Kolmogorov''s axiomatization of probability includes the familiarratio formula for conditional probability: 0).$$ " align="middle" border="0">.

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)

The relationship between machine learning and the philosophy of science can be classed as a dynamic interaction: a mutually beneficial connection between two autonomous fields that changes direction over time. I discuss the nature of this interaction and give a case study highlighting interactions between research on Bayesian networks in machine learning and research on causality and probability in the philosophy of science.

Is the common cause principle merely one of a set of useful heuristics for discovering causal relations, or is it rather a piece of heavy duty metaphysics, capable of grounding the direction of causation itself? Since the principle was introduced in Reichenbach’s groundbreaking work The Direction of Time (1956), there have been a series of attempts to pursue the latter program—to take the probabilistic relationships constitutive of the principle of the common cause and use them to ground the direction of (...) causation. These attempts have not all explicitly appealed to the principle as originally formulated; it has also appeared in the guise of independence conditions, counterfactual overdetermination, and, in the causal modelling literature, as the causal markov condition. In this paper, I identify a set of difficulties for grounding the asymmetry of causation on the principle and its descendents. The first difficulty, concerning what I call the vertical placement of causation, consists of a tension between considerations that drive towards the macroscopic scale, and considerations that drive towards the microscopic scale—the worry is that these considerations cannot both be comfortably accommodated. The second difficulty consists of a novel potential counterexample to the principle based on the familiar Einstein Podolsky Rosen (EPR) correlations in quantum mechanics. (shrink)

Darwinians are realists about the force of selection, but there has been surprisingly little discussion about what form this realism should take. Arguments about the units of selection in general and genic selectionism in particular reveal two realist assumptions: (1) for any selection process, there is a uniquely correct identification of the operative selective forces and the level at which each impinges; and (2) selective forces must satisfy the Pareto-style requirement of probabilistic causation. I argue that both assumptions are false; (...) we must temper realism about the force of selection and revise the way we think about probabilistic causation. (shrink)

The paper builds on the basically Humean idea that A is a cause of B iff A and B both occur, A precedes B, and A raises the metaphysical or epistemic status of B given the obtaining circumstances. It argues that in pursuit of a theory of deterministic causation this ‘status raising’ is best explicated not in regularity or counterfactual terms, but in terms of ranking functions. On this basis, it constructs a rigorous theory of deterministic causation that successfully deals (...) with cases of overdetermination and pre-emption. It finally indicates how the account's profound epistemic relativization induced by ranking theory can be undone. Introduction Variables, propositions, time Induction first Causation Redundant causation Objectivization. (shrink)

This paper outlines a general theory of efficient causation, a theory that deals in a unified way with traditional or deterministic, indeterministic, probabilistic, and other causal concepts. Theorists like Lewis, Salmon, and Suppes have attempted to broaden our causal perspective by reductively analysing causal notions in other terms. By contrast, the present theory rests in the first place on a non-reductive analysis of traditional causal concepts — into formal or structural components, on the one hand, and a physical or metaphysical (...) component, on the other. The analyzans is then generalised. The theory also affords a more general propensity notion than is standard, one that helps solve major problems facing propensity interpretations of probability. (shrink)

This paper attempts to set up a probabilistic framework for understanding the notion of causal necessity. What results is a relaxed and relativized probabilistic theory of epsilon-Causal necessity and an explicit attempt to avoid deterministic assumptions. The theory developed emphasizes the notions of partial cause, Causal contribution, And the degree of contribution. Implications for causal overdetermination, Causal preemption, And causal discourse are discussed.

