Complex organisms thwart the simple rectilinear causality paradigm of “necessary and sufficient,” with its experimental strategy of “knock down and overexpress.” This Essay organizes the eccentricities of biology into four categories that call for new mathematical approaches; recaps for the biologist the philosopher's recent refinements to the causation concept and the mathematician's computational tools that handle some but not all of the biological eccentricities; and describes overlooked insights that make causal properties of physical hierarchies such as emergence and downward causation (...) straightforward. Reviewing and extrapolating from similar situations in physics, it is suggested that new mathematical tools for causation analysis incorporating feedback, signal cancellation, nonlinear dependencies, physical hierarchies, and fixed constraints rather than instigative changes will reveal unconventional biological behaviors. These include “eigenisms,” organisms that are limited to quantized states; trajectories that steer a system such as an evolving species toward optimal states; and medical control via distributed “sheets” rather than single control points. (shrink)

We construct a new measure of voting power that yields reasonable measurements even if the individual votes are not cast independently. Our measure hinges on probabilities of counterfactuals, such as the probability that the outcome of a collective decision would have been yes, had a voter voted yes rather than no as she did in the real world. The probabilities of such counterfactuals are calculated on the basis of causal information, following the approach by Balke and Pearl. Opinion leaders whose (...) votes have causal influence on other voters' votes can have significantly more voting power under our measure. But the new measure of voting power is also sensitive to the voting rule. We show that our measure can be regarded as an average treatment effect, we provide examples in which it yields intuitively plausible results and we prove that it reduces to Banzhaf voting power in the limiting case of independent and equiprobable votes. (shrink)

There is a tension between, on the one hand, the view that natural selection refers to individual-level causes, and on the other hand, the view that it refers to a population-level cause. In this article, I make the case for the individual-level cause view. I respond to recent claims made by McLoone that the individual-level cause view is inconsistent. I show that if one were to follow his arguments, any causal claim in any context would have to be regarded as (...) vindicating a form of population-level cause view. I show why this is implausible and how a consistent individual-level cause position can be held within the interventionist account of causation. Finally, I argue that there is one sense in which natural selection might be said to refer to population-level causes of evolutionary change. The upshot is that, as noted by others, natural selection can be regarded as referring to a population-level cause in the context of frequency-dependent selection and other situations of fitness-altering interactions between the individuals of a population. But whether this statement is true will depend on the empirical case investigated, not some a priori conceptual distinction. Thus, even though situations of frequency dependence might be ubiquitous, it is orthogonal to the conceptual question of whether frequency-independent natural selection—McLoone’s target—refers to individual- or population-level causes. (shrink)

Back in 1987 the physicist/theoretical biologist Walter Elsasser reviewed a range of philosophical issues at the foundation of organismal biology above the molecular level. Two of these are particularly relevant to quantifications of form: the concept of ordered heterogeneity and the principle of nonstructural memory, the truism that typically the forms of organisms substantially resemble the forms of their ancestors. This essay attempts to weave Elsasser’s principles together with morphometrics for one prominent data type, the representation of animal forms by (...) positions of landmark points. I introduce a new spectrum of pattern descriptors of the shape variation of landmark configurations, ranging from the most homogeneous through growth gradients and focal features to a model of totally disordered heterogeneity incompatible with the rhetoric of functional explanation. An investigation may end up reporting its findings by one of these descriptors or by several. These descriptors all derive from one shared diagrammatic device: a log–log plot of sample variance against one standard formalism of today’s geometric morphometrics, the bending energies of the principal warps that represent all the scales of variability around the sample average shape. The new descriptors, which I demonstrate over a variety of contemporary morphometric examples, may help build the bridge we urgently need between the arithmetic of today’s burgeoning image-based data resources and the rhetoric of biological explanations aligned with the principles of Elsasser along with an even earlier philosopher of biology, the Viennese visionary Hans Przibram. (shrink)

