The thesis is defended that the theories of causation, time and space, and levels of reality are mutually interrelated in such a way that the difficulties internal to theories of causation and to theories of space and time can be understood better, and perhaps dealt with, in the categorial context furnished by the theory of the levels of reality. The structural condition for this development to be possible is that the first two theories be opportunely generalized.

This paper attempts to elucidate three characteristics of causal relationships that are important in biological contexts. Stability has to do with whether a causal relationship continues to hold under changes in background conditions. Proportionality has to do with whether changes in the state of the cause “line up” in the right way with changes in the state of the effect and with whether the cause and effect are characterized in a way that contains irrelevant detail. Specificity is connected both to (...) David Lewis’ notion of “influence” and also with the extent to which a causal relation approximates to the ideal of one cause–one effect. Interrelations among these notions and their possible biological significance are also discussed. (shrink)

Causation is a central topic in many areas of philosophy. In metaphysics, philosophers want to know what causation is, and how it is related to laws of nature, probability, action, and freedom of the will. In epistemology, philosophers investigate how causal claims can be inferred from statistical data, and how causation is related to perception, knowledge and explanation. In the philosophy of mind, philosophers want to know whether and how the mind can be said to have causal (...) efficacy, and in ethics, whether there is a moral distinction between acts and omissions and whether the moral value of an act can be judged according to its consequences. And causation is a contested concept in other fields of enquiry, such as biology, physics, and the law. This book provides an in-depth and comprehensive overview of these and other topics, as well as the history of the causation debate from the ancient Greeks to the logical empiricists. The chapters provide surveys of contemporary debates, while often also advancing novel and controversial claims; and each includes a comprehensive bibliography and suggestions for further reading. The book is thus the most comprehensive source of information about causation currently available, and will be invaluable for upper-level undergraduates through to professional philosophers. (shrink)

The subject of this edited volume is the idea of levels of organization: roughly, the idea that the natural world is segregated into part-whole relationships of increasing spatiotemporal scale and complexity. The book comprises a collection of essays that raise the idea of levels into its own topic of analysis. Owing to the wide prominence of the idea of levels, the scope of the volume is aimed at theoreticians, philosophers, and practicing researchers of all stripes in the (...) life sciences. The volume’s contributions reflect this diversity, and draw from fields such as developmental biology, evolutionary biology, molecular biology, ecology, cell biology, and neuroscience. The book presents wide-ranging novel insights on causation and levels, the hierarchical structure of evolution, the role of levels in biological theory, and more. (shrink)

In this paper, we critically analyze the mechanicist approach to scientific explanation and propose to complement this view with a conception of level as interval of quasi-decompositionality. This conception allows us to metaphysically base the mechanicist proposals on characteristic systemic features. By means of concrete examples, we claim that this proposal is able to overcome some of the alleged limitations of predominant models of mechanistic explanation.

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)

What exactly do social scientists and biologists say when they make causal claims? This question is one of the central puzzles in philosophy of science. Alexander Reutlinger sets out to answer this question. He aims to provide a theory of causation in the special sciences (that is, a theory causation in the social sciences, the biological sciences and other higher-level sciences). According one recent prominent view, causation is that causation is intimately tied to manipulability and the (...) possibility of intervene. Reutlinger's main negative target is to argue interventionist account of causation is not adequate. Where do interventionist accounts go wrong? Reutlinger argues that the central concept of the interventionist theories – that is, the very concept of an intervention – is tremendously problematic. Reutlinger's main positive claim consists in replacing the interventionist approach by an alternative explication of causation in the special sciences, the comparative variability theory of causation. This alternative preserves many insights of the interventionist account without a commitment to the claim that causation and interventions are intimately tied together. (shrink)

