Evidence-based medicine (EBM) makes use of explicit procedures for grading evidence for causal claims. Normally, these procedures categorise evidence of correlation produced by statistical trials as better evidence for a causal claim than evidence of mechanisms produced by other methods. We argue, in contrast, that evidence of mechanisms needs to be viewed as complementary to, rather than inferior to, evidence of correlation. In this paper we first set out the case for treating evidence of mechanisms alongside evidence of correlation in (...) explicit protocols for evaluating evidence. Next we provide case studies which exemplify the ways in which evidence of mechanisms complements evidence of correlation in practice. Finally, we put forward some general considerations as to how the two sorts of evidence can be more closely integrated by EBM. (shrink)

In this paper we give a positive answer to a problem posed by Hofer-Szabó and Rédei (Int. J. Theor. Phys. 43:1819–1826, 2004) regarding the existence of infinite Reichenbachian common cause systems (RCCSs). An example of a countably infinite RCCS is presented. It is also determined that no RCCSs of greater cardinality exist.

Mechanistic philosophy of science views a large part of scientific activity as engaged in modelling mechanisms. While science textbooks tend to offer qualitative models of mechanisms, there is increasing demand for models from which one can draw quantitative predictions and explanations. Casini et al. (Theoria 26(1):5–33, 2011) put forward the Recursive Bayesian Networks (RBN) formalism as well suited to this end. The RBN formalism is an extension of the standard Bayesian net formalism, an extension that allows for modelling the hierarchical (...) nature of mechanisms. Like the standard Bayesian net formalism, it models causal relationships using directed acyclic graphs. Given this appeal to acyclicity, causal cycles pose a prima facie problem for the RBN approach. This paper argues that the problem is a significant one given the ubiquity of causal cycles in mechanisms, but that the problem can be solved by combining two sorts of solution strategy in a judicious way. (shrink)

The mechanistic and causal accounts of explanation are often conflated to yield a ‘causal-mechanical’ account. This paper prizes them apart and asks: if the mechanistic account is correct, how can causal explanations be explanatory? The answer to this question varies according to how causality itself is understood. It is argued that difference-making, mechanistic, dualist and inferentialist accounts of causality all struggle to yield explanatory causal explanations, but that an epistemic account of causality is more promising in this regard.

According to Russo and Williamson (Int Stud Philos Sci 21(2):157–170, 2007, Hist Philos Life Sci 33:389–396, 2011a, Philos Sci 1(1):47–69, 2011b ), in order to establish a causal claim of the form, ‘_C_ is a cause of _E_’, one typically needs evidence that there is an underlying mechanism between _C_ and _E_ as well as evidence that _C_ makes a difference to _E_. This thesis has been used to argue that hierarchies of evidence, as championed by evidence-based movements, tend to (...) give primacy to evidence of difference making over evidence of mechanisms and are flawed because the two sorts of evidence are required and they should be treated on a par. An alternative approach gives primacy to evidence of mechanism over evidence of difference making. In this paper, we argue that this alternative approach is equally flawed, again because both sorts of evidence need to be treated on a par. As an illustration of this parity, we explain how scientists working in the ‘EnviroGenomarkers’ project constantly make use of the two evidential components in a dynamic and intertwined way. We argue that such an interplay is needed not only for causal assessment but also for policy purposes. (shrink)

The failure to recognize a correlation as spurious can lead people to adopt strategies to bring about a specific outcome that manipulate something other than a cause of the outcome. However, in a 2008 paper appearing in the journal Analysis, Bert Leuridan, Erik Weber and Maarten Van Dyck suggest that knowledge of spurious correlations can, at least sometimes, justify adopting a strategy aiming at bringing about some change. This claim is surprising and, if true, throws into question the claim of (...) Nancy Cartwright and others that knowledge of laws of association is insufficient for distinguishing effective and ineffective strategies. This paper examines the nature of spurious correlations and their value in crafting strategies for change. The conclusion of the paper is that while knowledge of a spurious correlation may have practical value, the value depends on either having knowledge of the causal structure underlying the correlation or it depends on the use of ‘causal criteria’. (shrink)

Part I of this paper introduced a range of mechanistic theories of causality, including process theories and the complex-systems theories, and some of the problems they face. Part II argues that while there is a decisive case against a purely mechanistic analysis, a viable theory of causality must incorporate mechanisms as an ingredient, and describes one way of providing an analysis of causality which reaps the rewards of the mechanistic approach without succumbing to its pitfalls.