In this paper I investigate whether the phenomenon of quantum decoherence, the vanishing of interference and detectable entanglement on quantum systems in virtue of interactions with the environment, can be understood as the manifestation of a disposition. I will highlight the advantages of this approach as a realist interpretation of the quantum formalism, and demonstrate how such an approach can benefit from advances in the metaphysics of dispositions. I will also confront some commonalities with and differences to the many worlds (...) interpretation, and address the difficulties induced by quantum non-locality. I conclude that there are ways to deal with these issues and that the proposal hence is an avenue worth pursuing. (shrink)

Using Jim Woodward's Counterfactual Dependency account as an example, I argue that causal claims about indeterministic systems cannot be satisfactorily analysed as including counterfactual conditionals among their truth conditions because the counterfactuals such accounts must appeal to need not have truth values. Where this happens, counterfactual analyses transform true causal claims into expressions which are not true.

Various results show the ‘formal equivalence’ of kin and group selectionist methodologies, but this does not preclude there being a real and useful distinction between kin and group selection processes. I distinguish individual- and population-centred approaches to drawing such a distinction, and I proceed to develop the latter. On the account I advance, the differences between kin and group selection are differences of degree in the structural properties of populations. A spatial metaphor provides a useful framework for thinking about these (...) differences: kin and group selection may be conceptualized as large, overlapping regions of K - G space. I then consider some implications of the account, defend it from possible objections, and further argue that the structural features characteristic of both kin and group selection may recur at multiple levels of biological organization. (shrink)

The study tests the hypothesis that conditional probability judgments can be influenced by causal links between the target event and the evidence even when the statistical relations among variables are held constant. Three experiments varied the causal structure relating three variables and found that (a) the target event was perceived as more probable when it was linked to evidence by a causal chain than when both variables shared a common cause; (b) predictive chains in which evidence is a cause of (...) the hypothesis gave rise to higher judgments than diagnostic chains in which evidence is an effect of the hypothesis; and (c) direct chains gave rise to higher judgments than indirect chains. A Bayesian learning model was applied to our data but failed to explain them. An explanation-based hypothesis stating that statistical information will affect judgments only to the extent that it changes beliefs about causal structure is consistent with the results. (shrink)

Philosophical works on actual causation make wide use of thought experiments. The principal aim of this paper is to show how thought experiments are used in the contemporary debate over actual causation and to discuss their role in relation to formal approaches in terms of causal models. I claim that a recourse to thought experiments is not something old fashioned or superseded by abstract models, but it is useful to interpret abstract models themselves and to use our intuitions to judge (...) the results of the model. Recent research on actual causation has stressed the importance of integrating formal models with some notion of normality; I suggest that thought experiments can be useful in eliciting intuitions where normality is not intended in a statistical sense. The first expository part gives a short presentation of the notion of actual causation, summarising some typical problems of counterfactual approaches and how they are treated in causal and structural models. The second part focuses on the problems of model isomorphism and criticises some radical ideas opposing the role of thought experiments, claiming that they may also be of use in evaluating formal models. (shrink)

The definition of metabolic syndrome has been, and still is, extremely controversial. My purpose is not to give a solution to the associated debate but to argue that the controversy is at least partially due to the different ‘causal content’ of the various definitions: their theoretical validity and practical utility can be evaluated by reconstructing or making explicit the underlying causal structure. I will therefore propose to distinguish the alternative definitions according to the kinds of causal content they carry: definitions (...) grounded on associations, definitions presupposing a causal model built upon statistical associations, and definitions grounded on underlying mechanisms. I suggest that analysing definitions according to their causal content can be helpful in evaluating alternative definitions of some diseases. I want to show how the controversy over MetS suggests a distinction among three kinds of definitions based on how explicitly they characterise the syndrome in causal terms, and on the type of causality involved. I will call ‘type 1 definitions’ those definitions that are purely associative; ‘type 2 definitions’ the definitions based on statistical associations, plus generic medical and causal knowledge; and ‘type 3 definitions’ the definitions based on mechanisms. These kinds of definitions, although different, can be related to each other. A definition with more specific causal content may be useful in the evaluation of definitions characterised by a lower degree of causal specificity. Moreover, the identification of the type of causality involved is of help to constitute a good criterion for choosing among different definitions of a pathological entity. In section I introduce the controversy about MetS, in section I propose some remarks about medical definitions and their ‘causal import’, and in section I suggest that the different attitudes towards the definition of MetS are relevant to evaluate their explicative power. (shrink)

