Much of the recent work on the epistemology of causation has centered on two assumptions, known as the Causal Markov Condition and the Causal Faithfulness Condition. Philosophical discussions of the latter condition have exhibited situations in which it is likely to fail. This paper studies the Causal Faithfulness Condition as a conjunction of weaker conditions. We show that some of the weaker conjuncts can be empirically tested, and hence do not have to be assumed a priori. Our results lead to (...) two methodologically significant observations: (1) some common types of counterexamples to the Faithfulness condition constitute objections only to the empirically testable part of the condition; and (2) some common defenses of the Faithfulness condition do not provide justification or evidence for the testable parts of the condition. It is thus worthwhile to study the possibility of reliable causal inference under weaker Faithfulness conditions. As it turns out, the modification needed to make standard procedures work under a weaker version of the Faithfulness condition also has the practical effect of making them more robust when the standard Faithfulness condition actually holds. This, we argue, is related to the possibility of controlling error probabilities with finite sample size (“uniform consistency”) in causal inference. (shrink)

At least historically, it was common for medical practitioners to believe causal hypotheses on the basis of standalone mechanistic reasoning. However, it is now widely acknowledged that standalone mechanistic reasoning is insufficient for appropriately believing a causal hypothesis in medicine, thanks in part to the so-called problem of masking. But standalone mechanistic reasoning is not the only type of mechanistic reasoning. When exactly then is it appropriate to believe a causal hypothesis on the basis of mechanistic reasoning? In this paper, (...) I argue that it has proved difficult to provide a satisfying answer to this question. I also argue that this difficulty is predicted by recent work in knowledge-first epistemology. I think this shows that recent work in epistemology has important implications for practice in the philosophy of science. It is therefore worth paying closer attention in the philosophy of science to this recent work in knowledge-first epistemology. (shrink)

It is tempting to analyse causality in terms of just one of the indicators of causal relationships, e.g., mechanisms, probabilistic dependencies or independencies, counterfactual conditionals or agency considerations. While such an analysis will surely shed light on some aspect of our concept of cause, it will fail to capture the whole, rather multifarious, notion. So one might instead plump for pluralism: a different analysis for a different occasion. But we do not seem to have lots of different concepts of cause (...) – just one eclectic notion. The resolution of this conundrum, I think, requires us to accept that our causal beliefs are generated by a wide variety of indicators, but to deny that this variety of indicators yields a variety of concepts of cause. This focus on the relation between evidence and causal beliefs leads to what I call epistemic causality. Under this view, certain causal beliefs are appropriate or rational on the basis of observed evidence; our notion of cause can be understood purely in terms of these rational beliefs. Causality, then, is a feature of our epistemic representation of the world, rather than of the world itself. This yields one, multifaceted notion of cause. (shrink)

A cause may influence its effect via multiple paths. Paradigmatically (Hesslow [1974]), taking birth control pills both decreases one’s risk of thrombosis by preventing pregnancy and increases it by producing a blood chemical. Building on Pearl ([2001]), I explicate the notion of a path-specific effect. Roughly, a path-specific effect of C on E via path P is the degree to which a change in C would change E were they to be transmitted only via P. Facts about such effects may (...) be gleaned from the structural equations commonly used to represent the causal relationships among variables. I contrast my analysis of the Hesslow case with those given by theorists of probabilistic causality, who mistakenly link it to issues of causal heterogeneity, token-causation and indeterminism. The reason probabilistic theories misdiagnose this case is that they pay inadequate attention to the structural relationships among variables. (shrink)

This paper argues that the semantic facts about ‘because’ are best explained via a metaphorical treatment of metaphysical explanation that treats causal explanation as explanation par excellence. Along the way, it defends a commitment to a unified causal sense of ‘because’ and offers a proprietary explanation of grounding skepticism. With the causal metaphor account of metaphysical explanation on the table, an extended discussion of the relationship between conceptual structure and metaphysics ends with a suggestion that the semantic facts about ‘because’ (...) tell against grounding-causation unity. (shrink)

This essay is concerned with concentrations of entities, which play an important—albeit often overlooked—role in scientific explanation. First, I discuss an example from molecular biology to show that concentrations can play an irreducible causal role. Second, I provide a preliminary philosophical analysis of this causal role, suggesting some implications for extant theories of causation. I conclude by introducing the concept of causation by concentration, a form of statistical causation whose widespread presence throughout the sciences has been unduly neglected and which (...) deserves to be studied in more depth. 1 Introduction2 Solving Lillie's Paradox: Lysogenic Induction in Phage λ3 Repressor Concentration and the Tuning of the Switch4 Concentration and Causality5 Preemption in Concentrations: Analysis and Implications6 Causation by Concentration: General Definition, Refinements, and Further Applications. (shrink)