According to Nancy Cartwright, a causal law holds just when a certain probabilistic condition obtains in all test situations which in turn satisfy a set of background conditions. These background conditions are shown to be inconsistent and, on separate account, logically incoherent. I offer a corrective reformulation which also incorporates a strategy for problems like Hesslow's thrombosis case. I also show that Cartwright's recent argument for modifying the condition to appeal to singular causes fails.Proposed modifications of the theory's probabilistic condition (...) to handle effects with extreme probabilities (0 or 1) are found unsatisfactory. I propose a unified solution which also handles extreme causes. Undefined conditional probabilities give rise to three good, but non-equivalent, ways of formulating the theory. Various formulations appear in the literature. I give arguments to eliminate all but one candidate. Finally, I argue for a crucial new condition clause, and show how to extend the results beyond a simple probabilistic framework. (shrink)

Bayesian networks are computer programs which represent probabilitistic relationships graphically as directed acyclic graphs, and which can use those graphs to reason probabilistically , often at relatively low computational cost. Almost every expert system in the past tried to support probabilistic reasoning, but because of the computational difficulties they took approximating short-cuts, such as those afforded by MYCIN's certainty factors. That all changed with the publication of Judea Pearl's Probabilistic Reasoning in Intelligent Systems, in 1988, which synthesized a decade of (...) research making accurate graphical probabilistic reasoning computationally achievable.Bayesian network technology is now one of the fastest growing fields of research in artificial intelligence. That it has become a publication industry in its own right is shown by a search on Google scholar :This development, together with a parallel related growth in the use of causal discovery algorithms which automate the learning of Bayesian networks from sample data, has generated considerable interest, and controversy, within the philosophy-of-science community.Three central questions bringing together AI researchers and philosophers of science are: Are Bayesian networks Bayesian? What is the relation between probability and causality? Are the assumptions behind causal discovery of Bayesian networks realistic or fantastical?Jon Williamson, as a philosopher of science with a keen interest in the technology, asks and answers these questions in his new book. Although it is self-contained, his book is not very likely as an introduction to the technology , nor is it optimal even as an introduction to the philosophical problems in interpreting Bayesian networks . Rather Williamson's book is an attempt to move the debate forward by solving the central problems of the …. (shrink)

Causal inference in the empiricalsciences is based on counterfactuals. The mostcommon approach utilizes a statistical model ofpotential outcomes to estimate causal effectsof treatments. On the other hand, one leadingapproach to the study of causation inphilosophical logic has been the analysis ofcausation in terms of counterfactualconditionals. This paper discusses and connectsboth approaches to counterfactual causationfrom philosophy and statistics. Specifically, Ipresent the counterfactual account of causationin terms of Lewis's possible-world semantics,and reformulate the statistical potentialoutcome framework using counterfactualconditionals. This procedure highlights variousproperties and (...) mechanisms of the statisticalmodel. (shrink)

This essay furthers debate about the burgeoning science of Probabilistic Event Attribution (PEA) and its relevance to imminent climate policy decisions. It critically examines Allen Thompson and Friederike Otto’s recent arguments concerning the implications of PEA studies for how the United Nations Framework Convention on Climate Change (UNFCCC) policy framework should be revised during the 2016 ‘review and decision.’ I show that their contention that PEA studies cannot usefully inform decision-making about adaptation policies and strategies is misguided and argue that (...) the current UNFCCC treaty, the “Paris Agreement,” supersedes their proposed revision. (shrink)

In the paper it will be shown that Reichenbach’s Weak Common Cause Principle is not valid in algebraic quantum field theory with locally finite degrees of freedom in general. Namely, for any pair of projections A, B supported in spacelike separated double cones ${\mathcal{O}}_{a}$ and ${\mathcal{O}}_{b}$ , respectively, a correlating state can be given for which there is no nontrivial common cause (system) located in the union of the backward light cones of ${\mathcal{O}}_{a}$ and ${\mathcal{O}}_{b}$ and commuting with the both (...) A and B. Since noncommuting common cause solutions are presented in these states the abandonment of commutativity can modulate this result: noncommutative Common Cause Principles might survive in these models. (shrink)

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)