Popper’s introduction of ‘‘propensity’’ was intended to provide a solid conceptual foundation for objective single-case probabilities. By considering the partly opposed contributions of Humphreys and Miller and Salmon, it is argued that when properly understood, propensities can in fact be understood as objective single-case causal probabilities of transitions between concrete events. The chief claim is that propensities are well-explicated by describing how they fit into the existing formal theory of branching space-times, which is simultaneously indeterministic and causal. Several problematic examples, (...) some commonsense and some quantum-mechanical, are used to make clear the advantages of invoking branching space-times theory in coming to understand propensities. (shrink)

In this paper, we examine the causal framework within which integrated information theory of consciousness makes it claims. We argue that, in its current formulation, IIT is threatened by the causal exclusion problem. Some proponents of IIT have attempted to thwart the causal exclusion problem by arguing that IIT has the resources to demonstrate genuine causal emergence at macro scales. In contrast, we argue that their proposed solution to the problem is damagingly circular as a result of inter-defining information and (...) causation. As a solution, we propose that IIT should adopt the specific interventionist causal framework that we offer and show how IIT can harness this interventionist framework to avoid the causal exclusion problem. We demonstrate how our argument remains fully compatible with the methodology, empirical data, and conceptual aims of the theory. (shrink)

While standard procedures of causal reasoning as procedures analyzing causal Bayesian networks are custom-built for (non-deterministic) probabilistic struc- tures, this paper introduces a Boolean procedure that uncovers deterministic causal structures. Contrary to existing Boolean methodologies, the procedure advanced here successfully analyzes structures of arbitrary complexity. It roughly involves three parts: first, deterministic dependencies are identified in the data; second, these dependencies are suitably minimalized in order to eliminate redundancies; and third, one or—in case of ambiguities—more than one causal structure is (...) assigned to the minimalized deterministic dependencies. (shrink)

It has become a popular view among non-reductive physicalists that it is possible to devise empirical tests generating evidence for the causal efficacy of the mental, whereby the exclusion worries that have haunted the position of non-reductive physicalism for decades can be dissolved once and for all. This paper aims to show that these evidentialist hopes are vain. I argue that, if the mental is taken to supervene non-reductively on the physical, there cannot exist empirical evidence for its causal efficacy. (...) While causal structures without non-reductive supervenience relations can be conclusively identified in ideal discovery circumstances, it is impossible, in principle, to generate evidence that would favour models with mental causation over models without. Ascribing causal efficacy to the mental, for the non-reductive physicalist, is a modelling choice that must be made on the basis of metaphysical background theories or pragmatic maxims guiding the selection among empirically indistinguishable models. (shrink)

This paper addresses a problem that arises when it comes to inferring deterministic causal chains from pertinent empirical data. It will be shown that to every deterministic chain there exists an empirically equivalent common cause structure. Thus, our overall conviction that deterministic chains are one of the most ubiquitous (macroscopic) causal structures is underdetermined by empirical data. It will be argued that even though the chain and its associated common cause model are empirically equivalent there exists an important asymmetry between (...) the two models with respect to model expansions. This asymmetry might constitute a basis on which to disambiguate corresponding causal inferences on non-empirical grounds. (shrink)