I defend what may loosely be called an eliminativist account of causation by showing how several of the main features of causation, namely asymmetry, transitivity, and necessitation, arise from the combination of fundamental dynamical laws and a special constraint on the macroscopic structure of matter in the past. At the microscopic level, the causal features of necessitation and transitivity are grounded, but not the asymmetry. At the coarse-grained level of the macroscopic physics, the causal asymmetry is grounded, but (...) not the necessitation or transitivity. Thus, at no single level of description does the physics justify the conditions that are taken to be constitutive of causation. Nevertheless, if we mix our reasoning about the microscopic and macroscopic descriptions, the structure provided by the dynamics and special initial conditions can justify the folk concept of causation to a significant extent. I explain why our causal concept works so well even though at bottom it is comprised of a patchwork of principles that don't mesh well. (shrink)

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

Several philosophers have embraced the view that high-level events—events like Zimbabwe's monetary policy and its hyper-inflation—are causally related if their corresponding low-level, fundamental physical events are causally related. I dub the view which denies this without denying that high-level events are ever causally related causal emergentism. Several extant philosophical theories of causality entail causal emergentism, while others are inconsistent with the thesis. I illustrate this with David Lewis's two theories of causation, one of which entails causal emergentism, the other (...) of which entails its negation. I then argue for causal emergentism on the grounds that it provides the only adequate means of squaring the apparent plenitude of causal relations between low-level events with the apparent scarcity of causal relations between high-level events. This tension between the apparent abundance of low-level causation and the apparent scarcity of high-level causation has been noted before. However, it has been thought that various theses about the semantics or the pragmatics of causal claims could be used to ameliorate the tension without going in for causal emergentism. I argue that none of the suggested semantic or pragmatic strategies meet with success, and recommend emergentist theories of causality in their stead. As Lewis's 1973 account illustrates, causal emergentism is consistent with the thesis that all facts reduce to microphysical facts. (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)

The idea of a higher level phenomenon having a downward causal influence on a lower level process or entity has taken a variety of forms. In order to discuss the relation between emergence and downward causation, the specific variety of the thesis of downward causation (DC) must be identified. Based on some ontological theses about inter-level relations, types of causation and the possibility of reduction, three versions of DC are distinguished. Of these, the `Strong' form of DC (...) is held to be in conflict with contemporary science; the `Medium' version of DC may for instance describe thoughts constraining neurophysiological states, while the `Weak' form of DC is physically acceptable but may not in practice be a feasible description of the mind/brain or the cell/molecule relation. All forms have their specific problems, but the Medium and the Weak version seems to be most promising. (shrink)

In this dissertation, I propose a reductive account of causation. This account may be stated as follows: -/- Causation:c is a cause of e within a possibility horizon H iff a) c is process-connected to e, and b) e security-depends on c within H. -/- More precisely, my suggestion is that there are two kinds of causal relata: instantaneous events (defined in Chapter 4) and possibility horizons (defined in Chapter 5). Causation is a ternary relation between two (...) actual instantaneous events – the cause c and the effect e – and a possibility horizon H. -/- I argue that causation has a dual nature: on the one hand, a cause must be connected to its effect via a genuine process; on the other hand, a cause must make a difference to its effect. The first condition – namely, the condition of process-connection (defined in Chapter 6) – captures the sense in which a cause must be connected to its effect via a genuine process. This condition allows my account to separate causation from mere correlation, distinguish genuine causes from preempted backups, and capture how a cause must be at the right level of detail relative to its effect (Chapter 7). -/- The second condition – namely, the condition of security-dependence (defined in Chapter 8) – captures the sense in which a cause must make a difference to its effect. This condition allows my account to yield intuitively correct verdicts on the counterexamples to the transitivity and intrinsicness of causation, resolve the problem of profligate omissions, accommodate structurally isomorphic but causally different cases, and handle contrastive causal claims (Chapter 9 and 10). -/- Finally, my proposed account of causation logically entails restricted versions of three important principles of causal reasoning concerning the sufficiency of counterfactual dependence for causation, and the transitivity and intrinsicness of causation (Chapter 11). (shrink)

