The Minimal Theory of Causation, presented in Graßhoff and May, 2001, aspires to be a version of a regularity analysis of causation able to correctly predict our causal intuitions. In my article, I will argue that it is unsuccessful in this respect. The second aim of the paper will be to defend Hitchcock’s proposal concerning divisions of causal relations against criticism made, in Jakob, 2006 on the basis of the Minimal Theory of Causation.

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)

I use some recent formal work on measuring causation to explore a suggestion by James Woodward: that the notion of causal specificity can clarify the distinction in biology between permissive and instructive causes. This distinction arises when a complex developmental process, such as the formation of an entire body part, can be triggered by a simple switch, such as the presence of particular protein. In such cases, the protein is said to merely induce or "permit" the developmental process, whilst (...) the causal "instructions" for guiding that process are already prefigured within the cells. I construct a novel model that expresses in a simple and tractable way the relevant causal structure of biological development and then use a measure of causal specificity to analyse the model. I show that the permissive-instructive distinction cannot be captured by simply contrasting the specificity of two causes as Woodward proposes, and instead introduce an alternative, hierarchical approach to analysing the interaction between two causes. The resulting analysis highlights the importance of focusing on gene regulation, rather than just the coding regions, when analysing the distinctive causal power of genes. (shrink)

The finding of fractal scaling (FS) in behavioral sequences has raised a debate on whether FS is a pervasive property of the cognitive system or is the result of specific processes. Inferences about the origins of properties in time sequences are causal. That is, as opposed to correlational inferences reflecting instantaneous symmetrical relations, causal inferences concern asymmetric relations lagged in time. Here, I integrate Granger‐causality with inferences about FS. Four simulations illustrate that causal analyses can isolate distinct (...) FS sources, whereas correlational techniques cannot. I then analyze three simultaneous sequences of responses from a database of word‐naming trials. I find that two, or perhaps three, distinct sources account for the presence of FS in these sequences, but FS is not a general property of the system. This suggests that FS arises due to the properties of a limited number of identifiable psychological and/or neural processes. Finally, I reanalyze a previously published dataset of acoustic frequency spectra using the new tools. The causality/criticality combination introduced here offers a new important perspective in the study of cognition. (shrink)

The finding of fractal scaling (FS) in behavioral sequences has raised a debate on whether FS is a pervasive property of the cognitive system or is the result of specific processes. Inferences about the origins of properties in time sequences are causal. That is, as opposed to correlational inferences reflecting instantaneous symmetrical relations, causal inferences concern asymmetric relations lagged in time. Here, I integrate Granger-causality with inferences about FS. Four simulations illustrate that causal analyses can isolate distinct (...) FS sources, whereas correlational techniques cannot. I then analyze three simultaneous sequences of responses from a database of word-naming trials. I find that two, or perhaps three, distinct sources account for the presence of FS in these sequences, but FS is not a general property of the system. This suggests that FS arises due to the properties of a limited number of identifiable psychological and/or neural processes. Finally, I reanalyze a previously published dataset of acoustic frequency spectra using the new tools. The causality/criticality combination introduced here offers a new important perspective in the study of cognition. (shrink)

The stoic fragments about the notion of cause describe general determinations of what a cause is, without distinguishing kinds of causes. This, for instance, is the case with Zeno’s and Chrysippus’ definitions conveyed by Stobaeus. On the other hand, many testimonies mention causal distinctions, but only related to the Stoics in general, or even without indicating any school. The interest of Cicero’s De fato is that this treatise refers precisely to some causal distinctions presented by Chrysippus (...) and points out the context in which they are developed, i.e the defence of human responsibility. The present study first analyses these causal distinctions linked to Chrysippus at the end of the preserved part of Cicero’s treatise. Secondly, it studies the academic reactions to these distinctions, which are carefully described by Cicero. Finally, these debates between Stoics and Academics are considered from the standpoint of the contrasting positions found in Plato’s dialogues, about the proper or improper usage of the word a‡tion. There are good reasons to think that Plato’s positions underlie the discussions presented by Cicero. (shrink)

This paper defends the acts/omissions distinction which underpins the present law on euthanasia, from various criticisms, and aims to show that it is supported by fundamental principles. After rejecting arguments that deny the coherence and/or legal relevance of the distinction, the discussion proceeds to focus on the causal relationship between the doctor and the patient's death in each case. Although previous analyses, challenging the causal efficacy of omissions generally, are shown to be deficient, it is argued that in (...) certain cases of causing death by omission the causal authorship of the doctor lapses. The final part of the paper examines why this should be morally significant and proposes an answer in terms of the principle of equality. Assuming all other factors are equal, the infringement of this principle provides an additional reason against actively killing a patient, which is not present in cases of passively letting die. (shrink)