In recent years, the debate on the problem of causal exclusion has seen an ‘interventionist turn’. Numerous non-reductive physicalists (e.g. Shapiro and Sober 2007) have argued that Woodward's (2003) interventionist theory of causation provides a means to empirically establish the existence of non-reducible mental-to-physical causation. By contrast, Baumgartner (2010) has presented an interventionist exclusion argument showing that interventionism is in fact incompatible with non-reductive physicalism. In response, a number of revised versions of interventionism have been suggested that are compatible with (...) non-reductive physicalism. The first part of this paper reconstructs the definitional details of these modified interventionist theories. The second part investigates whether the modification proposed in Woodward (2011) is not only compatible with, but moreover supports non-reductive physicalism. In particular, it is examined whether that newest variant of interventionism allows for empirically resolving the problem of causal exclusion as envisaged by Shapiro, Sober and others. (shrink)

An actual cause of some token effect is itself a token event that helped to bring about that effect. The notion of an actual cause is different from that of a potential cause – for example a pre-empted backup – which had the capacity to bring about the effect, but which wasn't in fact operative on the occasion in question. Sometimes actual causes are also distinguished from mere background conditions: as when we judge that the struck match was a cause (...) of the fire, while the presence of oxygen was merely part of the relevant background against which the struck match operated. Actual causation is also to be distinguished from type causation: actual causation holds between token events in a particular, concrete scenario; type causation, by contrast, holds between event kinds in scenario kinds. (shrink)

The essential precondition of implementing interventionist techniques of causal reasoning is that particular variables are identified as so-called intervention variables. While the pertinent literature standardly brackets the question how this can be accomplished in concrete contexts of causal discovery, the first part of this paper shows that the interventionist nature of variables cannot, in principle, be established based only on an interventionist notion of causation. The second part then demonstrates that standard observational methods that draw on Bayesian networks identify intervention (...) variables only if they also answer the questions that can be answered by interventionist techniques—which are thus rendered dispensable. The paper concludes by suggesting a way of identifying intervention variables that allows for exploiting the whole inferential potential of interventionist techniques. (shrink)

While ideal interventions are acknowledged by many as valuable tools for the analysis of causation, recent discussions have shown that, since there are no ideal interventions on upper-level phenomena that non-reductively supervene on their underlying mechanisms, interventions cannot—contrary to a popular opinion—ground an informative analysis of constitution. This has led some to abandon the project of analyzing constitution in interventionist terms. By contrast, this paper defines the notion of a horizontally surgical intervention, and argues that, when combined with some innocuous (...) metaphysical principles about the relation between upper and lower levels of mechanisms, that notion delivers a sufficient condition for constitution. This, in turn, strengthens the case for an interventionist analysis of constitution. (shrink)

The first part of this paper argues that if Craver’s ([2007a], [2007b]) popular mutual manipulability account (MM) of mechanistic constitution is embedded within Woodward’s ([2003]) interventionist theory of causation--for which it is explicitly designed--it either undermines the mechanistic research paradigm by entailing that there do not exist relationships of constitutive relevance or it gives rise to the unwanted consequence that constitution is a form of causation. The second part shows how Woodward’s theory can be adapted in such a way that (...) (MM) neither undermines the mechanistic paradigm nor reduces constitution to causation. However, it turns out that this modified theoretical embedding of (MM) makes it impossible to produce empirical evidence for constitutive relations. The paper ends by suggesting an additional criterion, the fat-handedness criterion, which, when combined with (MM), generates indirect empirical evidence for constitutive relevance. (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)

The majority of the currently flourishing theories of actual causation are located in a broadly counterfactual framework that draws on structural equations. In order to account for cases of symmetric overdeterminiation and preemption, these theories resort to rather intricate analytical tools, most of all, to what Hitchcock has labeled explicitly nonforetracking counterfactuals. This paper introduces a regularity theoretic approach to actual causation that only employs material conditionals, standard Boolean minimization procedures, and a stability condition that regulates the behavior of causal (...) models under model expansions. Notwithstanding its lightweight analytical toolbox, this regularity theory performs at least as well as the structural equations accounts with their heavy appliances. (shrink)

