The mind's best trick: how we experience conscious will

We often consciously will our own actions. This experience is so profound that it tempts us to believe that our actions are caused by consciousness. It could also be a trick, however - the mind's way of estimating its own apparent authorship by drawing causal inferences about relationships between thoughts and actions. Cognitive, social, and neuropsychological studies of apparent mental causation suggest that experiences of conscious will frequently depart from actual causal processes and so might not reflect direct perceptions of conscious thought causing action.     

Models of causation and the semantics of causal verbs

This research examines the relationship between the concept of CAUSE as it is characterized in psychological models of causation and the meaning of causal verbs, such as the verb cause itself. According to focal set models of causation (; ), the concept of CAUSE should be more similar to the concepts of ENABLE and PREVENT than either is to each other. According to a model based on theory of force dynamics, the force dynamic model, the concepts of CAUSE, ENABLE, and PREVENT should be roughly equally similar to one another. The relationship between these predictions and the meaning of causal verbs was examined by having participants sort causal verbs and rate them with respect to the dimensions specified by the two models. The results from five experiments indicated that the force dynamic model provides a better account of the meaning of causal verbs than do focal set models of causation. Implications for causal inference and induction are discussed.     

How agency can solve interventionism’s problem of circularity

Woodward’s interventionist theory of causation is beset by a problem of circularity: the analysis of causes is in terms of interventions, and the analysis of interventions is in terms of causes. This is not in itself an argument against the correctness of the analysis. But by requiring us to have causal knowledge prior to making any judgements about causation, Woodward’s theory does make it mysterious how we can ever start acquiring causal knowledge. We present a solution to this problem by showing how the interventionist notion of causation can be rationally generated from a more primitive agency notion of causation. The agency notion is easily and non-circularly applicable, but fails when we attempt to capture causal relations between non-actions. We show that the interventionist notion of causation serves as an appropriate generalisation of the agency notion. Furthermore, the causal judgements based on the latter generally remain true when rephrased in terms of the former, which allows one to use the causal knowledge gained by applying the agency notion as a basis for applying Woodward’s interventionist theory. We then present an overview of relevant empirical evidence from developmental psychology which shows that our proposed rational reconstruction lines up neatly with the actual development of causal reasoning in children. This gives additional plausibility to our proposal. The article thus provides a solution to one of the main problems of interventionism while keeping Woodward’s analysis intact.     

Explanation and Manipulation1

I argue that manipulationist theories of causation fail as accounts of causal structure, and thereby as theories of “actual causation” and causal explanation. I focus on two kinds of problem cases, which I call “Perceived Abnormality Cases” and “Ontological Dependence Cases.” The cases illustrate that basic facts about social systems—that individuals are sensitive to perceived abnormal conditions and that certain actions metaphysically depend on institutional rules—pose a challenge for manipulationist theories and for counterfactual theories more generally. I then show how law‐based accounts of causal structure can answer such challenges. The moral of the story is that the basic manipulationist idea that our interest in causal structure is driven by our interest in manipulating our environment faces decisive problems in a central domain of application, the social sciences.     

How Effects Depend on their Causes,Why Causal Transitivity Fails,and Why we Care About Causation

Despite recent efforts to improve on counterfactual theories of causation, failures to explain how effects depend on their causes are still manifest in a variety of cases. In particular, theories that do a decent job explaining cases of causal preemption have problems accounting for cases of causal intransitivity. Moreover, the increasing complexity of the counterfactual accounts makes it difficult to see why the concept of causation would be such a central part of our cognition. In this paper, I propose an account of our causal thinking that not only explains the hitherto puzzling variety of causal judgments, but also makes it intelligible why we would employ such an elusive concept.     

Computation and Causation

The computer's effect on our understanding of causation has been enormous. By the mid-1980s, philosophical and social-scientific work on the topic had left us with (1) no reasonable reductive account of causation and (2) a class of statistical causal models tied to linear regression. At this time, computer scientists were attacking the problem of equipping robots with models of the external that included probabilistic portrayals of uncertainty. To solve the problem of efficiently storing such knowledge, they introduced Bayes Networks and directed graphs. By attaching a causal interpretation to Bayes Networks, the philosophy of causation changed dramatically. We are now able to be extremely general about how causal structure connects to data, and systematic about when causal structures are empirically indistinguishable. In this essay I try to motivate and describe this synthesis.     