This paper is an investigation into the notion of degree of influence, and its application to the problem of pre-emption. In 'Causation as Influence', Lewis presented a new account of causation under determinism and some new observations on the problem of pre-emption. He claimed that, in cases of pre-emption, the pre-empting cause is much more of a cause than its pre-empted alternative; it has much more influence. I begin by trying to make sense of the notion of degree of influence. (...) Then I emend Lewis's approach to pre-emption in response to objections, compare it to Kvart's Sustainably Reducible Influence account, and finally conclude that all these accounts fail to solve the problem of pre-emption. (shrink)

This paper argues that the non-reductive monist need not be concerned about the ‘problem’ of mental causation; one can accept both the irreducibility of mental properties to physical properties and the causal closure of the physical. More precisely, it is argued that instances of mental properties can be causally efficacious, and that there is no special barrier to seeing mental properties whose instances are causally efficacious as being causally relevant to the effects they help to bring about. It is then (...) shown that the causal relevance of mental properties is consistent with there being no downward causation, so the dilemma of ‘epiphenomenalism or reduction’ can be avoided. Non-reductive monism lives on as a viable position in the philosophy of mind. (shrink)

Hitchcock (2001a) argues that the distinction between singular and general causation conflates the two distinctions ‘actual causation vs. causal tendencies’ and ‘wide vs. narrow causation’. Based on a recent regularity account of causation I will show that Hitchcock’s introduction of the two distinctions is an unnecessary multiplication of causal concepts.

Russo and Williamson claim that establishing causal claims requires mechanistic and difference-making evidence. In this article, I will argue that Russo and Williamson's formulation of their thesis is multiply ambiguous. I will make three distinctions: mechanistic evidence as type vs object of evidence; what mechanism or mechanisms we want evidence of; and how much evidence of a mechanism we require. I will feed these more precise meanings back into the Russo–Williamson thesis and argue that it is both true and false: (...) two weaker versions of the thesis are worth supporting, while the stronger versions are not. Further, my distinctions are of wider concern because they allow us to make more precise claims about what kinds of evidence are required in particular cases. (shrink)

There are many ways of attaching two objects together: for example, they can be connected, linked, tied or bound together; and the connection, link, tie or bind can be made of chain, rope, or cement. Every one of these binding methods has been used as a metaphor for causation. What is the real significance of these metaphors? They express a commitment to a certain way of thinking about causation, summarized in the following thesis: ‘In any concrete situation, there is an (...) objective fact of the matter as to whether two events are in fact bound by the causal relation. It is the aim of philosophical inquiry to analyze this objective relation.’ Through a variety of examples, I hope to cast doubt on this seemingly innocuous thesis. The problem lies not with the word ‘objective’, but with the word ‘the’. The goal of a philosophical account of causation should not be to capture the causal relation, but rather to capture the many ways in which the events of the world can be bound together. 1 The metaphors 2 Unpacking the metaphors 3 Theories of causation 4 The two assassins 5 The birth control pills 6 The smoker-protector gene 7 The bicycle thief 8 Further examples 8.1 Indeterminism 8.2 Probability-lowering causes 8.3 Parts vs wholes 8.4 Symmetric overdetermination 8.5 Delayers 8.6 Causation by omission 8.7 Double prevention/disconnection 8.8 Preemptive prevention 8.9 Quantitative variables 9 Conclusion. (shrink)

Nancy Cartwright offers an account of causal powers, and argues that it explains some important general features of scientific method. Patricia Cheng argues that this theory is superior as a psychological theory of learning to standard models of conditioning. I extend and develop the theory, and argue that it provides the best explanation of a number of problem cases for philosophical theories of causation, including preemption, overdetermination and puzzles about transitivity. Hitchcock and Halpern & Pearl on ‘actual causes’ Problems and (...) morals 2.1 Puzzles about prevention 2.2 Counterfactuals Causal powers 3.1 Generative causal power 3.2 Preventative causal power Net and component powers ‘Actual’ or ‘successful’ causes Solutions to puzzle cases Conclusion. (shrink)

Work on analogy has been done from a number of disciplinary perspectives throughout the history of Western thought. This work is a multidisciplinary guide to theorizing about analogy. It contains 1,406 references, primarily to journal articles and monographs, and primarily to English language material. classical through to contemporary sources are included. The work is classified into eight different sections (with a number of subsections). A brief introduction to each section is provided. Keywords and key expressions of importance to research on (...) analogy are discussed in the introductory material. Electronic resources for conducting research on analogy are listed as well. (shrink)