The basic question of this article is whether Thomas Aquinas's doctrine of divine providence through his understanding of primary and secondary causation can be understood as a theological causal or non-causal explanation. To answer this question, I will consider some contemporary discussions about the nature of causal and non-causal explanations in philosophy of science and metaphysics, in order to integrate them into a theological discourse that appeals to the classical distinction between God as first cause and (...) creatures as secondary causes to explain God's presence and providence in the created universe. My main argument will hold that, even if there are some philosophical models of explanation that seem to allow one to suggest that, at least partially, this doctrine could be seen as a non-causal theological explanation, there are other models that offer seemingly stronger reasons to see this doctrine in full as a causal theological explanation. (shrink)

Mayr’s proximate–ultimate distinction has received renewed interest in recent years. Here we discuss its role in arguments about the relevance of developmental to evolutionary biology. We show that two recent critiques of the proximate–ultimate distinction fail to explain why developmental processes in particular should be of interest to evolutionary biologists. We trace these failures to a common problem: both critiques take the proximate–ultimate distinction to neglect specific causal interactions in nature. We argue that this is implausible, and that the (...) distinction should instead be understood in the context of explanatory abstractions in complete causal models of evolutionary change. Once the debate is reframed in this way, the proximate–ultimate distinction’s role in arguments against the theoretical significance of evo-devo is seen to rely on a generally implicit premise: that the variation produced by development is abundant, small and undirected. We show that a “lean version” of the proximate–ultimate distinction can be maintained even when this isotropy assumption does not hold. Finally, we connect these considerations to biological practice. We show that the investigation of developmental constraints in evolutionary transitions has long relied on a methodology which foregrounds the explanatory role of developmental processes. It is, however, entirely compatible with the lean version of the proximate–ultimate distinction. (shrink)

We can perceive not only low-level features of events such as color and motion, but also seemingly higher-level properties such as causality. A prototypical example of causal perception is the ”launching effect’: one object moves toward a stationary second object until they are adjacent, at which point A stops and B starts moving in the same direction. Beyond these motions themselves --- and regardless of any higher-level beliefs --- this display induces a vivid visual impression of causality, wherein A (...) is seen to cause B’s motion. Do such percepts reflect a unitary category of visual processing, or might there be multiple distinct forms of causal perception? While launching is often simply equated with causal perception, researchers have sometimes described other phenomena such as ”triggering’ and ”entraining’. We used psychophysical methods to determine whether these labels really carve visual processing at its joints, and how putatively different forms of causal perception relate to each other. Previous research demonstrated retinotopically specific adaptation to causality: exposure to causal launching makes subsequent ambiguous events in that same location more likely to be seen as non-causal ”passing’. Here, after replicating this effect, we show that exposure to triggering also yields retinotopically specific adaptation for subsequent ambiguous launching displays, but that exposure to entraining does not. Collectively, these results reveal that visual processing distinguishes some types of causal interactions. (shrink)

It has now been over twenty years since Elizabeth Prior, Robert Pargetter, and Frank Jackson (1982) published their classic paper on dispositions, in which they defend the following theses: (1) The Distinctness Thesis: Each disposition is distinct from its base. (2) The Impotence Thesis: Dispositions are causally impotent.1..

We develop a new version of the causal theory of spacetime. Whereas traditional versions of the theory seek to identify spatiotemporal relations with causal relations, the version we develop takes causal relations to be the grounds for spatiotemporal relations. Causation is thus distinct from, and more basic than, spacetime. We argue that this non-identity theory, suitably developed, avoids the challenges facing the traditional identity theory.