The first part of this paper finds Craver’s (2007) mutual manipulability theory (MM) of constitution inadequate, as it definitionally ties constitution to the feasibility of idealized experiments, which, however, are unrealizable in principle. As an alternative, the second part develops an abductive theory of constitution (NDC), which exploits the fact that phenomena and their constituents are unbreakably coupled via common causes. The best explanation for this common-cause coupling is the existence of an additional dependence relation, viz. constitution. Apart from adequately (...) capturing the essential characteristics of constitution missed by MM, NDC has important ramifications for constitutional discovery—most notably, that there is no experimentum crucis for constitution, not even under ideal discovery circumstances. (shrink)

There are three distinct questions associated with Simpson's paradox, (i) Why or in what sense is Simpson's paradox a paradox? (ii) What is the proper analysis of the paradox? (iii) How one should proceed when confronted with a typical case of the paradox? We propose a "formar" answer to the first two questions which, among other things, includes deductive proofs for important theorems regarding Simpson's paradox. Our account contrasts sharply with Pearl's causal (and questionable) account of the first two questions. (...) We argue that the "how to proceed question?" does not have a unique response, and that it depends on the context of the problem. We evaluate an objection to our account by comparing ours with Blyth's account of the paradox. Our research on the paradox suggests that the "how to proceed question" needs to be divorced from what makes Simpson's paradox "paradoxical.". (shrink)

Neutral monism is a position in metaphysics defended by Mach, James, and Russell in the early twentieth century. It holds that minds and physical objects are essentially two different orderings of the same underlying neutral elements of nature. This paper sets out some of the central concepts, theses and the historical background of ideas that inform this doctrine of elements. The discussion begins with the classic neutral monism of Mach, James, and Russell in the first part of the paper, then (...) considers recent neo-Russellian versions in the second half. The chances for a revival of neutral monism are probably slight; its key ideas and starting points lie far from those in contemporary philosophy of mind. A better route might be through the philosophy of science and a deeper understanding of causation. (shrink)

Current debates surrounding the virtues and shortcomings of randomization are symptomatic of a lack of appreciation of the fact that causation can be inferred by two distinct inference methods, each requiring its own, specific experimental design. There is a non-statistical type of inference associated with controlled experiments in basic biomedical research; and a statistical variety associated with randomized controlled trials in clinical research. I argue that the main difference between the two hinges on the satisfaction of the comparability requirement, which (...) is in turn dictated by the nature of the objects of study, namely homogeneous or heterogeneous populations of biological systems. Among other things, this entails that the objection according to which randomized experiments fail to provide better evidence for causation because randomization cannot guarantee comparability is mistaken. (shrink)

The notion of probabilistic support is beset by well-known problems. In this paper we add a new one to the list: the problem of transitivity. Tomoji Shogenji has shown that positive probabilistic support, or confirmation, is transitive under the condition of screening off. However, under that same condition negative probabilistic support, or disconfirmation, is intransitive. Since there are many situations in which disconfirmation is transitive, this illustrates, but now in a different way, that the screening-off condition is too restrictive. We (...) therefore weaken this condition to what we call ‘partial’ screening off. We show that the domain defined by partial screening off comprises two mutually exclusive subdomains. In one subdomain disconfirmation is indeed transitive, but confirmation is then intransitive. In the other, confirmation is transitive, but here disconfirmation is once more intransitive. (shrink)

The relationship between individual and population health is partially built on the broad dichotomization of medicine into clinical medicine and public health. Potential drawbacks of current views include seeing both individual and population health as absolute and independent concepts. I will argue that the relationship between individual and population health is largely relative and dynamic. Their interrelated dynamism derives from a causally defined life course perspective on health determination starting from an individual’s conception through growth, development and participation in the (...) collective till death, all seen within the context of an adaptive society. Indeed, it will become clear that neither individual nor population health is identifiable or even definable without informative contextualization within the other. For instance, a person’s health cannot be seen in isolation but must be placed in the rich contextual web such as the socioeconomic circumstances and other health determinants of where they were conceived, born, bred, and how they shaped and were shaped by their environment and communities, especially given the prevailing population health exposures over their lifetime. We cannot discuss the “what” and “how much” of individual and population health until we know the cumulative trajectories of both, using appropriate causal language. (shrink)