Tinbergen’s classic “On Aims and Methods of Ethology” (_Zeitschrift für Tierpsychologie, 20_, 1963) proposed four levels of explanation of behavior, which he thought would soon apply to humans. This paper discusses the need for multilevel explanation; Huxley and Mayr’s prior models, and others that followed; Tinbergen’s differences with Lorenz on “the innate”; and Mayr’s ultimate/proximate distinction. It synthesizes these approaches with nine levels of explanation in three categories: phylogeny, natural selection, and genomics (ultimate causes); maturation, sensitive period effects, (...) and routine environmental effects (intermediate causes); and hormonal/metabolic processes, neural circuitry, and eliciting stimuli (proximate causes), as a respectful extension of Tinbergen’s levels. The proposed classification supports and builds on Tinbergen’s multilevel model and Mayr’s ultimate/proximate continuum, adding intermediate causes in accord with Tinbergen’s emphasis on ontogeny. It requires no modification of Standard Evolutionary Theory or The Modern Synthesis, but shows that much that critics claim was missing was in fact part of Neo-Darwinian theory (so named by J. Mark Baldwin in _The American Naturalist_ in 1896) all along, notably reciprocal causation in ontogeny, niche construction, cultural evolution, and multilevel selection. Updates of classical examples in ethology are offered at each of the nine levels, including the neuroethological and genomic findings Tinbergen foresaw. Finally, human examples are supplied at each level, fulfilling his hope of human applications as part of the biology of behavior. This broad ethological framework empowers us to explain human behavior—eventually completely—and vindicates the idea of human nature, and of humans as a part of nature. (shrink)

This paper tracks the commitments of mechanistic explanations focusing on the relation between activities at different levels. It is pointed out that the mechanistic approach is inherently committed to identifying causal connections at higher levels with causal connections at lower levels. For the mechanistic approach to succeed a mechanism as a whole must do the very same thing what its parts organised in a particular way do. The mechanistic approach must also utilise bridge principles connecting different causal (...) terms of different theoretical vocabularies in order to make the identities of causal connections transparent. These general commitments get confronted with two claims made by certain proponents of the mechanistic approach: William Bechtel often argues that within the mechanistic framework it is possible to balance between reducing higher levels and maintaining their autonomy at the same time, whereas, in a recent paper, Craver and Bechtel argue that the mechanistic approach is able to make downward causation intelligible. The paper concludes that the mechanistic approach imbued with identity statements is no better candidate for anchoring higher levels to lower ones while maintaining their autonomy at the same time than standard reductive accounts are, and that what mechanistic explanations are able to do at best is showing that downward causation does not exist. (shrink)

A regularity theory of causation analyses type-level causation in terms of Boolean difference-making. The essential ingredient that helps this theoretical framework overcome the problems of Hume’s and Mill’s classical accounts is a principle of non-redundancy: only Boolean dependency structures from which no elements can be eliminated track causation. The first part of this paper argues that the recent regularity theoretic literature has not consistently implemented this principle, for it disregarded an important type of redundancies: structural redundancies. Moreover, (...) it is shown that a regularity theory needs to be underwritten by a hitherto neglected metaphysical background assumption stipulating that the world's causal makeup is not ambiguous. Against that background, the second part then develops a new regularity theory that does justice to all types of redundancies and, thereby, provides the first all-inclusive notion of Boolean difference-making. (shrink)

Sober (1984) presents an account of selection motivated by the view that one property can causally explain the occurrence of another only if the first plays a unique role in the causal production of the second. Sober holds that a causal property will play such a unique role if it is a population level cause of its effect, and on this basis argues that there is selection for a trait T only if T is a population level cause of survival (...) and reproductive success. Sterelny and Kitcher (1988) claim against Sober that some traits directly subject to selection will not satisfy the probabilistic condition on population level causation. In this paper I show that Sober has the resources to resist the Sterelny-Kitcher complaint, but I argue that not all traits that satisfy the probabilistic condition play the required unique role in the production of their effects. (shrink)