Some cases show that counterfactual conditionals (‘counterfactuals’ for short) are inherently ambiguous, equivocating between forward-tracking and backtracking counterfactu- als. Elsewhere, I have proposed a causal modeling semantics, which takes this phenomenon to be generated by two kinds of causal manipulations. (Lee 2015; Lee 2016) In an important paper (Hiddleston 2005), Eric Hiddleston offers a different causal modeling semantics, which he claims to be able to explain away the inherent ambiguity of counterfactuals. In this paper, I discuss these (...) two semantic treatments and argue that my (bifurcated) semantics is theoretically more promising than Hiddleston’s (unified) semantics. (shrink)

The paper argues against the widely accepted assumption that the causal laws of (completed) physics, in contrast to those of the special sciences, are essentially strict. This claim played an important role already in debates about the anomalousness of the mental, and it currently experiences a renaissance in various discussions about mental causation, projectability of special science laws, and the nature of physical laws. By illustrating the distinction with some paradigmatic physical laws, the paper demonstrates that only law schemata (...) are strict whereas causal laws are generally non-strict. Several potential replies to this argument are discussed and rejected as unsound. (shrink)

We blame faulty brakes for a car crash, or rain for our bad mood. This “merely causal” blame is usually seen as uninteresting. I argue that it is crucial for understanding the interpersonal blame with which we target ourselves and each other. The two are often difficult to distinguish, in a way that plagues philosophical discussions of blame. And interpersonal blame is distinctive, I argue, partly in its causal focus: its attention to a person as cause. I argue (...) that this causal focus helps explain several central characteristics of interpersonal blame: its tendency to exaggerate a person’s causal role, its weakening through attention to personal history or thoughts about determinism, its characteristic ‘force’ or ‘sting’, and our sense that blame is often harmful or unfair. I conclude by drawing out one implication of blame's causal focus: in a certain range of cases, blame is partly under our voluntary control. (shrink)

Both philosophers and psychologists have argued for the existence of distinct kinds of explanations, including teleological explanations that cite functions or goals, and mechanistic explanations that cite causal mechanisms. Theories of causation, in contrast, have generally been unitary, with dominant theories focusing either on counterfactual dependence or on physical connections. This paper argues that both approaches to causation are psychologically real, with different modes of explanation promoting judgments more or less consistent with each approach. Two sets of experiments isolate (...) the contributions of counterfactual dependence and physical connections in causal ascriptions involving events with people, artifacts, or biological traits, and manipulate whether the events are construed teleologically or mechanistically. The findings suggest that when events are construed teleologically, causal ascriptions are sensitive to counterfactual dependence and relatively insensitive to the presence of physical connections, but when events are construed mechanistically, causal ascriptions are sensitive to both counterfactual dependence and physical connections. The conclusion introduces an account of causation, an "exportable dependence theory," that provides a way to understand the contributions of physical connections and teleology in terms of the functions of causal ascriptions. (shrink)

This article discusses fundamental problems in "rational choice theory," as outlined by Jon Elster. Elster's discussion of why institutions may not be said to act shows his fundamental presupposition that only "monolithic," unitary entities are capable of action. This is, for him, a reason why only individual human beings may be said to act. Furthermore, human beings may be said to act only insofar as they "maximize" (their "utility") on the basis of a unitary, complete, consistent "preference structure." All action (...) that is not maximization in this sense is for Elster not really human action, but rather instances of "pure causality." Elster distinguishes between the "real," intentional person, who "maximizes," and "purely causal forces" within the person. This article tries to show that this radical, sharp dichotomy between "intentionality," in this narrow sense, and "pure causality" is inadequate as a basis for understanding human action. This radical dichotomy is central to important arguments made by Elster more generally. (shrink)

This paper is not going to offer any criticism of the way Gaven Kerr treats Aquinas’ argument. Instead, it offers an alternative way of reconstructing Aquinas’ argument, intending to strengthen especially those controversial aspects of it that Kerr’s reconstruction left untreated or in relative obscurity. Accordingly, although the paper’s treatment will have to have some overlaps with Kerr’s, it will deal with issues essential to adequate replies to certain competent criticisms of his argument untreated by Kerr. For the sake of (...) the “formally inclined” reader, the paper’s treatment will also include an Appendix offering a formal reconstruction of both the main argument and its sub-arguments to demonstrate the formal rigor of Aquinas’ original. (shrink)