Additionally, the text shows how to develop computationally feasible methods to mesh with this framework.

The paper considers the legal tools that have been developed in German pharmaceutical regulation as a result of the precautionary attitude inaugurated by the Contergan decision. These tools are the notion of “well-founded suspicion”, which attenuates the requirements for safety intervention by relaxing the requirement of a proved causal connection between danger and source, and the introduction of the reversal of proof burden in liability norms. The paper focuses on the first and proposes seeing the precautionary principle as an instance (...) of the requirement that one should maximise expected utility. In order to maximise expected utility certain probabilities are required and it is argued that objective Bayesianism offers the most plausible means to determine the optimal decision in cases where evidence supports diverging choices. (shrink)

The notion of ‘causal web’ emerged in the epidemiological literature in the early Sixties and had to wait until the Nineties for a thorough critical appraisal. Famously, Nancy Krieger argued that such a notion isn’t helpful unless we specify what kind of spiders create the webs. This means, according to Krieger, (i) that the role of the spiders is to provide an explanation of the yarns of the web and (ii) that the sought spiders have to be biological and social. (...) This paper contributes to the development of the notion of causal web, elaborating on the two following points: (i) to catch the spiders we need multi-fold evidence—specifically, mechanistic and difference-making—and (ii) for the eco-social to be explanatory, the web has to be mechanistic in a sense to be specified. (shrink)

Hájek has recently presented the following paradox. You are certain that a cable guy will visit you tomorrow between 8 a.m. and 4 p.m. but you have no further information about when. And you agree to a bet on whether he will come in the morning interval (8, 12] or in the afternoon interval (12, 4). At first, you have no reason to prefer one possibility rather than the other. But you soon realise that there will definitely be a future (...) time at which you will (rationally) assign higher probability to an afternoon arrival than a morning one, due to time elapsing. You are also sure there may not be a future time at which you will (rationally) assign a higher probability to a morning arrival than an afternoon one. It would therefore appear that you ought to bet on an afternoon arrival. The paradox is based on the apparent incompatibility of the principle of expected utility and principles of diachronic rationality which are prima facie plausible. Hájek concludes that the latter are false, but doesn't provide a clear diagnosis as to why. We endeavour to further our understanding of the paradox by providing such a diagnosis. (shrink)

The paper examines definitions of ‘cause’ in the epidemiological literature. Those definitions all describe causes as factors that make a difference to the distribution of disease or to individual health status. In the philosophical jargon, causes in epidemiology are difference-makers. Two claims are defended. First, it is argued that those definitions underpin an epistemology and a methodology that hinge upon the notion of variation, contra the dominant Humean paradigm according to which we infer causality from regularity. Second, despite the fact (...) that causes be defined in terms of ‘difference-making’, this cannot fixes the causal metaphysics. Causality in epidemiology ought to be interpreted according to the epistemic theory. In this approach relations are deemed causal depending on the evidence and on the available methods. Indeed, evidence to establish causal claims requires difference-making considerations; furthermore, those definitions of cause reflect the ‘variational’ epistemology and methodology of epidemiology. (shrink)

All univocal analyses of causation face counterexamples. An attractive response to this situation is to become a pluralist about causal relationships. "Causal pluralism" is itself, however, a pluralistic notion. In this article, I argue in favor of pluralism about concepts of cause in the social sciences. The article will show that evidence for, inference from, and the purpose of causal claims are very closely linked. Key Words: causation • pluralism • evidence • methodology.

