This paper argues against Papineau's claim that causal relations can be reduced to correlations and defends Cartwright's thesis that they can be nevertheless boot-strapped from them, given sufficiently rich causal background knowledge.

Existing research suggests that people's judgments of actual causation can be influenced by the degree to which they regard certain events as normal. We develop an explanation for this phenomenon that draws on standard tools from the literature on graphical causal models and, in particular, on the idea of probabilistic sampling. Using these tools, we propose a new measure of actual causal strength. This measure accurately captures three effects of normality on causal judgment that have been observed in existing studies. (...) More importantly, the measure predicts a new effect ("abnormal deflation"). Two studies show that people's judgments do, in fact, show this new effect. Taken together, the patterns of people's causal judgments thereby provide support for the proposed explanation. (shrink)

This paper shows that causation in the sense of Lewis is a special case of causation in the sense of Spohn.

It is shown that, given any finite set of pairs of random events in a Boolean algebra which are correlated with respect to a fixed probability measure on the algebra, the algebra can be extended in such a way that the extension contains events that can be regarded as common causes of the correlations in the sense of Reichenbach's definition of common cause. It is shown, further, that, given any quantum probability space and any set of commuting events in it (...) which are correlated with respect to a fixed quantum state, the quantum probability space can be extended in such a way that the extension contains common causes of all the selected correlations, where common cause is again taken in the sense of Reichenbach's definition. It is argued that these results very strongly restrict the possible ways of disproving Reichenbach's Common Cause Principle. (shrink)

Philosophers have used the probabilistic relation of ’screening-off‘ to explicate concepts in the theories of causation and explanation. Brandon has used screening-off relations in an attempt to reconstruct an argument of Mayr and Gould that natural selection acts at the level of the organism. I argue that Brandon‘s reconstruction is unsuccessful.

I advance a new theory of causal relevance, according to which causal claims convey information about conditional probability functions. This theory is motivated by the problem of disjunctive factors, which haunts existing probabilistic theories of causation. After some introductory remarks, I present in Section 3 a sketch of Eells's (1991) probabilistic theory of causation, which provides the framework for much of the discussion. Section 4 explains how the problem of disjunctive factors arises within this framework. After rejecting three proposed solutions, (...) I offer in Section 6 a new approach to causation that avoids the problem. Decision-theoretic considerations also support the new approach. Section 8 develops the consequences of the new theory for causal explanation. The resulting theory of causal explanation incorporates the new insights while respecting important work on scientific explanation by Salmon (1971), Railton (1981), and Humphreys (1989). My conclusions are enumerated in Section 9. (shrink)

This paper discusses two challenges for a Boolean method for establishing constitutive regularity statements which, according to the regularity theory of mechanistic constitution, form the core of any mechanistic explanation in neuroscience. After presenting the regularity definition for the constitution relation and a methodology for constitutive inference, the paper discusses the problem of full variation of tested mechanistic factors and the problem of informational redundancy. A solution is offered for each problem. The first requires some adjustments to the original theory (...) by introducing the technical notion of a set of types satisfying independent instantiability. The second one is resolved by demonstrating that the problem of informational redundancy is based on a confusion that fails to challenge the theory. It is concluded that the methodology of constitutive inference is consistent and plausible with respect to actual practice in neuroscience. (shrink)

The notion of common cause closedness of a classical, Kolmogorovian probability space with respect to a causal independence relation between the random events is defined, and propositions are presented that characterize common cause closedness for specific probability spaces. It is proved in particular that no probability space with a finite number of random events can contain common causes of all the correlations it predicts; however, it is demonstrated that probability spaces even with a finite number of random events can be (...) common cause closed with respect to a causal independence relation that is stronger than logical independence. Furthermore it is shown that infinite, atomless probability spaces are always common cause closed in the strongest possible sense. Open problems concerning common cause closedness are formulated and the results are interpreted from the perspective of Reichenbach's Common Cause Principle. (shrink)