Analyses of factual causation face perennial problems, including preemption, overdetermination, and omissions. Arguably, the thorniest, are cases of omissive overdetermination, involving two independent omissions, each sufficient for the harm, and neither, independently, making a difference. A famous example is Saunders, where pedestrian was hit by a driver of a rental car who never pressed on the (unbeknownst to the driver) defective (and, negligently, never inspected) brakes. Causal intuitions in such cases are messy, reflected in disagreement about which omission mattered. (...) What these analyses mistakenly take for granted, is that at issue is the 'efficacy' of each omission. I argue, on the contrary, the puzzle of omissive overdetermination favors taking the act/omission distinction seriously. Factual causation, properly understood precludes omissions (i.e. omissions are not causal). Of course, the law also attaches liability to omissions, but this works differently from liability for real causes (e.g. omissions have a duty requirement, they also respond differentially to difference-making considerations). The manner in which liability attaches for omissions differs from that of straightforward causal liability, and is entirely dependent on the underlying causal structure. Attention to that structure (e.g. that the driver's hitting the pedestrian with his car is what actually caused the injury) sheds light on which omissions matter (e.g. driver's failure to press on the brakes) and why (because that failure removes a defense the driver would have to liability for the accident he caused). Other cases, where the parties' connection is entirely omissive (e.g. two physicians fail to detect independently lethal conditions), come out differently (tracking moralized elements). The analysis offered makes better sense of both why omissive determination cases are puzzling and how to resolve them. (shrink)

Causal accounts of scientific explanation are currently broadly accepted (though not universally so). My first task in this paper is to show that, even for a causal approach to explanation, significant features of explanatory practice are not determined by settling how causal facts bear on the phenomenon to be explained. I then develop a broadly causal approach to explanation that accounts for the additional features that I argue an explanation should have. This approach to explanation makes (...) sense of several aspects of actual explanatory practice, including the widespread use of equilibrium explanations, the formulation of distinct explanations for a single event, and the tight relationship between explanations of events and explanations of causal regularities. (shrink)

Newcomb's problem and similar cases show the need to incorporate causal distinctions into the theory of rational decision; the usual noncausal decision theory, though simpler, does not always give the right answers. I give my own version of causal decision theory, compare it with versions offered by several other authors, and suggest that the versions have more in common than meets the eye.

Since the ENCODE project published its final results in a series of articles in 2012, there is no consensus on what its implications are. ENCODE’s central and most controversial claim was that there is essentially no junk DNA: most sections of the human genome believed to be «junk» are functional. This claim was met with many reservations. If researchers disagree about whether there is junk DNA, they have first to agree on a concept of function and how function, given a (...) particular definition, can be discovered. The ENCODE debate centered on a notion of function that assumes a strong dichotomy between evolutionary and non-evolutionary function and causes, prevalent in the Modern Evolutionary Synthesis. In contrast to how the debate is typically portrayed, both sides share a commitment to this distinction. This distinction is, however, much debated in alternative approaches to evolutionary theory, such as the EES. We show that because the ENCODE debate is grounded in a particular notion of function, it is unclear how it connects to broader debates about what is the correct evolutionary frame- work. Furthermore, we show how arguments brought forward in the controversy, particularly arguments from mathematical population genetics, are deeply embedded in their particular disciplinary contexts, and reflect substantive assumptions about the evolution of genomes. With this article, we aim to provide an anatomy of the ENCODE debate that offers a new perspective on the notions of function both sides employed, as well as to situate the ENCODE debate within wider debates regarding the forces operating in evolution. (shrink)

The physical realm is causally closed, according to physicalists like me. But why is it causally closed, what metaphysically explains causal closure? I argue that reductive physicalists are committed to one explanation of causal closure to the exclusion of any independent explanation, and that as a result, they must give up on using a causal argument to attack mind–body dualism. Reductive physicalists should view dualism in much the way that we view the hypothesis that unicorns exist, or (...) that the Kansas City Royals won the 2003 World Series: false, but not objectionable in any distinctively causal way. My argument turns on connections between explanation, counterfactuals, and inductive confirmation. (shrink)

This article compares causal and constitutive explanation. While scientific inquiry usually addresses both causal and constitutive questions, making the distinction is crucial for a detailed understanding of scientific questions and their interrelations. These explanations have different kinds of explananda and they track different sorts of dependencies. Constitutive explanations do not address events or behaviors, but causal capacities. While there are some interesting relations between building and causal manipulation, causation and constitution are not to be confused. Constitution (...) is a synchronous and asymmetric relation between relata that cannot be conceived as independent existences. However, despite their metaphysical differences, the same key ideas about explanation largely apply to both. Causal and constitutive explanations face similar challenges (such as the problems of relevance and explanatory regress) and both are in the business of mapping networks of counterfactual dependence—i.e. mechanisms—although the relevant counterfactuals are of a different sort. In the final section the issue of developmental explanation is discussed. It is argued that developmental explanations deserve their own place in taxonomy of explanations, although ultimately developmental dependencies can be analyzed as combinations of causal and constitutive dependencies. Hence, causal and constitutive explanation are distinct, but not always completely separate forms of explanation. (shrink)