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

Weber argues that causal modelers face a dilemma when they attempt to model systems in which the underlying mechanism operates according to some set of differential equations. The first horn is that causal models of these systems leave out certain causal effects. The second horn is that causal models of these systems leave out time-dependent derivatives, and doing so distorts reality. Either way causal models of these systems leave something important out. I argue that Weber’s reasons for thinking causal modeling (...) is limited in this domain are lacking. (shrink)

Even though the evidence‐based medicine movement (EBM) labels mechanisms a low quality form of evidence, consideration of the mechanisms on which medicine relies, and the distinct roles that mechanisms might play in clinical practice, offers a number of insights into EBM itself. In this paper, I examine the connections between EBM and mechanisms from several angles. I diagnose what went wrong in two examples where mechanistic reasoning failed to generate accurate predictions for how a dysfunctional mechanism would respond to intervention. (...) I then use these examples to explain why we should expect this kind of mechanistic reasoning to fail in systematic ways, by situating these failures in terms of evolved complexity of the causal system(s) in question. I argue that there is still a different role in which mechanisms continue to figure as evidence in EBM: namely, in guiding the application of population‐level recommendations to individual patients. Thus, even though the evidence‐based movement rejects one role in which mechanistic reasoning serves as evidence, there are other evidentiary roles for mechanistic reasoning. This renders plausible the claims of some critics of evidencebased medicine who point to the ineliminable role of clinical experience. Clearly specifying the ways in which mechanisms and mechanistic reasoning can be involved in clinical practice frames the discussion about EBM and clinical experience in more fruitful terms. (shrink)

In this field guide, I distinguish five separate senses with which the term ‘mechanism’ is used in contemporary philosophy of science. Many of these senses have overlapping areas of application but involve distinct philosophical claims and characterize the target mechanisms in relevantly different ways. This field guide will clarify the key features of each sense and introduce some main debates, distinguishing those that transpire within a given sense from those that are best understood as concerning two distinct senses. The ‘new (...) mechanisms’ sense is the primary sense from which other senses will be distinguished. In part II of this field guide, I consider three further senses of the term that are ontologically ‘flat’ or at least not explicitly hierarchical in character: equations in structural equation models of causation, causal-physical processes, and information-theoretic constraints on states available to systems. After characterizing each sense, I clarify its ontological commitments, its methodological implications, how it figures in explanations, its implications for reduction, and the key manners in which it differs from other senses of mechanism. I conclude that there is no substantive core meaning shared by all senses, and that debates in contemporary philosophy of science can benefit from clarification regarding precisely which sense of mechanism is at stake. (shrink)

In the recent literature on causal and non-causal scientific explanations, there is an intuitive assumption according to which an explanation is non-causal by virtue of being abstract. In this context, to be ‘abstract’ means that the explanans in question leaves out many or almost all causal microphysical details of the target system. After motivating this assumption, we argue that the abstractness assumption, in placing the abstract and the causal character of an explanation in tension, is misguided in ways that are (...) independent of which view of causation or causal explanation one takes to be most accurate. On major accounts of causation, as well as on major accounts of causal explanation, the abstractness of an explanation is not sufficient for it being non-causal. That is, explanations are not non-causal by dint of being abstract. (shrink)

Showcasing original arguments for well-defined positions, as well as clear and concise statements of sophisticated philosophical views, this volume is an ...

I use a contrastive theory of causal explanation to analyze the notion of a genetic trait. The resulting definition is relational, an implication of which is that no trait is genetic always and everywhere. Rather, every trait may be either genetic or non-genetic, depending on explanatory context. I also outline some other advantages of connecting the debate to the wider causation literature, including how that yields us an account of the distinction between genetic traits and genetic dispositions.

