 3). Integrating causal and non-causal knowledge in unified structures ultimately leads to an approach towards solving problems of (causal) decision theory and at the same time facilitates the representation of logical-mathematical, synonymical, as well as reductive relationships in efficiently structured, operational nets of belief propagation (chapter 4). (shrink)

Fitness plays many roles throughout evolutionary theory, from a measure of populations in the wild to a central element in abstract theoretical presentations of natural selection. It has thus been the subject of an extensive philosophical literature, which has primarily centered on the way to understand the relationship between fitness values and reproductive outcomes. If fitness is a probabilistic or statistical quantity, how is it to be defined in general theoretical contexts? How can it be measured? Can a single conceptual (...) model for fitness be offered that applies in all biological cases, or must fitness measures be case-specific? Philosophers have explored these questions over the last several decades, largely in the context of an influential definition of fitness proposed in the late 1970s: the propensity interpretation. This interpretation as first described undeniably suffers from significant difficulties, and debate regarding the tenability of amendments and alternatives to it remains unsettled. (shrink)

Explanations in psychiatry often integrate various factors relevant to psychopathology. Identifying genuine causes among them is theoretically and clinically important, but epistemically challenging. Woodward’s interventionism appears to provide a promising tool to achieve this. However, Woodward’s interventionism is too demanding to be applied to psychiatry. I thus introduce difference-making interventionism, which detects relevance in general rather than causation, to make interventionist reasoning viable in clinical practice. DMI mirrors the empirical reality of psychiatry even more closely than interventionism, but it needs (...) to be supplied with additional heuristics to disambiguate between causes and other difference-makers. To achieve this, I suggest employing heuristics based on multiple experiments, temporal order and scientific domain. (shrink)

Non-reductive physicalism is the view that mental events cause other events in virtue of their mental properties and that mental properties supervene on, without being identical to, physical properties. Jaegwon Kim has presented several much-discussed arguments against this view. But the much simpler causal closure argument, which purports to establish that every mental property is identical to a physical property, has received less attention than Kim’s arguments. This paper aims to show how a non-reductive physicalist should rebut the causal closure (...) argument. A crucial premise in the argument is a principle stating that the physical world is causally closed. It states, roughly, that every physical event has a physical sufficient cause. I argue that when the principle is formulated in this way, the causal closure argument is invalid. Less frequently, the causal closure principle is formulated in terms of a difference-making conception of causation so that it states that every physical effect has a physical difference-making cause. I argue that the principle, so formulated, is false and the causal closure argument unsound. Either way the argument lacks the apodeictic force to compel acceptance of its conclusion. (shrink)

Discussions of “chance” and related concepts are found throughout philosophical work on evolutionary theory. By drawing attention to three very commonly-recognized distinctions, I separate four independent concepts falling under the broad heading of “chance”: randomness, epistemic unpredictability, causal indeterminism, and probabilistic causal processes. Far from a merely semantic distinction, however, it is demonstrated that conflation of these obviously distinct notions has an important bearing on debates at the core of evolutionary theory, particularly the debate over the interpretation of fitness, natural (...) selection, and genetic drift. (shrink)

I have two main aims. The first is general, and more philosophical. The second is specific, and more closely related to physics. The first aim is to state my general views about laws and causation at different ”levels’. The main task is to understand how the higher levels sustain notions of law and causation that ”ride free’ of reductions to the lower level or levels. I endeavour to relate my views to those of other symposiasts. The second aim is to (...) give a framework for describing dynamics at different levels, emphasizing how the various levels’ dynamics can mesh or fail to mesh. This framework is essentially that of elementary dynamical systems theory. The main idea will be, for simplicity, to work with just two levels, dubbed ”micro’ and ”macro’, which are related by coarse-graining. I use this framework to describe, in part, the first four of Ellis’ five types of top-down causation. (shrink)