The paper argues for a pragmatic account of genetic explanation. This is to say that when a disease or other trait is termed genetic, the reasons for singling out genes as causes over other, also necessary, genetic and nongenetic conditions are not wholly theoretical but include pragmatic dimensions. Whether the explanation is the presence of a trait in an individual or differences in a trait among individuals, genetic explanations are context-dependent in three ways: they are relative to a causal background (...) of genetic and nongenetic factors; they are relative to a population; and they are relative to the present state of knowledge. Criteria like causal priority, nonstandardness, and causal efficacy that purport to distinguish objectively between genetic causes and nongenetic conditions either incorporate pragmatic elements or fail for other reasons. When the pragmatic dimensions of genetic explanations are recognized, we come to understand the current phenomenon of geneticization to be a reflection of increased technological capacities to manipulate genes in the laboratory, and potentially the clinic, rather than theoretical progress in understanding how diseases and other traits arise. This calls into question the value of the search for theoretical definitions of designations like genetic disease or genetic susceptibility as directives for action. (shrink)

It is sometimes thought that randomized study group allocation is uniquely proficient at producing comparison groups that are evenly balanced for all confounding causes. Philosophers have argued that in real randomized controlled trials this balance assumption typically fails. But is the balance assumption an important ideal? I run a thought experiment, the CONFOUND study, to answer this question. I then suggest a new account of causal inference in ideal and real comparative group studies that helps clarify the roles of confounding (...) variables and randomization. 1Confounders and Causes2The Balance Assumption3The CONFOUND Study 3.1CONFOUND 13.2CONFOUND 24Disjunction C and the Ideal Study 4.1The ultimate ‘other cause’: C4.2The ideal comparative group study4.3Required conditions for causal inference5Confounders as Causes, Confounders as Correlates6Summary. (shrink)

Bertrand Russell famously argued that causation is not part of the fundamental physical description of the world, describing the notion of cause as “a relic of a bygone age”. This paper assesses one of Russell’s arguments for this conclusion: the ‘Directionality Argument’, which holds that the time symmetry of fundamental physics is inconsistent with the time asymmetry of causation. We claim that the coherence and success of the Directionality Argument crucially depends on the proper interpretation of the ‘ time symmetry’ (...) of fundamental physics as it appears in the argument, and offer two alternative interpretations. We argue that: if ‘ time symmetry’ is understood as the time -reversal invariance of physical theories, then the crucial premise of the Directionality Argument should be rejected; and if ‘ time symmetry’ is understood as the temporally bidirectional nomic dependence relations of physical laws, then the crucial premise of the Directionality Argument is far more plausible. We defend the second reading as continuous with Russell’s writings, and consider the consequences of the bidirectionality of nomic dependence relations in physics for the metaphysics of causation. (shrink)

I explore the problem of ``probabilistic causal preemption'' in the context of a``propensity trajectory'' theory of singular probabilistic causation. This involvesa particular conception of events and a substantive thesis concerning events soconceived.

Processes produce changes: rivers erode their banks and thunderstorms cause floods. If I am right that organisms are a kind of process, then the causally efficacious behaviours of organisms are also examples of processes producing change. In this paper I shall try to articulate a view of how we should think of causation within a broadly processual ontology of the living world. Specifically, I shall argue that causation, at least in a central class of cases, is the interaction of processes, (...) that such causation is the exercise of a capacity inherent in that process and, negatively, that causation should not be understood as the instantiation of universal laws. The approach I describe has substantial similarities with the process causality articulated by Wesley Salmon and Phil Dowe for physical causation, making it plausible that the basic approach can be applied equally to the non-living world. It is an approach that builds at crucial points on the criticisms of determinism and universal causality famously articulated by Elizabeth Anscombe. (shrink)

In this paper I offer an anti-Humean critique to Williamson and Russo’s approach to medical mechanisms. I focus on one of the specific claims made by Williamson and Russo, namely the claim that micro-structural ‘mechanisms’ provide evidence for the stability across populations of causal relationships ascertained at the (macro-) level of (test) populations. This claim is grounded in the epistemic account of causality developed by Williamson, an account which—while not relying exclusively on mechanistic evidence for justifying causal judgements—appeals nevertheless to (...) mechanisms, and rejects their anti-Humean interpretation in terms of capacities, powers, potencies, etc. By using (and expanding on) Cartwright’s basic critique against Humean mechanisms, I suggest that, in order to move beyond the level of plausibility, Williamson and Russo’s position is in need of a clarification as to the occurent reading of the components, functioning and interferences of mechanisms. Relatedly, as concerns Williamson’s epistemic account of causation, I argue that this account is in need of a more straightforward answer as to what truth-makers its causal claims should have. (shrink)