To explain phenomenon R by showing how mechanism M yields output R each time it is triggered by circumstances C, is to give a causal explanation of R. This paper analyses what mechanistic analysis can contribute to our understanding of causation in general and of downward causation in particular. It is first shown, against Glennan, that the concept of causation cannot be reduced to that of mechanism. Second it is shown, against Craver and Bechtel, that mechanistic explanation (...) allows us to make sense of causal processes that cut across levels, either in bottom-up direction where a change in a part of a system causes a change in the whole, or in downward direction where a change at the level of the system causes a change at the level of its parts. I suggest construing a decision's influence on molecules in muscle cells as a global constraint. Microscopic laws determine the detailed evolution of muscle cells and glucose molecules, but this evolution is constrained by the fact that it must be compatible with the action caused by the decision. (shrink)

A regularity theory of causation analyses type-level causation in terms of Boolean difference-making. The essential ingredient that helps this theoretical framework overcome the problems of Hume’s and Mill’s classical accounts is a principle of non-redundancy: only Boolean dependency structures from which no elements can be eliminated track causation. The first part of this article argues that the recent regularity-theoretic literature has not consistently implemented this principle, for it disregarded an important type of redundancies: structural redundancies. Moreover, it (...) is shown that a regularity theory needs to be underwritten by a hitherto neglected metaphysical background assumption stipulating that the world’s causal makeup is not ambiguous. Against that background, the second part then develops a new regularity theory that does justice to all types of redundancies and, thereby, provides the first all-inclusive notion of Boolean difference-making. (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)

I argue that Mumford and Anjum’s recent theory of simultaneous causation among powerful meso-level objects is problematic in several respects: it is based on a false dichotomy, it is incompatible with standard meso-level physics, it is explanatory deficient, and it threatens to render the powers metaphysics incoherent. Powers theorists are advised, therefore, to adopt a purely sequential conception of causation.

Lack of clarity about underlying philosophical commitments leads to lack of clarity at other levels of analysis. Here I show that the literature on so-called “causal mechanisms” is rife with conceptual problems, stemming from insufficient rigor with respect to the metaphysics of causation.

One of Stuart Glennan's most prominent contributions to the new mechanist debate consists in his reductive analysis of higher-level causation in terms of mechanisms (Glennan, 1996). In this paper I employ the causal Bayes net framework to reconstruct his analysis. This allows for specifying general assumptions which have to be satis ed to get Glennan's approach working. I show that once these assumptions are in place, they imply (against the background of the causal Bayes net machinery) that higher-level (...) class='Hi'>causation indeed reduces to interactions between component parts of mechanisms. I also briefly discuss the plausibility of these assumptions and some consequences for the mechanism debate. (shrink)

In this doctoral thesis, I will argue that in his De motu (1721, ‘On motion’), Bishop George Berkeley (c.1684–1753) develops a pragmatist theory of causation regarding mechanical theories outlined previously with Newtonianism. I place chief emphasis on the importance of logic and mathematics in Berkeley’s scientific approach, on which the other levels of semantics, epistemology, and mechanics build up. On my rendering, Berkeley’s pragmatic method to conceive or mathematically imagine causation makes sense in terms of mechanical causes (...) or ‘mathematical hypotheses’. For the mechanist maintains the usefulness and truthfulness of causation by the following definition. Definition. A pragmatist theory of causation is one which holds that: 1 Causal terms are indispensable in scientific deliberation for their usefulness; they cannot be eliminated [contra reductionism]. 2 What a cause is is defined by one’s temporal deliberative practices, independent of a temporal structure that theories hold [contra structuralism]. 3 Causal laws (theories formulated in causal terms) are genuinely true, not fictitious, when one confirms and deduces them [contra instrumentalism]. By justifying this definition, I will object to three rival readings—reductionism, structuralism, and instrumentalism—to my reading of Berkeley as a pragmatist about causation. In particular, my pragmatist reading criticises the most popular instrumentalist reading because, according to the latter, talk of causal terms like forces can be false or merely fictitious inasmuch as one can hold the utility of theories in mechanical practices. The instrumentalist reading is then compatible with mathematical formalism, according to which it is not truth or meaning that counts as formal manipulation or game of meaningless symbols, thereby eschewing a platonist attitude towards mathematical objects. However, I rebut the formalistic instrumentalism from Berkeley’s logical and realist standpoint, maintaining the irreducibility of occult qualities that mathematical objects have in their formulation from hypotheses to propositions. Light shall be shed on the tenet I propose that law-propositions formulated in hypothetical, causal terms must be true, neither false nor fictitious, when we (1) frame, (2) confirm, and (3) express them to the extent of our discursive thinking (in three steps). [339 words]. (shrink)