This paper outlines a theory and computer implementation of causal meanings and reasoning. The meanings depend on possibilities, and there are four weak causal relations: A causes B, A prevents B, A allows B, and A allows not‐B, and two stronger relations of cause and prevention. Thus, A causes B corresponds to three possibilities: A and B, not‐A and B, and not‐A and not‐B, with the temporal constraint that B does not precede A; and the stronger relation conveys only the (...) first and last of these possibilities. Individuals represent these relations in mental models of what is true in the various possibilities. The theory predicts a number of phenomena, and, contrary to many accounts, it implies that the meaning of causation is not probabilistic, differs from the meaning of enabling conditions, and does not depend on causal powers or mechanisms. The theory also implies that causal deductions do not depend on schemas or rules. (shrink)

The starting point in the development of probabilistic analyses of token causation has usually been the naïve intuition that, in some relevant sense, a cause raises the probability of its effect. But there are well-known examples both of non-probability-raising causation and of probability-raising non-causation. Sophisticated extant probabilistic analyses treat many such cases correctly, but only at the cost of excluding the possibilities of direct non-probability-raising causation, failures of causal transitivity, action-at-a-distance, prevention, and causation by absence and omission. I show that (...) an examination of the structure of these problem cases suggests a different treatment, one which avoids the costs of extant probabilistic analyses. (shrink)

I argue that there are non-trivial objective chances (that is, objective chances other than 0 and 1) even in deterministic worlds. The argument is straightforward. I observe that there are probabilistic special scientific laws even in deterministic worlds. These laws project non-trivial probabilities for the events that they concern. And these probabilities play the chance role and so should be regarded as chances as opposed, for example, to epistemic probabilities or credences. The supposition of non-trivial deterministic chances might seem to (...) land us in contradiction. The fundamental laws of deterministic worlds project trivial probabilities for the very same events that are assigned non-trivial probabilities by the special scientific laws. I argue that any appearance of tension is dissolved by recognition of the level-relativity of chances. There is therefore no obstacle to accepting non-trivial chance-role-playing deterministic probabilities as genuine chances. (shrink)

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

In their article 'Causes and Explanations: A Structural-Model Approach. Part I: Causes', Joseph Halpern and Judea Pearl draw upon structural equation models to develop an attractive analysis of 'actual cause'. Their analysis is designed for the case of deterministic causation. I show that their account can be naturally extended to provide an elegant treatment of probabilistic causation.

ABSTRACT Joseph Halpern and Judea Pearl draw upon structural equation models to develop an attractive analysis of ‘actual cause’. Their analysis is designed for the case of deterministic causation. I show that their account can be naturally extended to provide an elegant treatment of probabilistic causation. 1Introduction 2Preemption 3Structural Equation Models 4The Halpern and Pearl Definition of ‘Actual Cause’ 5Preemption Again 6The Probabilistic Case 7Probabilistic Causal Models 8A Proposed Probabilistic Extension of Halpern and Pearl’s Definition 9Twardy and Korb’s Account 10Probabilistic (...) Fizzling 11Conclusion. (shrink)

In this paper I offer an 'integrating account' of singular causation, where the term 'integrating' refers to the following program for analysing causation. There are two intuitions about causation, both of which face serious counterexamples when used as the basis for an analysis of causation. The 'process' intuition, which says that causes and effects are linked by concrete processes, runs into trouble with cases of 'misconnections', where an event which serves to prevent another fails to do so on a particular (...) occasion and yet the two events are linked by causal processes. The chance raising intuition, according to which causes raise the chance of their effects, easily accounts for misconnections but faces the problem of chance lowering causes, a problem easily accounted for by the process approach. The integrating program attempts to provide an analysis of singular causation by synthesising the two insights, so as to solve both problems. In this paper I show that extant versions of the integrating program due to Eells, Lewis, and Menzies fail to account for the chance-lowering counterexample. I offer a new diagnosis of the chance lowering case, and use that as a basis for an integrating account of causation which does solve both cases. In doing so, I accept various assumptions of the integrating program, in particular that there are no other problems with these two approaches. As an example of the process account, I focus on the recent CQ theory of Wesley Salmon (1997). (shrink)