Concerning any object of philosophical analysis, we can ask several questions, including the two posed in the title of this paper. Despite difficulties in formulating a precise criterion to distinguish causal processes from pseudoprocesses, and causal interactions from mere spatiotemporal intersections, I argue that Salmon answered the first of these questions with extraordinary clarity. The second question, by contrast, has received very little attention. I will present two problems: in the first, it seems that Salmon has provided exactly the conceptual (...) resources needed to solve the problem; in the second, it is difficult to see how causal processes and interactions may be used to shed any light. In general, the way to carry Salmon's program forward will be to demonstrate that these resources can be made to do real philosophical work. (shrink)

There is no such thing as moral luck or everyone is profoundly mistaken about its nature and a radical rethinking of moral luck is needed. The argument to be developed is not complicated, and relies almost entirely on premises that should seem obviously correct to anyone who follows the moral luck literature. The conclusion, however, is surprising and disturbing. The classic cases of moral luck always involve an agent who lacks control over an event whose occurrence affects her praiseworthiness or (...) blameworthiness. Close examination of what it is to have control or to lack it reveals the logical space for counterexamples that do not fit the pattern constitutive of moral luck, and so unravel the whole. (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)

The role of measure theoretic atomicity in common cause closedness of general probability theories with non-distributive event structures is raised and investigated. It is shown that if a general probability space is non-atomic then it is common cause closed. Conditions are found that entail that a general probability space containing two atoms is not common cause closed but it is common cause closed if it contains only one atom. The results are discussed from the perspective of the Common Cause Principle.

A probability space is common cause closed if it contains a Reichenbachian common cause of every correlation in it and common cause incomplete otherwise. It is shown that a probability space is common cause incomplete if and only if it contains more than one atom and that every space is common cause completable. The implications of these results for Reichenbach's Common Cause Principle are discussed, and it is argued that the principle is only falsifiable if conditions on the common cause (...) are imposed that go beyond the requirements formulated by Reichenbach in the definition of common cause. (shrink)

The analyses of explanation and causal beliefs are heavily dependent on using probability functions as models of epistemic states. There are, however, several aspects of beliefs that are not captured by such a representation and which affect the outcome of the analyses. One dimension that has been neglected in this article is the temporal aspect of the beliefs. The description of a single event naturally involves the time it occurred. Some analyses of causation postulate that the cause must not occur (...) later than the effect. If we want this kind of causality it is easy to add the appropriate clause to ( CAUS ). An alternative is not to rule out backwards causation or causal loops a priori , but expect that ( CAUS ), via the properties of the contraction P C - , will result in the desired temporal relation between C and E . One way of ensuring this is to postulate that when the probability function P is contracted to P C - , the probabilities of all events that occurred before C remain the same in P C - as in P . This means that all beliefs about the history of events up to C are left unaltered in the construction of the hypothetical state of belief P C - . In conclusion, I hope to have shown that, in spite of these limitations, ( EXP ) and ( CAUS ) provide viable analyses of explanation and causality between single events for the case when epistemic states can be described by probability functions. I have also shown that the two analyses can be used to explicate the close connections between the two notions. These analyses reduce the problems of explanation and causality, hopefully in a non-circular way, to the problem of identifying contractions of states of belief. (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 development of causal modelling since the 1950s has been accompanied by a number of controversies, the most striking of which concerns the Markov condition. Reichenbach's conjunctive forks did satisfy the Markov condition, while Salmon's interactive forks did not. Subsequently some experts in the field have argued that adequate causal models should always satisfy the Markov condition, while others have claimed that non-Markovian causal models are needed in some cases. This paper argues for the second position by considering the multi-causal (...) forks, which are widespread in contemporary medicine (Section 2). A non-Markovian causal model for such forks is introduced and shown to be mathematically tractable (Sections 6, 7, and 8). The paper also gives a general discussion of the controversy about the Markov condition (Section 1), and of the related controversy about probabilistic causality (Sections 3, 4, and 5). (shrink)

This paper investigates the relations between causality and propensity. Aparticular version of the propensity theory of probability is introduced, and it is argued that propensities in this sense are not causes. Some conclusions regarding propensities can, however, be inferred from causal statements, but these hold only under restrictive conditions which prevent cause being defined in terms of propensity. The notion of a Bayesian propensity network is introduced, and the relations between such networks and causal networks is investigated. It is argued (...) that causal networks cannot be identified with Bayesian propensity networks, but that causal networks can be a valuable heuristic guide for the construction of Bayesian propensity networks. (shrink)

Two kinds of causal inference rules which are widely used by social scientists are investigated. Two conceptions of causation also widely used are explicated — the INUS and probabilistic conceptions of causation. It is shown that the causal inference rules which link correlation, a kind of partial correlation, and a conception of causation areinvalid. It is concluded anew methodology is required for causal inference.