I put forward several desiderata that a philosophical theory of causality should satisfy: it should account for the objectivity of causality, it should underpin formalisms for causal reasoning, it should admit a viable epistemology, it should be able to cope with the great variety of causal claims that are made, and it should be ontologically parsimonious. I argue that Nancy Cartwright’s dispositional account of causality goes part way towards meeting these criteria but is lacking in important respects. I go on (...) to argue that my epistemic account, which ties causal relationships to an agent’s knowledge and ignorance, performs well in the light of the desiderata. Such an account, I claim, is all we require from a theory of causality. (shrink)

We argue that the health sciences make causal claims on the basis of evidence both of physical mechanisms, and of probabilistic dependencies. Consequently, an analysis of causality solely in terms of physical mechanisms or solely in terms of probabilistic relationships, does not do justice to the causal claims of these sciences. Yet there seems to be a single relation of cause in these sciences - pluralism about causality will not do either. Instead, we maintain, the health sciences require a theory (...) of causality that unifies its mechanistic and probabilistic aspects. We argue that the epistemic theory of causality provides the required unification. (shrink)

Bayesian epistemology addresses epistemological problems with the help of the mathematical theory of probability. It turns out that the probability calculus is especially suited to represent degrees of belief (credences) and to deal with questions of belief change, confirmation, evidence, justification, and coherence. Compared to the informal discussions in traditional epistemology, Bayesian epis- temology allows for a more precise and fine-grained analysis which takes the gradual aspects of these central epistemological notions into account. Bayesian epistemology therefore complements traditional epistemology; it (...) does not re- place it or aim at replacing it. (shrink)

Philosophical analyses of causation have been centred on the question of what causation is. More precisely speaking, philosophers tend to address four different issues: metaphysical (what is causation out there?), epistemological (how can a causal claim be established and assessed?), conceptual (what does the word ‘cause’ mean?), and methodological (what methods ought one to use in order to establish and assess causal claims?). This chapter argues that the practical issue of causation (what is a causal claim for in practice?) is (...) highly relevant to the metaphysical, epistemological, conceptual, and methodological issues of causation. Any philosophical enquiry into causation without an examination of this practical issue is incomplete. In other words, a promising approach to causation ought to take all of the metaphysical, epistemological, conceptual, methodological, and practical issues into account. (shrink)

Theory of illness causation is an important issue in all biomedical sciences, and solid etiological explanations are needed in order to develop therapeutic approaches in medicine and preventive interventions in public health. Until now, the literature about the theoretical underpinnings of illness causation research has been scarce and fragmented, and lacking a convenient summary. This interdisciplinary book provides a convenient and accessible distillation of the current status of research into this developing field, and adds a personal flavor to the discussion (...) by proposing the etiological stance as a comprehensive approach to identify modifiable causes of illness. (shrink)

The epistemic probability of A given B is the degree to which B evidentially supports A, or makes A plausible. This paper is a first step in answering the question of what determines the values of epistemic probabilities. I break this question into two parts: the structural question and the substantive question. Just as an object’s weight is determined by its mass and gravitational acceleration, some probabilities are determined by other, more basic ones. The structural question asks what probabilities are (...) not determined in this way—these are the basic probabilities which determine values for all other probabilities. The substantive question asks how the values of these basic probabilities are determined. I defend an answer to the structural question on which basic probabilities are the probabilities of atomic propositions conditional on potential direct explanations. I defend this against the view, implicit in orthodox mathematical treatments of probability, that basic probabilities are the unconditional probabilities of complete worlds. I then apply my answer to the structural question to clear up common confusions in expositions of Bayesianism and shed light on the “problem of the priors.”. (shrink)

Permissivism is the view that there are evidential situations that rationally permit more than one attitude toward a proposition. In this paper, I argue for Intrapersonal Belief Permissivism (IaBP): that there are evidential situations in which a single agent can rationally adopt more than one belief-attitude toward a proposition. I give two positive arguments for IaBP; the first involves epistemic supererogation and the second involves doubt. Then, I should how these arguments give intrapersonal permissivists a distinct response to the toggling (...) objection. I conclude that IaBP is a view that philosophers should take seriously. (shrink)