This article reveals that explanatory practice in software engineering is in accordance with pragmatic explanatory pluralism, which states that explanations should at least partially be evaluated by their practical use. More specifically, I offer a defense of the idea that several explanation-types are legitimate in software engineering, and that the appropriateness of an explanation-type depends on (a) the engineer’s interests, and (b) the format of the explanation-seeking question he asks, with this format depending on his interests. This idea is defended (...) by considering examples that are representative for explanatory practice in software engineering. Different kinds of technological explanation are spelled out, and the dependence of their appropriateness on interests and question-formats is extensively illustrated. (shrink)

Epidemiologists’ discussions on causation are not always very enlightening with regard to the notion of ‘cause’ in epidemiology. Epidemiologists rightly work from a science-based approach to causation in epidemiology, but largely disagree about the matter. Disagreement may be partly due to confusion of the question of useful concepts for causal inference in epidemiological practice with the question of the metaphysical presuppositions of causal concepts used in epidemiology. In other words, epidemiologists seem to confuse the practical results of epidemiological research at (...) the population level with the metaphysical views about the reality of disease causation at the individual level in their writings on causation. (shrink)

I focus on token, deterministic causal claims as they feature in causal explanations. Adequately handling absences is difficult for most causal theories, including theories of causal explanation. Yet so is adequately handling cases of late preemption. The best account of absence-causal claims as they appear in causal explanations is Jonathan Schaffer's quaternary, contrastive account. Yet Schaffer's account cannot handle preemption. The account that best handles late preemption is James Woodward's interventionist account. Yet Woodward's account is inadequate when it comes to (...) absences. I propose an account that handles both absences and preemption by transposing Schaffer's account into an interventionist framework. (shrink)

Causal slingshots are formal arguments advanced by proponents of an event ontology of token-level causation which, in the end, are intended to show two things: (i) The logical form of statements expressing causal dependencies on token level features a binary predicate ‘‘... causes ...’’ and (ii) that predicate takes events as arguments. Even though formalisms are only revealing with respect to the logical form of natural language statements, if the latter are shown to be adequately captured within a corresponding formalism, (...) proponents of slingshots usually take the adequacy of their formalizations for granted without justifying it. The first part of this paper argues that the most discussed version of a causal slingshot, viz. the one e.g. presented by Davidson (Essays on actions and events. Oxford, Clarendon Press, 1980), can indeed be refuted for relying on an inadequate formal apparatus. In contrast, the formal means of Gödel’s (The philosophy of Betrand Russell. New York, Tudor, 1944) often neglected slingshot are shown to stand on solid ground in the second part of the paper. Nonetheless, I contend that Gödel’s slingshot does only half the work friends of event causation would like it to do. It provides good reasons for (i) but not for (ii). (shrink)

An adequate understanding of the ubiquitous practice of mechanistic explanation requires an account of what Craver termed “constitutive relevance.” Entities or activities are constitutively relevant to a phenomenon when they are parts of the mechanism responsible for that phenomenon. Craver’s mutual manipulability account extended Woodward’s account of manipulationist counterfactuals to analyze how interlevel experiments establish constitutive relevance. Critics of MM argue that applying Woodward’s account to this philosophical problem conflates causation and constitution, thus rendering the account incoherent. These criticisms, we (...) argue, arise from failing to distinguish the semantic, epistemic, and metaphysical aspects of the problem of constitutive relevance. In distinguishing these aspects of the problem and responding to these critics accordingly, we amend MM into a refined epistemic criterion, the “matched interlevel experiments” account. Further, we explain how this epistemological thesis is grounded in the plausible metaphysical thesis that constitutive relevance is causal betweenness. (shrink)