Philosophers and scientists have maintained that causation, correlation, and partial correlation are essentially related. These views give rise to various rules of causal inference. This essay considers the claims of several philosophers and social scientists for causal systems with dichotomous variables. In section 2 important commonalities and differences are explicated among four major conceptions of correlation. In section 3 it is argued that whether correlation can serve as a measure of A's causal influence on B depends upon the conception of (...) causation being used and upon certain background assumptions. In section 4 five major kinds of partial correlation are explicated, and some of the important relations are established among two conceptions of partial correlation, the conception of screening off, the conception of partitioning, and the measures of causal influence which have been suggested by advocates of path analysis or structural equation methods. In section 5 it is argued that whether any of these five conceptions of partial correlation can serve as a measure of causal influence depends upon the conception of causation being used and upon certain background assumptions.The important conclusion is that each of the approaches (considered here) to causal inference for causal systems with dichotomous variables stands in need of important qualifications and revisions if they are to be justified. (shrink)

During the past decades several philosophers of science and social scientists have been interested in the problems of causation. Recently attention has been given to probabilistic causation in dichotomous causal systems. The paper uses the basic features of probabilistic causation to argue that the causal modeling approaches developed by such researchers as Blalock and Duncan can provide, when an additional assumption is added, adequate qualitative measures of one variableś causal influence upon another. Finally, some of the difficulties and issues involved (...) in developing adequate quantitative measures are discussed, and it is concluded that the causal modeling measures cannot provide adequate quantitative measures. (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)

We characterize, by easily verifiable properties, abstract ternary relations isomorphic to the causal betweenness introduced by Hans Reichenbach.

Epistemologies and research methods are not free of metaphysics. This is to say that they are both, supported by (or presumed by), and support (or presume) fundamental ontologies. A discussion of the epistemological foundations of "multimethod" research in the social sciences—in as much as such research claims to unearth "causal" relations—therefore cannot avoid the ontological presuppositions or implications of such a discussion. But though there isn’t necessarily a perfect correspondence between ontology, epistemology, and methodology, they do constrain each other. As (...) such it is possible to make methodological choices that are at odds with one’s (implicit) ontology or argue from an ontology that is inconsistent one’s choice of methods.Yet lack of recognition of this fact has hampered methodological discussions in political science, especially with respect to the discussion on the merits of multimethod research. The ontology implicitly accepted in such discussions is "reductionist" and "regularist," that is, one that respectively defines causes in terms of noncausal relations and states of affair and affirms that such noncausal relations are regularities in nature. This article will argue that any attempt to fit "multimethod" research (where "multimethod" signifies some combination of inferential statistics and case studies) within this narrow ontology is destined to fail since such a metaphysics logically cannot accord case studies a necessary or sufficient role in the in the establishment of causal relations. However, there are metaphysical positions within the ambit of an empiricist philosophy of science that can accommodate multiple methods without contradiction. The article discusses two such ontologies and suggests ways in which they might allow the establishment of a coherent epistemological foundation for multimethod research, however, within a decidedly empiricist philosophy of science. (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)