Philosophy of medicine has traditionally examined two issues: the scientific ontology for medicine and the epistemic significance of the types of evidence used in medical research. In answering each question, philosophers have typically brought to bear tools from traditional analytic philosophy. In contrast, this volume explores medical knowledge from the perspective offered by social epistemology.While many of the same issues are addressed, the approach to these issues generates both fresh questions and new insights into old debates. In addition, the broader (...) purview offered by social epistemology opens up opportunities to address new topics such as the role of consensus conferences, epistemic injustice, the value of medical knowledge, continuing medical education, and industry funding. This article situates and summarizes the contributions to this special issue. (shrink)

We consider the use of interventions for resolving a problem of unidentified statistical models. The leading examples are from latent variable modelling, an influential statistical tool in the social sciences. We first explain the problem of statistical identifiability and contrast it with the identifiability of causal models. We then draw a parallel between the latent variable models and Bayesian networks with hidden nodes. This allows us to clarify the use of interventions for dealing with unidentified statistical models. We end by (...) discussing the philosophical and methodological import of our result. (shrink)

It can be argued (cf. Dizadji‑Bahmani et al. 2010) that an increase in coherence is one goal that drives reductionist enterprises. Consequently, the question if or how well this goal is achieved can serve as an epistemic criterion for evaluating both a concrete case of a purported reduction and our model of reduction : what conditions on the model allow for an increase in coherence ? In order to answer this question, I provide an analysis of the relation between the (...) reduction and the coherence of two theories. The underlying model of reduction is a (generalised) Nagelian model (cf. Nagel 1970, Schaffner 1974, Dizadji‑Bahmani et al. 2010). For coherence, different measures have been put forward (e.g. Shogenji 1999, Olsson 2002, Fitelson 2003, Bovens & Hartmann 2003). However, since there are counterexamples to each proposed coherence measure, we should be careful that the analysis be sufficiently stable (in a sense to be specified). It will turn out that this can be done. (shrink)

Objective Bayesian probability is often defined over rather simple domains, e.g., finite event spaces or propositional languages. This paper investigates the extension of objective Bayesianism to first-order logical languages. It is argued that the objective Bayesian should choose a probability function, from all those that satisfy constraints imposed by background knowledge, that is closest to a particular frequency-induced probability function which generalises the λ = 0 function of Carnap’s continuum of inductive methods.

In his Bayesian Nets and Causality, Jon Williamson presents an ‘Objective Bayesian’ interpretation of probability, which he endeavours to distance from the logical interpretation yet associate with the subjective interpretation. In doing so, he suggests that the logical interpretation suffers from severe epistemological problems that do not affect his alternative. In this paper, I present a challenge to his analysis. First, I closely examine the relationship between the logical and ‘Objective Bayesian’ views, and show how, and why, they are highly (...) similar. Second, I argue that the logical interpretation is not manifestly inferior, at least for the reasons that Williamson offers. I suggest that the key difference between the logical and ‘Objective Bayesian’ views is in the domain of the philosophy of logic; and that the genuine disagreement appears to be over Platonism versus nominalism. (shrink)

Mechanisms are usually viewed as inherently hierarchical, with lower levels of a mechanism influencing, and decomposing, its higher-level behaviour. In order to adequately draw quantitative predictions from a model of a mechanism, the model needs to capture this hierarchical aspect. The recursive Bayesian network formalism was put forward as a means to model mechanistic hierarchies by decomposing variables. The proposal was recently criticized by Gebharter and Gebharter and Kaiser, who instead propose to decompose arrows. In this paper, I defend the (...) RBN account from the criticism and argue that it offers a better representation of mechanistic hierarchies than the rival account. (shrink)

The foundations of probability are viewed through the lens of the subjectivist interpretation. This article surveys conditional probability, arguments for probabilism, probability dynamics, and the evidential and subjective interpretations of probability.