The pivotal problem of comorbidity research lies in the psychometric foundation it rests on, that is, latent variable theory, in which a mental disorder is viewed as a latent variable that causes a constellation of symptoms. From this perspective, comorbidity is a (bi)directional relationship between multiple latent variables. We argue that such a latent variable perspective encounters serious problems in the study of comorbidity, and offer a radically different conceptualization in terms of a network approach, where comorbidity is hypothesized to (...) arise from direct relations between symptoms of multiple disorders. We propose a method to visualize comorbidity networks and, based on an empirical network for major depression and generalized anxiety, we argue that this approach generates realistic hypotheses about pathways to comorbidity, overlapping symptoms, and diagnostic boundaries, that are not naturally accommodated by latent variable models: Some pathways to comorbidity through the symptom space are more likely than others; those pathways generally have the same direction (i.e., from symptoms of one disorder to symptoms of the other); overlapping symptoms play an important role in comorbidity; and boundaries between diagnostic categories are necessarily fuzzy. (shrink)

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)

Economists reason causally. Like many other scientists, they aim at formulating justified causal claims about their object of study. This thesis contributes to our understanding of how causal reasoning proceeds in economics. By using the research on the causes of unemployment as a case study, three questions are adressed. What are the meanings of causal claims? How can a causal claim be adequately supported by evidence? How are causal beliefs affected by incoming facts? In the process of answering these semantic, (...) epistemic and dynamical questions, the richness of causal reasoning in economics is brought to the foreground. In the part on semantics, it is argued that the meaning of causal generalizations in policy-oriented economics is best captured by using the concept of ‘inferential relation’ rather than the one of ‘referential relation’. This part contributes to develop an inferentialist semantics by distinguishing among types of inferential relations. In the part on epistemology, it is argued that justification in sciences like economics often relies, and ought to rely, on evidential variety―i.e. the combination of evidence from multiple sources. An interpretation of independence among evidential sources is offered: two evidential sources are fully independent if and only if the reasons why they would be unreliable do not overlap. It is then shown that the variety-of-evidence thesis does not hold under extreme circumstances. The part on dynamics focuses on deviant-case study. A storyline is provided for what deviant-case study aims at and how it proceeds in what is characterized as an ‘eclectic science’. (shrink)

I argue, contrary to standard claims, that accomplice liability need not be a causal relation. One can be an accomplice to another’s crime without causally contributing to the criminal act of the principal. This is because the acts of aid and encouragement that constitute the basis for accomplice liability typically occur in contexts of under- and over-determination, where causal analysis is confounded. While causation is relevant to justifying accomplice liability in general, only potential causation is necessary in particular cases. I (...) develop this argument through the example of the role of U.S. legal officials in abetting the acts of unlawful interrogation that have taken place since 2001. I also suggest that there may be a limited justification for ex post ratificatory accomplice liability. (shrink)

This paper defends the need for evidential diversity and the mix of methods that that can in train require. The focus is on causal claims, especially ‘singular’ claims about the effects of causes in a specific setting—either what will happen or what has happened. I do so by offering a template that categorises kinds of evidence that can support these claims. The catalogue is generated by considering what needs to happen for a causal process to carry through from putative cause (...) at the start to the targeted effect at the end. The usual call for mixed methods focusses on a single overall claim and argues that we increase certainty by the use of different methods with compensating strengths and weaknesses. My proposals instead focus on the evidence that supports the great many subsidiary claims that must hold if the overall one is to be true. As is typical for singular causal claims, the mix of methods that will generally be required to collect the kinds of evidence I urge will usually have little claim to the kind of rigour that is now widely demanded in evidencing causal claims, especially those for policy/treatment effectiveness. So I begin with an exploration of what seems to be intended by ‘rigour’ in such discussions, since it is seldom made clear just what makes the favoured methods especially rigorous. I then argue that the emphasis on rigour can be counterproductive. Rigour is often the enemy of evidential diversity, and evidential diversity—lots of it—can make for big improvements in the reliability of singular causal predictions and post hoc evaluations. I illustrate with the paragon of rigour for causal claims, randomised controlled trials (RCTs), rehearsing at some length what they can and cannot do to make it easier to assess the importance of rigour in warranting singular causal claims. (shrink)