Przedmowa Problematyka związana z zależnościami przyczynowymi, ich modelowaniem i odkrywa¬niem, po długiej nieobecności w filozofii i metodologii nauk, budzi współcześnie duże zainteresowanie. Wiąże się to przede wszystkim z dynamicznym rozwojem, zwłaszcza od lat 1990., technik obli¬czeniowych. Wypracowane w tym czasie sieci bayesowskie uznaje się za matematyczny język przyczynowości. Pozwalają one na daleko idącą auto¬matyzację wnioskowań, co jest także zachętą do podjęcia prób algorytmiza¬cji odkrywania przyczyn. Na potrzeby badań naukowych, które pozwalają na przeprowadzenie eksperymentu z randomizacją, standardowe metody ustalania zależności przyczynowych (...) opracowano na początku XX wieku. Zupełnie inaczej sprawa przedstawia się w przypadku badań nieeksperymentalnych, gdzie podobne rozwiązania pozostają kwestią przyszłości. Zadaniem tej książki jest podanie warunków, które powinny być spełnione przez te rozwiązania, oraz sformułowanie proceduralnego kryterium zależności przy¬czynowych jako szczegółowej realizacji tych warunków. Pociąga ono waż¬kie konsekwencje dla filozofii i metodologii nauk, które ujawnia – podany w Części II – zarys me-todolo¬gii proceduralnej. W literaturze przedmiotu brakuje w miarę wszechstronnego i systema¬tycznego omówie¬nia najnowszych filozoficznych i metodologicznych dys¬kusji na temat przy¬czynowości, co niech będzie wytłumaczeniem, dlaczego w niektórych punktach obecnej książki szczegółowo referuję trudno dos¬tępne teksty źró¬dłowe. Przymiotnik „proceduralny” używam tu w znaczeniu węższym niż Huw Price (w którego pracach właściwszy byłby termin „kryterialny”) dla podkre¬ślenia – zgodnie z łacińskim źródłosłowem procedo – że dla ustalenia przy¬czyny niezbędne jest podjęcie przez uczonych określonych interakcji z ba¬daną rzeczywistością. Zalążki zamysłu prezentowanego w tej książce przedstawiłem podczas warsztatów filozoficznych „Philosophy and Probability” w roku 2002, zor¬ganizowanych przez Instytut Filozofii Uniwersytetu w Konstancji. Wdzięczny jestem uczestnikom tych warsztatów za uwagi, a przede wszyst¬kim następującym osobom: Luc Bovens, Brandon Fitelson, Alan Hájek, Stephan Hartmann oraz Jon Williamson. Podczas międzynarodowej konferencji „Analytical Pragmatism”, zorgani¬zowanej w Lublinie w roku 2003 przez Wydział Filo¬zofii Katolickiego Uniwersytetu Lubelskiego, odniosłem swoją koncepcję do prac Nancy Cartwright. Szczególnie inspirujący okazał się komentarz Huw Price’a do mojego referatu i przeprowadzona z nim dysku¬sja. Ujęcie koncepcji metodologii proceduralnej na szerszym tle współ-czes¬nego nurtu empirystycznego w filozofii nauki przedstawiłem w roku 2004 podczas konferencji „5th Quadrennial Fellows Conference”, zorgani¬zowanej przez Instytut Filozofii Uniwersytetu Jagiellońskiego oraz Centrum Filozofii Nauki w Pittsburghu. Szczególnie pomocne w dalszych moich pra¬cach były uwagi Jamesa Bogena, Janet Kourany, Jamesa Lennoxa, Johna Nortona, Thomasa Bonka, Jana Woleńskiego i Johna Worralla, za które wyra¬żam swoją wdzięczność. Korpus książki powstał podczas mojego stażu w Centrum Filozofii Nauki w Pittsburghu, który odbyłem jako stypendysta Fundacji na Rzecz Nauki Polskiej w roku akademickim 2004-2005. Uczestniczyłem w tym czasie w życiu naukowym Centrum i w pracach badawczych zespołu z Instytutu Filozofii Uniwersytetu Carnegie-Mellon w Pittsburghu kierowanego przez Clarka Glymoura. Na jego ręce składam podziękowanie za wiele po¬mocnych uwag do moich wy¬stąpień oraz tekstów i za dyskusje przede wszystkim z nim samym i z jego najbliższymi współpracownikami: Peterem Spirtesem oraz Richardem Scheinesem, a także pozostałymi członkami tego zes¬połu, doktorantami i uczestnikami seminarium badawczego „Causality in the Social Sciences”. Za wieloletnie wsparcie, wielopłaszczyznowe inspiracje towarzyszące pi¬saniu tej książki, a także liczne pomocne uwagi do jej wcześniejszych wersji dziękuję przede wszystkim Księdzu Profesorowi Andrzejowi Bronkowi oraz Księdzu Profesorowi Józefowi Herbutowi, współprowadzącemu seminarium doktorskie w Katedrze Metodologii Nauk Katolickiego Uniwersytetu Lubel¬skiego im. Jana Pawła II, jak również pozostałym uczestnikom tego semina¬rium. Dziękuję mojej Żonie, dr Annie Kawalec za wiele wysiłku włożonego w ulepszenie redakcji – językowej i merytorycznej – obecnej książki. Książkę tę można czytać na kilka sposobów. Czytelnikom zainteresowa¬nym przede wszystkim prowadzeniem badań empirycznych polecałbym rozpoczęcie od Rozdziału 2. i kontynuację pozostałych rozdziałów Części I, a następnie Dodatków. Czytelnikom zainteresowanym problemami filozo¬fii i metodologii nauk polecałbym rozpoczęcie lektury książki od Części II i uzupełniającą lekturę Rozdziału 2., a następnie Wprowadzenia i Zakończenia. Czytelnikom mniej zainteresowanym zagadnieniami teoretycznymi pole¬całbym zapoznanie się z fascynującymi dziejami odkrycia przyczyn cholery przez Johna Snowa, które rekonstruuję w Rozdziale 1. W dalszej części nato¬miast polecałbym przejście do Wprowadzenia i Zakończenia, które w mniej specjalistyczny sposób przybliżają proponowane tu rozstrzygnięcia. Tekst książki nie był dotąd publikowany. Wyjątkiem są pewne fragmenty Rozdziału 8. oraz 9., które w zmienionej postaci ukazały się w Rocznikach Filozoficznych (Kawalec 2004). -/- Lublin, luty 2006 r. (shrink)