I argue that high level causal relationships are often more fundamental than low level causal relationships. My argument is based on some general principles governing when one causal relationship will metaphysically ground another—a phenomenon I term derivative causation. These principles are in turn based partly on our intuitive judgments concerning derivative causation in a series of representative examples, and partly on some powerful theoretical considerations in their favour. I show how these principles entail that low level causation (...) can derive from high level causation, and in particular that neural causation can derive from mental causation. I then draw out several important consequences of this result. Most immediate among these are the implications the result has for aspirations to reduce high level causation to its low level counterpart. But the result also bears on the possibility of downward causation, the relationship between counterfactuals and causation, and the idea—familiar from both the literature on the exclusion problem and the literature on proportionality constraints on causation—that causal relationships at different levels compete for their existence. (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)

Supporters of the autonomy of higher-level causation (or explanation) often appeal to proportionality, arguing that higher-level causes are more proportional than their lower-level realizers. Recently, measures based on information theory and causal modeling have been proposed that allow one to shed new light on proportionality and the related notion of specificity. In this paper we apply ideas from this literature to the issue of higher vs. lower-level causation (and explanation). Surprisingly, proportionality turns out to be irrelevant for the (...) question of whether higher-level causes (or explanations) can be autonomous; specificity is a much more informative notion for this purpose. (shrink)

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)

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)

The causal exclusion argument supports the notion that causation should be thought of as a purely low-level affair. Here we argue instead in favour of high-level causation as a natural and meaningful notion that may even be more useful than causation at more fundamental physical levels. Our argument is framed in terms of a broadly interventionist conception of causation. Its essence is that causal relations at an appropriately high level can in a certain sense be (...) less sensitive than those at a fundamental, microscopic level. This means that in settings where causal relations at the physical level are not considered in the context of some suitable macro-level interpretation, statements concerning the low-level relations may be highly sensitive with respect to changes in background conditions. Using an example of accelerator experiments in particle physics, we consider what it means to characterize extremely sensitive low-level events as causal. (shrink)

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

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)

Causation is important. It is, as Hume said, the cement of the universe, and lies at the heart of our conceptual structure. Causation is one of the most fundamental tools we have for organizing our apprehension of the external world and ourselves. But philosophers' disagreement about the correct interpretation of causation is as limitless as their agreement about its importance. The history of attempts to elucidate the nature of this concept and to situate it with respect to (...) other fundamental concepts is almost as long as the history of philosophy itself. In this first English translation of Causalite; et lois de la nature Max Kistler seeks to reconstruct a unified concept of causation that is general enough to adequately deal with both elementary physical processes and the macroscopic level of phenomena we encounter in everyday life. It will be of great interest to philosophers of science and metaphysics; and also to students and scholars of philosophy of mind where concepts of causation and law play a prominent role. (shrink)

This is the first English translation of _Causalite´ et Lois de La Nature,_ and is an important contribution to the theory of causation_._ Max Kistler reconstructs a unified concept of causation that is general enough to adequately deal with both elementary physical processes, and the macroscopic level of phenomena we encounter in everyday life. This book will be of great interest to philosophers of science and metaphysics, and also to students and scholars of philosophy of mind where concepts of (...) causation and law play a prominent role. (shrink)

After briefly presenting Ronald Giere's (1979, 1980) recent counterfactual characterization of population-level causation, I present two counterexamples to the characterization. The difficulty discussed stems from nonaccidental correlations that can obtain between causally effective and causally neutral factors.