We show that five important elements of the ‘nomological package’— laws, counterfactuals, chances, dispositions, and counterfactuals—needn’t be a problem for the Growing-Block view. We begin with the framework given in Briggs and Forbes (in The real truth about the unreal future. Oxford studies in metaphysics. Oxford University Press, Oxford, 2012 ), and, taking laws as primitive, we show that the Growing-Block view has the resources to provide an account of possibility, and a natural semantics for non-backtracking causal counterfactuals. We show (...) how objective chances might ground a more fine-grained concept of feasibility, and furnished a places in the structure where causation and dispositions might fit. The Growing-Block view, thus understood, provides the resources to explain the close link between modality and tense, so that it predicts modal change as time passes. This account lets us capture not only what the future might hold for us, and also what might have been. (shrink)

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 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. (shrink)

This article illustrates instrumental variable (IV) estimation by examining an unexpected finding of the research on career adaptability and job satisfaction. Theoretical and empirical arguments suggest that in the general population, people’s abilities to adapt their careers are beneficial to their job satisfaction. However, a recent meta-analysis unexpectedly found no effect when personality traits are controlled for. We argue that a reverse effect of job satisfaction on career adaptability, originating from affective tendencies tied to personality, might explain this null effect. (...) Our argument implies that the estimates obtained with traditional ordinary least squares (OLS) regressions are biased by endogeneity, a correlation between an explanatory variable and the error term in a regression model. When experimental manipulations are impossible, IV estimations, such as two-stage least squares (2SLS) regressions, are one possible solution to the endogeneity problem. Analyzing three waves of data from a sample of 836 adults, the concurrent and time-lagged effect of job satisfaction on career adaptability was revealed to be more consistent than the reverse. Our results provide an explanation, rooted in affective dispositions, as to why recent meta-analytical estimates unexpectedly found that career adaptability does not predict job satisfaction at the interindividual level. We also discuss IV estimation in terms of its limits, weight the interpretation of its estimates against the temporality criterion for causal inference, and consider its possible extension to analyses of change. (shrink)

Once upon a time, coherentism was the dominant response to the regress problem in epistemology, but in recent decades the view has fallen into disrepute: now almost everyone is a foundationalist (with a few infinitists sprinkled here and there). In this paper, I sketch a new way of thinking about coherentism, and show how it avoids many of the problems often thought fatal for the view, including the isolation objection, worries over circularity, and concerns that the concept of coherence is (...) too vague or metaphorical for serious theoretical use. The key to my approach is to take a familiar tool from discussions of the regress problem -- namely, directed graphs depicting the support relations between beliefs -- and to use that tool in a more sophisticated manner than it is standardly employed. (shrink)

We discuss the latent variables construct, particularly in regard to the following: that latent variables are considered as the sole explanatory factor of a disorder; that pragmatic concerns are ignored; and that the relationship of these variables to biological markers is not addressed. Further, we comment on the relationship between bridge symptoms and causality, and discuss the proposal in relationship to other constructs (endophenotypes, connectionist-inspired networks).

We present a logic, \, for the discovery of deterministic causal regularities starting from empirical data. Our approach is inspired by Mackie’s theory of causes as INUS-conditions, and implements a more recent adjustment to Mackie’s theory according to which the left-hand side of causal regularities is required to be a minimal disjunction of minimal conjunctions. To derive such regularities from a given set of data, we make use of the adaptive logics framework. Our knowledge of deterministic causal regularities is, as (...) Mackie noted, most often gappy or elliptical. The adaptive logics framework is well-suited to explicate both the internal and the external dynamics of the discovery of such gappy regularities. After presenting \, we first discuss these forms of dynamics in more detail. Next, we consider some criticisms of the INUS-account and show how our approach avoids them, and we compare \ with the CNA algorithm that was recently proposed by Michael Baumgartner. (shrink)

For a long time, regularity accounts of causation have virtually vanished from the scene. Problems encountered within other theoretical frameworks have recently induced authors working on causation, laws of nature, or methodologies of causal reasoning – as e.g. May (Kausales Schliessen. Eine Untersuchung über kausale Erklärungen und Theorienbildung. Ph.D. thesis, Universität Hamburg, Hamburg, 1999), Ragin (Fuzzy-set social science. Chicago: University of Chicago Press, 2000), Graßhoff and May (Causal regularities. In W. Spohn, M. Ledwig, & M. Esfeld (Eds.), Current issues in (...) causation (pp. 85–114). Paderborn: Mentis, 2001), Swartz (The concept of physical law (2nd ed.). http://www.sfu.ca/philosophy/physical-law/, 2003), Halpin (Erkenntnis, 58, 137–168, 2003) – to direct their attention back to regularity theoretic analyses. In light of the latest proposals of regularity theories, the paper at hand therefore reassesses the criticism raised against regularity accounts since the INUS theory of causation of Mackie (The cement of the universe. A study of causation. Oxford: Clarendon Press, 1974). It is shown that most of these objections target strikingly over-simplified regularity theoretic sketches. By outlining ways to refute these objections it is argued that the prevalent conviction as to the overall failure of regularity theories has been hasty. (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)