There is a major debate as to whether there are non-causal mathematical explanations of physical facts that show how the facts under question arise from a degree of mathematical necessity considered stronger than that of contingent causal laws. We focus on Marc Lange’s account of distinctively mathematical explanations to argue that purported mathematical explanations are essentially causal explanations in disguise and are no different from ordinary applications of mathematics. This is because these explanations work not by appealing (...) to what the world must be like as a matter of mathematical necessity but by appealing to various contingent causal facts. (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)

We argue that two well-known examples (strawberry distribution and Konigsberg bridges) generally considered genuine cases of distinctively _mathematical_ explanation can also be understood as cases of distinctively _generic_ explanation. The latter answer resemblance questions (e.g., why did neither person A nor B manage to cross all bridges) by appealing to ‘generic task laws’ instead of mathematical necessity (as is done in distinctively mathematical explanations). We submit that distinctively generic explanations derive their explanatory force from their role in ontological unification. Additionally, (...) we argue that distinctively generic explanations are better seen as standardly mathematical instead of distinctively mathematical. Finally, we compare and contrast our proposal with the work of Christopher Pincock on abstract explanations in science and the views of Michael Strevens on abstract causal event explanations. (shrink)

We start this paper by arguing that causality should, in analogy with force in Newtonian physics, be understood as a theoretical concept that is not explicated by a single definition, but by the axioms of a theory. Such an understanding of causality implicitly underlies the well-known theory of causal nets and has been explicitly promoted by Glymour. In this paper we investigate the explanatory warrant and empirical content of TCN. We sketch how the assumption of directed cause–effect relations can (...) be philosophically justified by an inference to the best explanation. We then ask whether the explanations provided by TCN are merely post-facto or have independently testable empirical content. To answer this question we develop a fine-grained axiomatization of TCN, including a distinction of different kinds of faithfulness. A number of theorems show that although the core axioms of TCN are empirically empty, extended versions of TCN have successively increasing empirical content. (shrink)

In what follows, I shall presuppose the ecumenical core of the causal powers metaphysics. The argument of this paper concerns what may appear at first to be a wholly unrelated matter, the metaphysics of free will. However, an adequate account of freedom requires, in my judgment, a notion of a distinctive variety of causal power, one which tradition dubs ‘agent-causal power’. I will first develop this notion and clarify its relationship to other notions. I will then respond (...) to a number of objections either to the possibility of a power so explicated or to its sufficiency for grounding an adequate account of human freedom. (shrink)

The problem of structure and agency has been the subject of intense debate in the social sciences for over 100 years. This book offers a solution. Using a critical realist version of the theory of emergence, Dave Elder-Vass argues that, instead of ascribing causal significance to an abstract notion of social structure or a monolithic concept of society, we must recognise that it is specific groups of people that have social structural power. Some of these groups are entities with (...) emergent causal powers, distinct from those of human individuals. Yet these powers also depend on the contributions of human individuals, and this book examines the mechanisms through which interactions between human individuals generate the causal powers of some types of social structures. The Causal Power of Social Structures makes particularly important contributions to the theory of human agency and to our understanding of normative institutions. (shrink)

This paper discusses several distinct process theories of causality offered in recent years by Phil Dowe and me. It addresses problems concerning the explication of causal process, causal interaction, and causal transmission, whether given in terms of transmission of marks, transmission of invariant or conserved quantities, or mere possession of conserved quantities. Renouncing the mark-transmission and invariant quantity criteria, I accept a conserved quantity theory similar to Dowe's--differing basically with respect to causal transmission. This paper also (...) responds to several fundamental constructive criticisms contained in Christopher Hitchcock's discussion of both the mark-transmission and the conserved quantity theories. (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 last two decades few topics in philosophy of science have received as much attention as mechanistic explanation. A significant motivation for these accounts is that scientists frequently use the term “mechanism” in their explanations of biological phenomena. While scientists appeal to a variety of causal concepts in their explanations, many philosophers argue or assume that all of these concepts are well understood with the single notion of mechanism. This reveals a significant problem with mainstream mechanistic accounts– although (...) philosophers use the term “mechanism” interchangeably with other causal concepts, this is not something that scientists always do. This paper analyses two causal concepts in biology–the notions of “mechanism” and “pathway”–and how they figure in biological explanation. I argue that these concepts have unique features, that they are associated with distinct strategies of causal investigation, and that they figure in importantly different types of explanation. (shrink)

Graphical AbstractMicrobiome research attributes to whole microbiomes a causal role in the occurrence of different health outcomes. I argue, following some distinctions about causal relationships and explanations made within a philosophical account of causation, the “interventionist account,” that such claims need more scrutiny.