Causality in medicine: Towards a theory and terminology

One of the cornerstones of modern medicine is the search for what causes diseases to develop. A conception of multifactorial disease causes has emerged over the years. Theories of disease causation, however, have not quite been developed in accordance with this view. It is the purpose of this paper to provide a fundamental explication of aspects of causation relevant for discussing causes of disease. The first part of the analysis will discuss discrimination between singular and general causality. Singular causality, as in the specific patient, is a relation between a concrete sequence of causally linked events. General causation, e.g. as in disease etiology, means various categories of causal relations between event types. The paper introduces the concept of a reference case serving as a source for causal inference, reaching beyond the concept of general causality. The second part of the analysis provides exemplification of a theory of causation suitable for discussing singular causation. The chain of events that induce a disease state can be identified as effective causal complexes, each complex composed of nonredundant components, which separately contribute to the effect of the complex, without the individual component being necessary or sufficient in itself to produce the effect. In the third part of the analysis the theory is elaborated further. Causes, defined as nonredundant components, can furthermore be differentiated according to their avoidability, according to theories about human error or by the potential of eradication. Multifactorial models of disease creates a need for systematic approaches to causal factors. The paper proposes a taxonomical terminology that serves this purpose.     

How Could There Be True Causal Claims Without There Being Special Causal Facts in the World?

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.     

Suicide Causation: Pies,Paths, and Pointless Polemics

Most people readily agree that suicide is caused by a complex web of many different factors. However, for many people the concept of a single event resulting from the combined effect of a constellation of different factors (multiple causation) is imperfectly understood. Unfortunately, a naive understanding of multiple causation can lead to needless arguments about what “really” causes suicide, and pointless debate about the “right” point for preventive intervention. In this paper, I review several simple conceptual models of multiple causation as they relate to suicide prevention. I suggest that a more explicit understanding of the nature of multiple causation has the potential to obviate some of these misguided arguments and to facilitate cooperative prevention efforts among person who choose to apply their energies at different points in the causal chain of suicide.     

Causes,Counterfactuals, and Non-Locality

In order to motivate the thesis that there is no single concept of causation that can do justice to all of our core intuitions concerning that concept, Ned Hall has argued that there is a conflict between a counterfactual criterion of causation and the condition of causal locality. In this paper I critically examine Hall's argument within the context of a more general discussion of the role of locality constraints in a causal conception of the world. I present two strategies that defenders of counterfactual accounts of causation can pursue to respond to Hall's challenge—including the adoption of a counterfactual condition that is sufficient for causal action-at-a-distance in place of Hall's ‘process’ condition—and conclude that Hall's argument against counterfactual accounts of causation is unsuccessful.     

Degrees of Causation

The primary aim of this paper is to analyze the concept of degrees of causal contribution for actual events and examine the way in which it can be formally defined. This should go some way to filling out a gap in the legal and philosophical literature on causation. By adopting the conception of a cause as a necessary element of a sufficient set (the so-called NESS test) we show that the concept of degrees of causation can be given clear and even empirical meaning. We then apply a game theoretical framework to derive a measure of causal contribution. Our favoured measure turns out to be a generalised version of the normalized Penrose–Banzhaf index of voting power.     

Quasi-Realism and Inductive Scepticism in Hume’s Theory of Causation

Interpreters of Hume on causation consider that an advantage of the ‘quasi-realist’ reading is that it does not commit him to scepticism or to an error theory about causal reasoning. It is unique to quasi-realism that it maintains this positive epistemic result together with a rejection of metaphysical realism about causation: the quasi-realist supplies an appropriate semantic theory in order to justify the practice of talking ‘as if’ there were causal powers in the world. In this paper, I problematise the quasi-realist reading of Hume on causation by showing how quasi-realism does not speak to inductive scepticism. I also offer evidence that Hume takes inductive scepticism to result from his theory of causation, and that his scepticism is tied to his rejection of metaphysical causal realism.     