This paper argues against the view that the standard explanation of phase transitions in statistical mechanics may be considered a causal explanation, a distortion that can nevertheless successfully represent causal relations.

A crucial question for a process view of life is how to identify a process and how to follow it through time. The genidentity view can contribute decisively to this project. It says that the identity through time of an entity X is given by a well-identified series of continuous states of affairs. Genidentity helps address the problem of diachronic identity in the living world. This chapter describes the centrality of the concept of genidentity for David Hull and proposes an (...) extension of Hull’s view to the ubiquitous phenomenon of symbiosis. Finally, using immunology as a key example, it shows that the genidentity view suggests that the main interest of a process approach is epistemological rather than ontological and that its principal claim is one of priority, namely that processes precede and define things, and not vice versa. (shrink)

This article is about Avicenna’s account of syllogisms comprising opposite premises. We examine the applications and the truth conditions of these syllogisms. Finally, we discuss the relation between these syllogisms and the principle of non-contradiction.

To clarify and illuminate the place of probability in science Ellery Eells and James H. Fetzer have brought together some of the most distinguished philosophers ...

The anti-causal prophecies of last century have been disproved. Causality is neither a ‘relic of a bygone’ nor ‘another fetish of modern science’; it still occupies a large part of the current debate in philosophy and the sciences. This investigation into causal modelling presents the rationale of causality, i.e. the notion that guides causal reasoning in causal modelling. It is argued that causal models are regimented by a rationale of variation, nor of regularity neither invariance, thus breaking down the dominant (...) Human paradigm. The notion of variation is shown to be embedded in the scheme of reasoning behind various causal models: e.g. Rubin’s model, contingency tables, and multilevel analysis. It is also shown to be latent – yet fundamental – in many philosophical accounts. Moreover, it has significant consequences for methodological issues: the warranty of the causal interpretation of causal models, the levels of causation, the characterisation of mechanisms, and the interpretation of probability. This book offers a novel philosophical and methodological approach to causal reasoning in causal modelling and provides the reader with the tools to be up to date about various issues causality rises in social science. (shrink)

Hume is known for his claim that our idea of causation is nothing beyond constant conjunction, and that our idea of necessary connection is nothing beyond a felt determination of the mind. In short, Hume endorses a "thin" conception of causation and necessary connection. In recent years, however, a sizeable number of philosophers have come to view Hume as someone who believes in the existence of thick causal connections - that is, causal connections that allow one to infer a priori (...) the effect from the cause, and vice versa. Hume doesn't wish to deny such connections, said philosopher's claim, he only seeks to demonstrate that we can't know anything about the nature of the thick causal connections that make up the natural world. In this dissertation, I defend the old or traditional interpretation of Hume on causation. I draw attention to the important but neglected role of clear and distinct perception in Hume's thought, arguing that for Hume our impressions are clear and distinct perceptions, whereas our ideas are faint and obscure. Accordingly, Hume's copy principle - the thesis that our ideas are copies of our impressions - is Hume's way of rendering our naturally obscure and confused ideas distinct. One need only discern the impression from which said ideas are copied. In this way, I show that Hume's opinion concerning our idea of thick causation is that it's an obscure and confused idea, and that the only clear and distinct idea we can have of causation is thin causation. Furthermore, since meaning for Hume is a matter of a word's being associated with an idea, Hume thinks that an expression such as "thick causation" is meaningless or confused. In one sense, then, Hume is a positivist, and as such doesn't believe in thick causal connections. (shrink)