I present an overview of emotion theories, organised around the question of emotion causation. I argue that theories of emotion causation should ideally address the problems of elicitation, intensity, and differentiation. Each of these problems can be divided into a subquestion that asks about the relation between stimuli and emotions (i.e., the functional level of process description, cf. Marr, 1982) and a subquestion that asks about the mechanism and representations that intervene (i.e., the algorithmic level of process description). (...) The overview reveals that theories of emotion causation sometimes differ with regard to the kind of process that they hold responsible for emotion causation. More precisely, they hold different assumptions regarding the conditions under which the process is supposed to operate (optimal versus suboptimal), the format of the representations involved (propositional versus perceptual), and the object or input of the central process (stimulus versus responses/experience). Further, the overview reveals that theories of emotion causation sometimes differ with regard to the level of process description that they focus on. Finally, the overview brings to light several similarities among the theories discussed. (shrink)

According to the new mechanistic approach, an acting entity is at a lower mechanistic level than another acting entity if and only if the former is a component in the mechanism for the latter. Craver and Bechtel :547–563, 2007. doi:10.1007/s10539-006-9028-8) argue that a consequence of this view is that there cannot be causal interactions between acting entities at different mechanistic levels. Their main reason seems to be what I will call the Metaphysical Argument: things at different levels of (...) a mechanism are related as part and whole; wholes and their parts cannot be related as cause and effect; hence, interlevel causation in mechanisms is impossible. I will analyze this argument in more detail and show under which conditions it is valid. This analysis will reveal that interlevel causation in mechanisms is indeed possible, if we take seriously the idea that the relata of the mechanistic level relation are acting entities and accept a slightly modified notion of a mechanistic level that is highly plausible in the light of the first clarification. (shrink)

In this paper I examine Salmon's response to two counterexamples to his conserved quantity (CQ) theory of causation. The first counterexample that I examine involves a time‐wise gerrymandered world line of a series of patches of wall that is absorbing energy as a result of being illuminated in an astrodome. Salmon says that since the gerrymandered world line does not fulfill his “no‐interaction requirement,” his CQ theory does not suffer from the counterexample. But I will argue that his response (...) fails both at a theoretical level and at a practical level. In so doing I point out a problem for CQ theorists' definition of a causal interaction. The second counterexample is concerned with a time‐wise gerrymandered world line of a series of patches that are in shadow, in Hitchcock's well‐known example. Salmon's response is based on a principle that Salmon thinks is derivable from the concept of a conserved quantity. However, I argue that the principle has a counterexample. (shrink)

The paper aims to demonstrate the possibility of consistently accepting the existence of effective mental causality in the fundamentally physical world. We suppose that the concept of causality in J. Kim’s exclusion argument against mental causation, which implies а generative conception of causal relations, can be revised taking into account the specificity of the multilevel organization of living objects. Rejection of the mechanistic model of causality as a linear process, allows you to maintain commitment to the principle of causal (...) closure of the physical world and at the same time explain how top-down causality at the macro level is possible. For this, we use the model of a fractal tree of causal chains by J. Lowe, in which mental causality plays the role of an indirect cause of a fact. We carry out a meaningful distinction between the causality of facts and events by resorting to the multilevel model of J. Ellis, in which mental causality can be considered as a macro-level fact that has a selective effect on physical events of lower levels, taking into account a wide environmental context. (shrink)