Current philosophical accounts of causation suggest that the same causal assertion can have different meanings. Yet, in actual social-scientific practice, the possible meanings of some causal generalisations intended to support policy prescriptions are not always spelled out. In line with a standard referentialist approach to semantics, we propose and elaborate on four questions to systematically elucidate the meaning of causal generalisations. The analysis can be useful to a host of agents, including social scientists, policy-makers, and philosophers aiming at being socially (...) relevant. To illustrate our proposal, we analyse the complexities related to the meaning of causal generalisations in the context of a concrete case of economic research which is explicitly intended to guide public policy, namely, the OECD research on the causes of unemployment. (shrink)

Our concept of actual causation plays a deep, ever-present role in our experiences. I first argue that traditional philosophical methods for understanding this concept are unlikely to be successful. I contend that we should instead use functional analyses and an understanding of the cognitive bases of causal cognition to gain insight into the concept of actual causation. I additionally provide initial, programmatic steps towards carrying out such analyses. The characterization of the concept of actual causation that results is quite different (...) from many standard views: it is graded, context-sensitive, and extrinsic. (shrink)

In this article, I present some new group level interpretations of probability, and champion one in particular: a consensus-based variant where group degrees of belief are construed as agreed upon betting quotients rather than shared personal degrees of belief. One notable feature of the account is that it allows us to treat consensus between experts on some matter as being on the union of their relevant background information. In the course of the discussion, I also introduce a novel distinction between (...) intersubjective and interobjective interpretations of probability. (shrink)

This paper responds to Achinstein’s criticism of the thesis that the only empirical fact that can affect the truth of an objective evidence claim such as ‘e is evidence for h’ (or ‘e confirms h to degree r’) is the truth of e. It shows that cases involving evidential flaws, which form the basis for Achinstein’s objections to the thesis, can satisfactorily be accounted for by appeal to changes in background information and working assumptions. The paper also argues that the (...) a priori and empirical accounts of evidence are on a par when we consider scientific practice, but that a study of artificial intelligence might serve to differentiate them. (shrink)

How should probabilities be interpreted in causal models in the social and health sciences? In this paper we take a step towards answering this question by investigating the case of cancer in epidemiology and arguing that the objective Bayesian interpretation is most appropriate in this domain.

Philosophical work on free will, contemporary as well as historical, is inevitably framed by the problem of free will and determinism. One of my goals in what follows is to give a feel for the main lines of that debate in philosophy today. I will also be outlining a particular perspective on free will. Many working philosophers consider themselves Compatibilists; the perspective outlined, building on a number of arguments in the recent literature, is a contemporary form of such a view. (...) It cannot, however, claim to be the contemporary philosophical perspective. There is no such thing. Against a background of the perennial problem of free will and determinism, through ongoing argument and debate, philosophers continue to try to work toward an understanding of precisely what it means for an action to be free. (shrink)

The Recursive Bayesian Net formalism was originally developed for modelling nested causal relationships. In this paper we argue that the formalism can also be applied to modelling the hierarchical structure of mechanisms. The resulting network contains quantitative information about probabilities, as well as qualitative information about mechanistic structure and causal relations. Since information about probabilities, mechanisms and causal relations is vital for prediction, explanation and control respectively, an RBN can be applied to all these tasks. We show in particular how (...) a simple two-level RBN can be used to model a mechanism in cancer science. The higher level of our model contains variables at the clinical level, while the lower level maps the structure of the cell's mechanism for apoptosis. (shrink)

After describing the disorder of psychopathy, I examine the theories and the evidence concerning the psychopaths’ deficient moral capacities. I first examine whether or not psychopaths can pass tests of moral knowledge. Most of the evidence suggests that they can. If there is a lack of moral understanding, then it has to be due to an incapacity that affects not their declarative knowledge of moral norms, but their deeper understanding of them. I then examine two suggestions: it is their deficient (...) practical reason or their stunted emotions that are at fault. The evidence supports both explanations. I conclude with an overview of the debate concerning whether they are morally or legally responsible for their actions. (shrink)