Causation is defined as a relation between facts: C causes E if and only if C and E are nomologically independent facts and C is a necessary part of a nomologically sufficient condition for E. The analysis is applied to problems of overdetermination, preemption, trumping, intransitivity, switching, and double prevention. Preventing and allowing are defined and distinguished from causing. The analysis explains the direction of causation in terms of the logical form of dynamic laws. Even in a universe that is (...) deterministic in both temporal directions, not every fact must have a cause and present facts may have no future causes. (shrink)

The essay is an attempt to make sense of the apparently special relation between self-knowledge and agency. To achieve that goal, the essay translates the account of what it is like to be a human self offered by Sartre into the language of evolutionary psychology. In L’être et le néant, Sartre describes the phenomenology of the self as a series of inescapable choices in a contingent set of circumstances. This essay identifies Sartre’s description with what Baumeister, Maranges and Sjåstad call (...) a matrix of maybe: the mechanism of nonfactual pragmatic prospection found in humans. Consequently, it defines the self as a matrix of maybe operating within a contingency matrix and reflecting on its own operation. Self-knowledge, the essay concludes, seems special because we routinely and erroneously ascribe to the self features of its contingency matrix. Most of our true first-person claims should not be read as I PREDICATE. Instead, they can be explicated as I have to act in a world where C PREDICATE, where C is the relevant part of the contingency matrix. (shrink)

Externalist theories in natural language semantics have become the orthodoxy since Kripke is widely thought to have refuted descriptive theories involving internal cognitive representation of meaning. This shift may be seen in developments in philosophy of language of the 1970s – the direct reference “revolution against Frege”. I consider Fodor’s heretical thought that something has gone “awfully wrong” in this philosophical consensus, perhaps confirming Chomsky’s view that the whole field of philosophical semantics is “utterly wrongheaded” and “crazy” by virtue of (...) its non-naturalist assumptions and “methodological dualism.” Kripke acknowledges that he was led to his views by his “natural intuition”. Accordingly, I take up the aetiological question Chomsky poses, suggesting that we may go beyond the usual analysis of those doctrines that have been assumed too uncritically “to ask why they seem so compelling”. I suggest that the externalist orthodoxy is a kind of cognitive illusion seen elsewhere in philosophy and cognitive science. (shrink)

In "The Comparative Method" Ragin (1987) has outlined a procedure of Boolean causal reasoning operating on pure coincidence data that has meanwhile become widely known as QCA (Qualitative Comparative Analysis) among social scientists. QCA -- also in its recent form as presented in Ragin (2000) -- is designed to analyze causal structures featuring one effect and a possibly complex configuration of mutually independent direct causes of that effect. The paper at hand presents a procedure of causal reasoning that operates on (...) the same type of empirical data as QCA and that implements Boolean techniques related to the ones resorted to by QCA, yet, in contrast to QCA, the procedure introduced here successfully identifies causal structures involving both mutually dependent causes, i.e. causal chains, and multiple effects, i.e. epiphenomena. In this sense, the paper at hand generalizes QCA. (shrink)

I argue that the Carroll-Chen cosmogonic model does not provide a plausible scientific explanation of our universe's initial low-entropy state.

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)

This paper is on the problem of causal selection and comments on Collingwood's classic paper "The so-called idea of causation". It discusses the relevance of Collingwood’s control principle in contemporary life sciences and defends that it is not the ability to control, but the willingness to control that often biases us towards some rather than other causes of a phenomenon. Willingness to control is certainly only one principle that influences causal selection, but it is an important one. It shows how (...) norms make causes. (shrink)

A thoroughly physical view on reality and our common sense view on agency and free will seem to be in a direct conflict with each other: if everything that happens is determined by prior physical events, so too are all our actions and conscious decisions; you have no choice but to do what you are destined to do. Although this way of thinking has intuitive appeal, and a long history, it has recently began to gain critical attention. A number of (...) arguments have been raised in defense of the idea that our will could be genuinely free even if the universe is governed by deterministic laws of physics. Determinism and free will have been argued to be compatible before, of course, but these recent arguments seem to take a new step in that they are relying on a more profound and concrete view on the central elements of the issue, the fundamental laws of physics and the nature of causal explanation in particular. The basic idea of this approach is reviewed in here, and it is shown how a careful analysis of physics and causal explanation can indeed enhance our understanding of the issue. Although it cannot be concluded that the problem of free will would now be completely solved (or dissolved), it is clear that these recent developments can bring significant advancement to the debate. (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)