Russell famously argued that causation should be dispensed with. He gave two explicit arguments for this conclusion, both of which can be defused if we loosen the ties between causation and determinism. I show that we can define a concept of causation which meets Russell’s conditions but does not reduce to triviality. Unfortunately, a further serious problem is implicit beneath the details of Russell’s arguments, which I call the causal exclusion problem. Meeting this problem involves deploying a minimalist pragmatic account (...) of the nature and function of modal language. Russell’s scruples about causation can be accommodated, even as we partially legitimise the pervasive causal explanations in folk and scientific practice. (shrink)

Laws of nature take center stage in philosophy of science. Laws are usually believed to stand in a tight conceptual relation to many important key concepts such as causation, explanation, confirmation, determinism, counterfactuals etc. Traditionally, philosophers of science have focused on physical laws, which were taken to be at least true, universal statements that support counterfactual claims. But, although this claim about laws might be true with respect to physics, laws in the special sciences (such as biology, psychology, economics etc.) (...) appear to have—maybe not surprisingly—different features than the laws of physics. Special science laws—for instance, the economic law “Under the condition of perfect competition, an increase of demand of a commodity leads to an increase of price, given that the quantity of the supplied commodity remains constant” and, in biology, Mendel's Laws—are usually taken to “have exceptions”, to be “non-universal” or “to be ceteris paribus laws”. How and whether the laws of physics and the laws of the special sciences differ is one of the crucial questions motivating the debate on ceteris paribus laws. Another major, controversial question concerns the determination of the precise meaning of “ceteris paribus”. Philosophers have attempted to explicate the meaning of ceteris paribus clauses in different ways. The question of meaning is connected to the problem of empirical content, i.e., the question whether ceteris paribus laws have non-trivial and empirically testable content. Since many philosophers have argued that ceteris paribus laws lack empirically testable content, this problem constitutes a major challenge to a theory of ceteris paribus laws. (shrink)

Casini, Illari, Russo, and Williamson (2011) suggest to model mechanisms by means of recursive Bayesian networks (RBNs) and Clarke, Leuridan, and Williamson (2014) extend their modelling approach to mechanisms featuring causal feedback. One of the main selling points of the RBN approach should be that it provides answers to questions concerning manipulation and control. In this paper I demonstrate that the method to compute the effects of interventions the authors mentioned endorse leads to absurd results under the additional assumption of (...) faithfulness, which can be expected to hold for many RBN models of mechanisms. (shrink)

Arguably no concept is more fundamental to science than that of causality, for investigations into cases of existence, persistence, and change in the natural world are largely investigations into the causes of these phenomena. Yet the metaphysics and epistemology of causality remain unclear. For example, the ontological categories of the causal relata have been taken to be objects (Hume 1739), events (Davidson 1967), properties (Armstrong 1978), processes (Salmon 1984), variables (Hitchcock 1993), and facts (Mellor 1995). (For convenience, causes and effects (...) will usually be understood as events in what follows.) Complicating matters, causal relations may be singular (Socrates’s drinking hemlock caused Socrates’s death) or general (Drinking hemlock causes death); hence the relata might be tokens (e.g., instances of properties) or types (e.g., types of events) of the category in question. Other questions up for grabs are: Are singular causes metaphysically and/or epistemologically prior to general causes or vice versa (or neither)? What grounds the intuitive asymmetry of the causal relation? Are macro-causal relations reducible to micro-causal relations? And perhaps most importantly: Are causal facts (e.g., the holding of causal relations) reducible to non-causal facts (e.g., the holding of certain spatiotemporal relations)? (shrink)

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

In this paper I offer a criticism of Carnap's inductive logic which also applies to other formal methods of inductive inference. Criticisms of Carnap's views have typically centered upon the justification of his particular choice of inductive method. I argue that the real problem is not that there is an agreed upon method for which no justification can be found, but that different methods are justified in different circumstances.