Objective standards for justification or for being a reason would be desirable, but inductive skepticism tells us that they cannot be presupposed. Rather, we have to start from subjective-relative notions of justification and of being a reason. The paper lays out the strategic options we have given this dilemma. The paper explains the requirements for this subject-relative notion and how they may be satisfied. Then it discusses four quite heterogeneous ways of providing more objective standards, which combine without guaranteeing complete (...) success. (shrink)

This article examines how specific realist and projectivist versions of manipulability theories of causation deal with the problem of objectivity. Does an agent-dependent concept of manipulability imply that conflicting causal claims made by agents with different capacities can come out as true? In defence of the projectivist stance taken by the agency view, I argue that if the agent’s perspective is shown to be uniform across different agents, then the truth-values of causal claims do not vary arbitrarily and, thus, reach (...) a satisfactory level of objectivity. My argument connects Price’s considerations on the situation of deliberation, whose structure, common to all agents, is the same with respect to both decision making and causal claims on a concept inspired by Douglas’s classification of objectivity of thought processes: the perspective of the detached agent. I further argue that, despite his agent-independent concept of intervention, Woodward’s claim of a stronger objectivity standard cannot be achieved, as the relativity of causal concepts to a variable set brings about the issue of the agent’s choice of variables. Consequently, a more permissive objectivity standard applies to both views. (shrink)

The prospects of a causal interpretation of probability are examined. Various accounts both from the history of scientific method and from recent developments in the tradition of the method of arbitrary functions, in particular by Strevens, Rosenthal, and Abrams, are briefly introduced and assessed. I then present a specific account of causal probability with the following features: First, the link between causal probability and a particular account of induction and causation is established, namely eliminative induction and the related difference-making account (...) of causation in the tradition of Bacon, Herschel, and Mill. Second, it is shown how a causal approach is useful beyond applications of the method of arbitrary functions and is able to deal with various shades of both ontic and epistemic probabilities. Furthermore, I clarify the notion of causal symmetry as a central element of an objective version of the principle of indifference and relate probabilistic independence to causal irrelevance. (shrink)

Part I of this paper introduces a range of mechanistic theories of causality, including process theories and the complex-systems theories, and some of the problems they face. Part II argues that while there is a decisive case against a purely mechanistic analysis, a viable theory of causality must incorporate mechanisms as an ingredient, and describes one way of providing an analysis of causality which reaps the rewards of the mechanistic approach without succumbing to its pitfalls.

This paper addresses questions about how the levels of causality (generic and single-case causality) are related. One question is epistemological: can relationships at one level be evidence for relationships at the other level? We present three kinds of answer to this question, categorised according to whether inference is top-down, bottom-up, or the levels are independent. A second question is metaphysical: can relationships at one level be reduced to relationships at the other level? We present three kinds of answer to this (...) second question, categorised according to whether single-case relations are reduced to generic, generic relations are reduced to single-case, or the levels are independent. We then explore causal inference in autopsy. This is an interesting case study, we argue, because it refutes all three epistemologies and all three metaphysics. We close by sketching an account of causality that survives autopsy—the epistemic theory. (shrink)

This dissertation aims to determine the optimal level of granularity for the variables used in probabilistic causal models. These causal models are useful for generating explanations in a number of scientific contexts. In Chapter 1, I argue that there is rarely a unique level of granularity at which a given phenomenon can be causally explained, thereby rejecting various causal exclusion arguments. In Chapter 2, I consider several recent proposals for measuring the explanatory power of causal explanations, and show that these (...) measures fail to track the comparative depth of explanations given at different levels of granularity. In Chapter 3, I offer a pragmatic account of how to partition the measure space of a causal variable so as to optimally explain its effect. My account uses the decision-theoretic notion of value of information, and indexes the relative depth of an explanation to a particular agent faced with a particular decision problem. Chapter 4 applies this same decisiontheoretic framework to answer the epistemic question of how to discover constitutive relationships in nature. In Chapter 5, I describe the formal details of the relationship between random variables that are meant to be coarse-grained and fine-grained representations of the same type of phenomenon. I use this formal framework to rebut a popular argument for the view that special science probabilities can be objective chances. Chapter 6 discusses challenges related to the causal interpretation of Bayes nets that use imprecise rather than precise probabilities. (shrink)