In this paper, we analyse the fruitfulness of Ronald Giere’s comparative model for causation in populations. While the original model was primarily developed to capture the meaning of causal claims in the biomedical and health sciences, we want to show that the model is not only useful in these domains, but can also fruitfully be applied to other scientific domains. Specifically, we demonstrate that the model is fruitful for characterizing the meaning of causal claims found in classical genetics, epidemiology (...) and electoral sociology. Additionally, we propose an adapted comparative model which is needed to get a grip on higher level causal claims. We show that such claims are present in population genetics, epidemiology and electoral systems research. We conclude with some reflections on the implications of our findings for the issue of causal pluralism. (shrink)

In this paper, we advocate the idea that an adequate explanation of biological systems requires appealing to organizational closure as an emergent causal regime. We first develop a theoretical justification of emergence in terms of relatedness, by arguing that configurations, because of the relatedness among their constituents, possess ontologically irreducible properties, providing them with distinctive causal powers. We then focus on those emergent causal powers exerted as constraints, and we claim that biological systems crucially differ from other natural systems in (...) that they realize a closure of constraints, i.e. a second-order emergent regime of causation such that the constituents, each of them acting as a constraint, realize a mutual dependence among them, and are collectively able to self-maintain. Lastly, we claim that closure can be justifiably taken as an emergent regime of causation, without admitting that it inherently involves whole-parts causation, which would require to commit to stronger ontological and epistemological assumptions. (shrink)

This paper takes issue with a widely accepted view of mental causation. This is the view that mental causation is either reducible to physical causation or ultimately untenable, because incompatible with the causal completeness of physics The paper examines, first, why recent attempts to save the phenomena of mental causation by way of the notion of supervenient causation fail The result of t/us examination is the claim that any attempted specification of the most basic causal (...) factors which supposedly underlie a causal transaction cannot account for the counterfactually necessary connections with the effect m question. By contrast, the specification of these factors at a higher-level would allow establishing such connections. The paper doses with a discussion of how the view of autonomous higher-level causation grounded on counterfactual relations can be made compatible with the physicalistic commitment to a complete specification of the particular causes of any physical effect exclusively in physical terms. (shrink)

The discovery of high-level causal relations seems a central activity of the special sciences. Those same sciences are less successful in formulating strict laws. If causation must be underwritten by strict laws, we are faced with a puzzle, which might be dubbed the 'no strict laws' problem for high-level causation. Attempts have been made to dissolve this problem by showing that leading theories of causation do not in fact require that causation be underwritten by strict laws. (...) But this conclusion has been too hastily drawn. Philosophers have tended to equate non-strict laws with ceteris paribus laws. I argue that there is another category of non-strict law that has often not been properly distinguished: namely, minutiae rectus laws. If, as it appears, many special science laws are minutiae rectus laws, then this poses a problem for their ability to underwrite causal relations in a way that their typically ceteris paribus nature does not. I argue that the best prospect for resolving the resurgent 'no strict laws' problem is to argue that special science laws are in fact typically probabilistic, rather than being minutiae rectus laws. (shrink)

The Many-Worlds Interpretation is a theory in physics which proposes that, rather than quantum-level events being resolved randomly as according to the Copenhagen Interpretation, the universe constantly divides into different versions or worlds. All physically possible worlds occur, though some outcomes are more likely than others, and therefore all possible histories exist. This paper explores some implications of this for history, especially concerning causation. Unlike counterfactuals, which concern different starting conditions, MWI concerns different outcomes of the same starting conditions. (...) It is argued that analysis of causation needs to take into account the divergence of outcomes and the possibility that we inhabit a less probable world. Another implication of MWI is convergent history: for any given world there will be similar worlds which are the result of different pasts which are, however, more or less probable. MWI can assist in thinking about historical causation and indicates the importance of probabilistic causation. (shrink)

One part of the true theory of actual causation is a set of conditions responsible for eliminating all of the non-causes of an effect that can be discerned at the level of counterfactual structure. I defend a proposal for this part of the theory.