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)

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

I present Aristotle’s theory of causation in a way that privileges a comparison with contemporary discussion on causation. I do so by selecting in Aristotle’s theory points that are interesting to contemporary discussion and by translating Aristotle in the contemporary philosophical terminology. I compare Aristotle’s views with Mackie’s (1993/1965) and Sosa’s (1993/1980). Mackie is a humean regularist regarding the metaphysics of causal necessity, but his theory postulates some formal aspects of the causal relation which are similar to the Aristotelian theory. (...) By introducing the notion of causal field as a third causal relatum – a sample in which the cause must be picked out as a explanation coextensive to the effect –, Mackie holds a point very similar to Aristotle, inasmuch as both defend that the causal relation is triadic and both have the extensional desideratum. Sosa (1993/1980) defends that every cause necessitates its effect, arguing against classical Humeanism, and he also proposes a causal pluralism. Both these theses are clearly Aristotelian. Aristotle comprehends that the causal relation has three relata: a subjacent C, a property of that subjacent A and a cause B that explains why such property is attributed to that subjacent. The subjacent is similar to Mackie’s notion of causal field, for in regard to it the cause must be coextensive to the property. But Aristotle also says that for each explanandum (property attributed to a subjacent of which one aims to investigate a cause) there is only one cause, which necessitates it. Sosa and Aristotle are similar because both develop a causal pluralism from a theory of causes as having intrinsic necessitation. For Aristotle, causes/explanations [aitiai] are central for attaining scientific knowledge, and its triadic structure determines the syllogistic structure of scientific demonstrations. Aristotle’s theory of causation also involves comprehending the actualisation of capacities (dispositional properties of objects) affirming that the causal relation is resultant from intrinsic properties of the objects, and the cause B is the essence of the explanandum. (shrink)