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)

Tim Crane's ‘Cosmic Hermeneutics vs. Emergence: The Challenge of the Explanatory Gap’ claims that non‐reductive physicalism must either close the explanatory gap, addressing the challenge famously posed by Levine's argument, or become identical to emergentism. Since no way to close the gap is available, the result is that there can be no interesting philosophical position intermediate between physicalism and emergentism. This chapter argues that if we look at the relation between physicalism and emergentism from the vantage point of reduction, Crane's (...) analysis is rather persuasive. However, if we switch from reduction to causality, its conclusions appear more disputable. In particular, if we shift from ‘novelty and explanation’ to ‘novelty and causality’ as key features of emergent properties, we may introduce a distinction between two kinds of emergentism (moderate and radical) based on their attitude towards the causal inheritance principle. If the causal inheritance principle is accepted (some versions of) moderate emergentism may be considered as non‐trivial forms of non‐reductive physicalism. (shrink)

My aim in this paper is to make a case for the singularist view from the perspective of a mechanical theory of causation, and to explain what, from this perspective, causal generalizations mean, and what role they play within the mechanical theory.

Scientific explanation is an important goal of scientific practise. Philosophers have proposed a striking diversity of seemingly incompatible accounts of explanation, from deductive-nomological to statistical relevance, unification, pragmatic, causal-mechanical, mechanistic, causal intervention, asymptotic, and model-based accounts. In this dissertation I apply two novel methods to reexamine our evidence about scientific explanation in practise and thereby address the fragmentation of philosophical accounts. I start by collecting a data set of 781 articles from one year of the journal Science. Using automated text (...) mining techniques I measure the frequency and distribution of several groups of philosophically interesting words, such as "explain", "cause", "evidence", "theory", "law", "mechanism", and "model". I show that "explain" words are much more common in scientific writing than in other genres, occurring in roughly half of all articles, and that their use is very often qualified or negated. These results about the use of words complement traditional conceptual analysis. Next I use random samples from the data set to develop a large number of small case studies across a wide range of scientific disciplines. I use a sample of "explain" sentences to develop and defend a new general philosophical account of scientific explanation, and then test my account against a larger set of randomly sampled sentences and abstracts. Five coarse categories can classify the explanans and explananda of my cases: data, entities, kinds, models, and theories. The pair of the categories of the explanans and explanandum indicates the "form" of an explanation. The explain-relation supports counterfactual reasoning about the dependence of qualities of the explanandum on qualities of the explanans. But for each form there is a different "core relation" between explanans and explanandum that supports the explain-relation. Causation, modelling, and argument are the core relations for different forms of scientific explanation between different categories of explanans and explananda. This flexibility allows me to resolve some of the fragmentation in the philosophical literature. I provide empirical evidence to show that my general philosophical account successfully describes a wide range of scientific practise across a large number of scientific disciplines. (shrink)

As the demand for explainable deep learning grows in the evaluation of language technologies, the value of a principled grounding for those explanations grows as well. Here we study the state-of-the-art in explanation for neural models for natural-language processing (NLP) tasks from the viewpoint of philosophy of science. We focus on recent evaluation work that finds brittleness in explanations obtained through attention mechanisms.We harness philosophical accounts of explanation to suggest broader conclusions from these studies. From this analysis, we assert the (...) impossibility of causal explanations from attention layers over text data. We then introduce NLP researchers to contemporary philosophy of science theories that allow robust yet non-causal reasoning in explanation, giving computer scientists a vocabulary for future research. (shrink)

There are three questions associated with Simpson’s Paradox (SP): (i) Why is SP paradoxical? (ii) What conditions generate SP?, and (iii) What should be done about SP? By developing a logic-based account of SP, it is argued that (i) and (ii) must be divorced from (iii). This account shows that (i) and (ii) have nothing to do with causality, which plays a role only in addressing (iii). A counterexample is also presented against the causal account. Finally, the causal and logic-based (...) approaches are compared by means of an experiment to show that SP is not basically causal. (shrink)