The epistemic theory of causality is analogous to epistemic theories of probability. Most proponents of epistemic probability would argue that one's degrees of belief should be calibrated to chances, insofar as one has evidence of chances. The question arises as to whether causal beliefs should satisfy an analogous calibration norm. In this paper, I formulate a particular version of a norm requiring calibration to chances and argue that this norm is the most fundamental evidential norm for epistemic probability. I then (...) develop an analogous calibration norm for epistemic causality, argue that it is the *only* evidential norm required for epistemic causality, and show how an epistemic account of causality that incorporates this norm can be used to analyse objective causal relationships. (shrink)

In this paper we investigate some mathematical consequences of the Equivocation Principle, and the Maximum Entropy models arising from that, for first order languages. We study the existence of Maximum Entropy models for these theories in terms of the quantifier complexity of the theory and will investigate some invariance and structural properties of such models.

It is still a matter of controversy whether the Principle of the Common Cause (PCC) can be used as a basis for sound causal inference. It is thus to be expected that its application to quantum mechanics should be a correspondingly controversial issue. Indeed the early 90’s saw a flurry of papers addressing just this issue in connection with the EPR correlations. Yet, that debate does not seem to have caught up with the most recent literature on causal inference generally, (...) which has moved on to consider the virtues of a generalised PCC-inspired condition, the so-called Causal Markov Condition (CMC). In this paper we argue that the CMC is an appropriate benchmark for debating possible causal explanations of the EPR correlations. But we go on to take issue with some pronouncements on EPR by defenders of the CMC. (shrink)

Some philosophers of physics recently expressed their skepticism about causation (Norton 2003b, 2007). However, this is not new. The view that causation does not refer to any ontological category perhaps can be attributed to Hume, Kant and Russell. On the other hand, some philosophers (Wesley Salmon and Phil Dowe) view causation as a physical process and some others (Cartwright) view causation as making claims about capacities possessed by objects. The issue about the ontological status of causal claims involves issues concerning (...) the ontological status of capacity, modality and dispositional claims. In this paper, my goal is to show that without engaging metaphysical debates about the ontological status of causal claims, it can be shown that we can objectively assign truth values to these statements. I argue that for causal claims to be objective we don't need to postulate the existence of special facts (specific to causal claims) in addition to ordinary physical facts described by physical theories. This, I think, is enough to justify the usefulness of this concept in certain branches (may be all) of science. Once this is achieved, there is no need to engage in unnecessary metaphysical debates. So, even if advanced physical theories don't mention this notion, causal reasoning can still be important in understanding the world not in the sense that science discovers special ontological category called causation but in the sense that we come to know certain facts about the world. (shrink)

Both Popper and van Fraassen have used evolutionary analogies to defend their views on the aim of science, although these are diametrically opposed. By employing Price's equation in an illustrative capacity, this paper considers which view is better supported. It shows that even if our observations and experimental results are reliable, an evolutionary analogy fails to demonstrate why conjecture and refutation should result in: (1) the isolation of true theories; (2) successive generations of theories of increasing truth-likeness; (3) empirically adequate (...) theories; or (4) successive generations of theories of increasing proximity to empirical adequacy. Furthermore, it illustrates that appeals to induction do not appear to help. It concludes that an evolutionary analogy is only sufficient to defend the notion that the aim of science is to isolate a particular class of false theories, namely those that are empirically inadequate. (shrink)