Much has been written on the role of causal notions and causal reasoning in the so-called 'special sciences' and in common sense. But does causal reasoning also play a role in physics? Mathias Frisch argues that, contrary to what influential philosophical arguments purport to show, the answer is yes. Time-asymmetric causal structures are as integral a part of the representational toolkit of physics as a theory's dynamical equations. Frisch develops his argument partly through a critique of anti-causal arguments and partly (...) through a detailed examination of actual examples of causal notions in physics, including causal principles invoked in linear response theory and in representations of radiation phenomena. Offering a new perspective on the nature of scientific theories and causal reasoning, this book will be of interest to professional philosophers, graduate students, and anyone interested in the role of causal thinking in science. (shrink)

Modular approaches to the architecture of the mind claim that some mental mechanisms, such as sensory input processes, operate in special-purpose subsystems that are functionally independent from the rest of the mind. This assumption of modularity seems to be in tension with recent claims that the mind has a predictive architecture. Predictive approaches propose that both sensory processing and higher-level processing are part of the same Bayesian information-processing hierarchy, with no clear boundary between perception and cognition. Furthermore, it is not (...) clear how any part of the predictive architecture could be functionally independent, given that each level of the hierarchy is influenced by the level above. Both the assumption of continuity across the predictive architecture and the seeming non-isolability of parts of the predictive architecture seem to be at odds with the modular approach. I explore and ultimately reject the predictive approach’s apparent commitments to continuity and non-isolation. I argue that predictive architectures can be modular architectures, and that we should in fact expect predictive architectures to exhibit some form of modularity. (shrink)

The paper displays the similarity between the theory of probabilistic causation developed by Glymour et al. since 1983 and mine developed since 1976: the core of both is that causal graphs are Bayesian nets. The similarity extends to the treatment of actions or interventions in the two theories. But there is also a crucial difference. Glymour et al. take causal dependencies as primitive and argue them to behave like Bayesian nets under wide circumstances. By contrast, I argue the behavior of (...) Bayesian nets to be ultimately the defining characteristic of causal dependence. (shrink)

Causal claims in biomedical contexts are ubiquitous albeit they are not always made explicit. This paper addresses the question of what causal claims mean in the context of disease. It is argued that in medical contexts causality ought to be interpreted according to the epistemic theory. The epistemic theory offers an alternative to traditional accounts that cash out causation either in terms of “difference-making” relations or in terms of mechanisms. According to the epistemic approach, causal claims tell us about which (...) inferences (e.g., diagnoses and prognoses) are appropriate, rather than about the presence of some physical causal relation analogous to distance or gravitational attraction. It is shown that the epistemic theory has important consequences for medical practice, in particular with regard to evidence-based causal assessment. (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)

In this thesis, I give a metascientific account of causality in medicine. I begin with two historical cases of causal discovery. These are the discovery of the causation of Burkitt’s lymphoma by the Epstein-Barr virus, and of the various viral causes suggested for cervical cancer. These historical cases then support a philosophical discussion of causality in medicine. This begins with an introduction to the Russo- Williamson thesis (RWT), and discussion of a range of counter-arguments against it. Despite these, I argue (...) that the RWT is historically workable, given a small number of modifications. I then expand Russo and Williamson’s account. I first develop their suggestion that causal relationships in medicine require some kind of evidence of mechanism. I begin with a number of accounts of mechanisms and produce a range of consensus features of them. I then develop this consensus position by reference to the two historical case studies with an eye to their operational competence. In particular, I suggest that it is mechanistic models and their representations which we are concerned with in medicine, rather than the mechanism as it exists in the world. -/- I then employ these mechanistic models to give an account of the sorts of evidence used in formulating and evaluating causal claims. Again, I use the two human viral oncogenesis cases to give this account. I characterise and distinguish evidence of mechanism from evidence of difference-making, and relate this to mechanistic models. I then suggest the relationship between types of evidence presents us with a means of tackling the reference-class problem. This sets the scene for the final chapter. Here, I suggest the manner in which these two different classes of evidence become integrated is also reflected in the way that developing research programmes change as their associated causal claims develop. (shrink)