Ernst Mayr’s classical work on the nature of causation in biology has had a huge influence on biologists as well as philosophers. Although his distinction between proximate and ultimate causation recently came under criticism from those who emphasize the role of development in evolutionary processes, the formal relationship between these two notions remains elusive. Using causal graph theory, this paper offers a unified framework to systematically translate a given “proximate” causal structure into an “ultimate” evolutionary response, and illustrates (...) evolutionary implications of various kinds of causal mechanisms including epigenetic inheritance, maternal effects, and niche construction. These results not only reveal the essential interplay between proximate and ultimate causation in the study of evolution, but also provide a formal method to evaluate or discover non-standard or yet unknown evolutionary phenomena. (shrink)

Book synopis: A collection of more than 30 specially commissioned essays, this volume surveys the work of the 17th-century philosopher-scientist commonly regarded as the founder of modern philosophy, while integrating unique essays detailing the context and impact of his work. Covers the full range of historical and philosophical perspectives on the work of Descartes Discusses his seminal contributions to our understanding of skepticism, mind-body dualism, self-knowledge, innate ideas, substance, causality, God, and the nature of animals Explores the philosophical significance of (...) his contributions to mathematics and science Concludes with a section on the impact of Descartes's work on subsequent philosophers. (shrink)

While scientific realism generally assumes that successful scientific explanations yield information about reality, realists also have to admit that not all information acquired in this way is equally well warranted. Some versions of scientific realism do this by saying that explanatory posits with which we have established some kind of causal contact are better warranted than those that merely appear in theoretical hypotheses. I first explicate this distinction by considering some general criteria that permit us to distinguish causal (...) warrant from theoretical warrant. I then apply these criteria to a specific case from particle physics, claiming that scientific realism has to incorporate the distinction between causal and theoretical warrant if it is to be an adequate stance in the philosophy of particle physics. (shrink)

Jaegwon Kim’s causal exclusion argument says that if all physical effects have sufficient physical causes, and no physical effects are caused twice over by distinct physical and mental causes, there cannot be any irreducible mental causes. In addition, Kim has argued that the nonreductive physicalist must give up completeness, and embrace the possibility of downward causation. This paper argues first that this extra argument relies on a principle of property individuation, which the nonreductive physicalist need not accept, and second (...) that once we get clear on overdetermination, there is a way to reject the exclusion principle upon which the causal exclusion argument depends, but third that this should not lead to the belief that mental causation is easily accounted for in terms of counterfactual dependencies. (shrink)

Ernst Mayr proposed a distinction between “proximate”, mechanistic, and “ultimate”, evolutionary, causes of biological phenomena. This dichotomy has influenced the thinking of many biologists, but it is increasingly perceived as impeding modern studies of evolutionary processes, including study of “niche construction” in which organisms alter their environments in ways supportive of their evolutionary success. Some still find value for this dichotomy in its separation of answers to “how?” versus “why?”questions about evolution. But “why is A?” questions about evolution necessarily take (...) the form “how does A occur?”, so this separation is illusory. Moreover, the dichotomy distorts our view of evolutionary causality, in that, contra Mayr, the action of natural selection, driven by genotype-phenotype-environment interactions which constitute adaptations, is no less “proximate” than the biological mechanisms which are altered by naturally selected genetic variants. Mayr’s dichotomy thus needs replacement by more realistic, mechanistic views of evolution. From a mechanistic viewpoint, there is a continuum of adaptations from those evolving as responses to unchanging environmental pressures to those evolving as the capacity for niche construction, and intermediate stages of this can be identified. Some biologists postulate an association of “phenotypic plasticity” (phenotype-environment covariation with genotype held constant) with capacity for niche construction. Both “plasticity” and niche construction comprise wide ranges of adaptive mechanisms, often fully heritable and resulting from case-specific evolution. Association of “plasticity” with niche construction is most likely to arise in systems wherein capacity for complex learning and behavioral flexibility have already evolved. (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)