Granger Causality—Statistical Analysis Under a Configural Perspective

The concept of Granger causality can be used to examine putative causal relations between two series of scores. Based on regression models, it is asked whether one series can be considered the cause for the second series. In this article, we propose extending the pool of methods available for testing hypotheses that are compatible with Granger causation by adopting a configural perspective. This perspective allows researchers to assume that effects exist for specific categories only or for specific sectors of the data space, but not for other categories or sectors. Configural Frequency Analysis (CFA) is proposed as the method of analysis from a configural perspective. CFA base models are derived for the exploratory analysis of Granger causation. These models are specified so that they parallel the regression models used for variable-oriented analysis of hypotheses of Granger causation. An example from the development of aggression in adolescence is used. The example shows that only one pattern of change in aggressive impulses over time Granger-causes change in physical aggression against peers.     

Causal Reasoning and Clinical Practice: Challenges from Molecular Biology

Not only has the philosophical debate on causation been gaining ground in the last few decades, but it has also increasingly addressed the sciences. The biomedical sciences are among the most prominent fields that have been considered, with a number of works tackling the understanding of the notion of cause, the assessment of genuinely causal relations and the use of causal knowledge in applied contexts. Far from denying the merits of the debate on causation and the major theories it comprises, this paper is meant as a stimulus for theorists of causation in the philosophy of biomedicine, with a focus on clinical matters. Without aiming at putting forward an original theory of causation and starting from the narration of two actual but paradigmatic cases at the joints between biomedical research and clinical practice, we want to point out that some pathological situations addressed by molecular medicine actually prove resistant to (at least) some of our major epistemological accounts of causal explanation. Given this scenario, which is very frequent in our hospitals, our analysis aims to provide a stimulus for the debate among theorists of causation in biomedicine interested in real cases in science in practice. We believe that this might in turn encourage some more general rethinking of the complex intertwinement of science, philosophy of science and ethics, as well as of the role of philosophy of science for clinical medicine itself.

     

Contiguity and the causal theory of memory

In Memory: A Philosophical Study, Bernecker argues for an account of contiguity. This Contiguity View is meant to solve relearning and prompting, wayward causation problems plaguing the causal theory of memory. I argue that Bernecker’s Contiguity View fails in this task. Contiguity is too weak to prevent relearning and too strong to allow prompting. These failures illustrate a problem inherent in accounts of memory causation. Relearning and prompting are both causal relations, wayward only with respect to our interest in specifying remembering’s requirements. Solving them requires saying more about remembering, not causation. I conclude by sketching such an account.     

Causation as Property Acquisition

Persistence theories of causation – such as transference theory, conserved-quantity theory, and Douglas Ehring's theory – attempt to analyzecausation in terms of some persisting entityconnecting cause and effect. While mostpersistence accounts are intended as empiricaltheories, this article develops a persistenceanalysis of the concept of causation. The basic idea is that the central concept ofdirect causation can be analyzed in terms ofproperty acquisition. The analysis cohereswith our ordinary causal judgments andprovides a straightforward explanation of thedirection of causation. It also explains whybackwards causation is conceptually problematic.     

Causal Sufficiency and Actual Causation

Journal of Philosophical Logic - Pearl opened the door to formally defining actual causation using causal models. His approach rests on two strategies: first, capturing the widespread intuition...     

Causal foundationalism, physical causation, and difference-making

An influential tradition in the philosophy of causation has it that all token causal facts are, or are reducible to, facts about difference-making. Challenges to this tradition have typically focused on pre-emption cases, in which a cause apparently fails to make a difference to its effect. However, a novel challenge to the difference-making approach has recently been issued by Alyssa Ney. Ney defends causal foundationalism, which she characterizes as the thesis that facts about difference-making depend upon facts about physical causation. She takes this to imply that causation is not fundamentally a matter of difference-making. In this paper, I defend the difference-making approach against Ney’s argument. I also offer some positive reasons for thinking, pace Ney, that causation is fundamentally a matter of difference-making.