In the philosophical tradition, the notions of determinism and causality are strongly linked: it is assumed that in a world of deterministic laws, causality may be said to reign supreme; and in any world where the causality is strong enough, determinism must hold. I will show that these alleged linkages are based on mistakes, and in fact get things almost completely wrong. In a deterministic world that is anything like ours, there is no room for genuine causation. Though there may (...) be stable enough macro-level regularities to serve the purposes of human agents, the sense of “causality” that can be maintained is one that will at best satisfy Humeans and pragmatists, not causal fundamentalists. (shrink)

It so happens that classical physical theories can be interpreted as a representation of local interactions between systems with determinate properties. Orthodox quantum mechanics, which is one of our most experimentally well-confirmed theories, is notoriously resistant to being interpreted in terms of the above framework. Bell-type theorems and Bell-type experiments have made such an interpretation impossible. In the early sixties, John Bell demonstrated that any theory that represents its domain in terms of the above framework satisfies a set of inequalities, (...) the so-called Bell inequalities. Experiments on quantum phenomena violate Bell-type inequalities. By a simple modus tollens, the upshot is that no theory that includes all the elements of the above framework can recover all statistical predictions of quantum mechanics. Philosophers have been trying to interpret this result, that is, to understand what the world might be like if it is true that physical interactions between systems are non-local, or that physical systems do not possess determinate properties. This line of thought found its climax in program of Òexperimental metaphysicsÓ that developed after the violation of Bell-type inequalities was observed. Experimental metaphysics consists in deriving metaphysical conclusions from the Bell-type experimental results. The mainstream interpretation within experimental metaphysics is that Bell-type experiments force us to accept the existence of a form of non-locality at the ontological level, but a form that we can consider benign because it is of a non-causal type. In my dissertation, I assess to what extent philosophical investigation can help us decide what the world is like on the basis of our best physical theories, from the point of view of the quantum domain and with an emphasis on Bell-type phenomena. My conclusions point to a more modest view on the possible achievements of philosophy of physics than the experimental metaphysics program would have us believe. In the first part of my dissertation, I investigate what role philosophy of physics can legitimately hope to play in the development and evaluation of various accounts of quantum phenomena. I claim that it is not the role of philosophy of physics to impose criteria of acceptability on physical theories, in addition to coherence and empirical adequacy. By contrast, I take in my dissertation that the legitimate role of philosophy of physics is to clearly determine what is imposed by the phenomena and our best theories from what is a matter of preference on the basis of the structural analysis of the phenomena and theories. In the second part of my dissertation, I turn to the more specific case of the interpretation of Bell-type theorems and Bell-type phenomena. I undertake a systematic examination of the mainstream interpretation. I show that the mainstream interpretation includes three claims, one about locality, another one about causation and a last one about holism. I utilize theories of locality and causation in order to assess these three claims. On the one hand, the upshot of my analysis is that the claim about locality can be supported by a rigorous theory of locality. On the other hand, no theory of probabilistic causation can support the claims of the mainstream interpretation about causation when it is construed as a strong program of experimental metaphysics yielding conclusions about the ontology of the world. That said, weakened versions of the mainstream interpretation, those that do without conclusions about the ontology of the world, can be made compatible with some theories of probabilistic causation. In particular, the mainstream interpretation can be rigorously supported if its claims are restricted to the empirical level. (shrink)