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 distinction between causal role and selected effect functions is typically framed in terms of their respective explanatory roles. However, much of the controversy over functions in genomics takes place in an investigative, not an explanatory context. Specifically, the process of component-driven functional investigation begins with the designation of some genetic or epigenetic element as functional —i.e. not junk— because it possesses properties that, arguably, suggest some biologically interesting organismal effect. The investigative process then proceeds, in a bottom-up fashion, (...) to search for those effects. I argue that this process encounters a problem reminiscent of one that Gould and Lewontin associated with the adaptationist program. Just as their stereotypical adaptationst became trapped in the myopic pursuit of one selectionist hypothesis after another, so can the investigation of CR functions in genomics lead to an unending series putative organism-level CR functions for junk DNA. This is an acute problem for genomics, because eukaryotic genomes are littered with transposable elements and their deactivated descendants which often masquerade as interesting CR-functional components and it is experimentally onerous to determine whether they lack such a function. I further argue that selectionist reasoning about TE-host coevolutionary dynamics can greatly streamline the investigative process. Importantly, selectionist hypotheses need not be well confirmed to be illuminating in this context. Informed selectionist reasoning about the strategic roles of TEs in the genome offers a corrective to the idea that most of our DNA is somehow CR functional for the organism. (shrink)

There are two concepts of causes, property causation and token causation. The principle I want to discuss describes an epistemological connection between the two concepts, which I call the Connecting Principle. The rough idea is that if a token event of type Cis followed by a token event of type E, then the support of the hypothesis that the first event token caused the second increases as the strength of the property causal relation of C to E does. I (...) demonstrate the principle, illustrate its application to phylogenies, infections, and rumours, and discuss its consequence for the conceptual distinctness of causal processes from the events they connect. Although I am by no means confident that the Connecting Principle is ultimately correct, it seems to be a useful point of departure into an important aspect of the epistemology of causality. (shrink)

Causal compatibilism claims that even though physics is causally closed, and even though mental properties are multiply realizable and are not identical to physical causal properties, mental properties are causal properties nonetheless. This position asserts that there is genuine causation at multiple descriptive/ontological levels; physics-level causal claims are not really incompatible with mentalistic causal claims. I articulate and defend a version of causal compatibilism that incorporates three key contentions. First, causation crucially involves robust patterns (...) of counterfactual dependence among properties.Second, often several distinct such patterns, all subsuming a single phenomenon, exist at different descriptive/ontological levels (e.g., microphysical, neurobiological, macrobiological, and psychological). Third, the concept of causation is governed by an implicit contextual parameter that normally determines a specific descriptive/ontological level as the contextually relevant level, for the context-sensitive semantic evaluation of causal statements. (shrink)

According to one conception of strong emergence, strongly emergent properties are nomologically necessitated by their base properties and have novel causal powers relative to them. In this paper, I raise a difficulty for this conception of strong emergence, arguing that these two features are incompatible. Instead of presenting this as an objection to the friends of strong emergence, I argue that this indicates that there are distinct varieties of strong emergence: causal emergence and epiphenomenal emergence. I then explore (...) the prospects of emergentism with this distinction in the background. (shrink)

Do component forces exist in conjoined circumstances? Cartwright (1980) says no; Creary (1981) says yes. I'm inclined towards Cartwright's side in this matter, but find several problems with her argumentation. My primary aim here is to present a better, distinctly causal, argument against component forces: very roughly, I argue that the joint posit of component and resultant forces in conjoined circumstances gives rise to a threat of causal overdetermination, avoidance of which best proceeds via eliminativism about component forces. (...) A secondary aim is to show that rejecting component forces does not require, pace Cartwright, rejecting certain attractive theses about what laws of nature express and the role such laws play in scientific explanations. (shrink)

One contentious debate in the philosophy of biology is that between the statisticalists and causalists. The former understand core evolutionary concepts like fitness and selection to be mere statistical summaries of underlying causal processes. In this view, evolutionary changes cannot be causally explained by selection or fitness. The causalist side, on the other hand, holds that populations can change in response to selection—one can cite fitness differences or driftability in causal explanations of evolutionary change. But, on the causalist (...) side, it is often not clear how, precisely, one should understand these causes. Thus, much more could be said about what sort of causes fitness and driftability are. In this paper, I borrow Dretske's distinction between structuring and triggering causes and I suggest that fitness and driftability are structuring causes of evolution. (shrink)