In Making Things Happen, James Woodward influentially combines a causal modeling analysis of actual causation with an interventionist semantics for the counterfactuals encoded in causal models. This leads to circularities, since interventions are defined in terms of both actual causation and interventionist counterfactuals. Circularity can be avoided by instead combining a causal modeling analysis with a semantics along the lines of that given by David Lewis, on which counterfactuals are to be evaluated with respect to worlds in which their antecedents (...) are realized by miracles. I argue, pace Woodward, that causal modeling analyses perform just as well when combined with the Lewisian semantics as when combined with the interventionist semantics. Reductivity therefore remains a reasonable hope. (shrink)

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

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. (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)

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

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

This paper considers the applicability of standard accounts of causation to living systems. In particular it examines critically the increasing tendency to equate causal explanation with the identification of a mechanism. A range of differences between living systems and paradigm mechanisms are identified and discussed. While in principle it might be possible to accommodate an account of mechanism to these features, the attempt to do so risks reducing the idea of a mechanism to vacuity. It is proposed that the solution (...) to this problem requires the development of a philosophical account of process adequate to apply to living systems. (shrink)

This paper considers the applicability of standard accounts of causation to living systems. In particular it examines critically the increasing tendency to equate causal explanation with the identification of a mechanism. A range of differences between living systems and paradigm mechanisms are identified and discussed. While in principle it might be possible to accommodate an account of mechanism to these features, the attempt to do so risks reducing the idea of a mechanism to vacuity. It is proposed that the solution (...) to this problem requires the development of a philosophical account of process adequate to apply to living systems. (shrink)

This paper considers the applicability of standard accounts of causation to living systems. In particular it examines critically the increasing tendency to equate causal explanation with the identification of a mechanism. A range of differences between living systems and paradigm mechanisms are identified and discussed. While in principle it might be possible to accommodate an account of mechanism to these features, the attempt to do so risks reducing the idea of a mechanism to vacuity. It is proposed that the solution (...) to this problem requires the development of a philosophical account of process adequate to apply to living systems. (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)

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

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)

Cases of overdetermination or preemption continue to play an important role in the debate about the proper interpretation of causal claims of the form "C was a cause of E". I argue that the best treatment of preemption cases is given by Mackie's venerable INUS account of causal claims. The Mackie account suffers, however, from problems of its own. Inspired by its ability to handle preemption, I propose a dramatic revision to the Mackie account – one that Mackie himself would (...) certainly have rejected – to solve these difficulties. The result is, I contend, a very attractive account of singular causal claims. (shrink)

Negative causation occurs when an absence serves as cause, effect, or causal intermediary. Negative causation is genuine causation, or so I shall argue. It involves no physical connection between cause and effect. Thus causes need not be physically connected to their effects.

In this thesis I investigate causal inquiry in the social sciences, drawing on examples from various disciplines and in particular from conflict studies. In a backlash against the pervasiveness of statistical methods, in the last decade certain social scientists have focused on finding the causal mechanisms behind observed correlations. To provide evidence for such mechanisms, researchers increasingly rely on ‘process tracing’, a method which attempts to give evidence for causal relations by specifying the chain of events connecting a putative cause (...) and effect of interest. I will ask whether the causal claims process tracers make are defensible, and where they are not defensible I will ask how we can improve the method. Throughout these investigations, I show that the conclusions of process tracing are constrained both by the causal structure ofthe social world and by social scientists’ aims and values. My central argument is this: all instances of social phenomena have causally relevant differences, which implies that any research design that requires some comparison between cases is limited by how we systematize these phenomena. Moreover, such research cannot rely on stable regularities. Nevertheless, to forego causal conclusions altogether is not the right response to these limitations; by carefully outlining our epistemic assumptions we can make progress in causal inquiry. While I use philosophical theories of causation to comment on the feasibility of a social scientific method, I also do the reverse: by investigating a popular contemporary method in the social sciences, I show to what extent our philosophical theories of causation are workable in practice. Thus, this thesis is both a methodological and a philosophical work. Every chapter discusses both a fundamental philosophical position on the social sciences and a relevant case study from the social sciences. (shrink)

Mental causation is a problem and not just a problem for the nonphysicalist. One of the many lessons learned from Jaegwon Kim’s writings in the philosophy of mind is that mental causation is a problem for the nonreductive physicalist as well. A central component of the common sense picture we have of ourselves as persons is that our beliefs and desires causally explain our actions. But the completeness of the “brain sciences” threatens this picture. If all of our actions are (...) causally explained by neurophysiological events occurring in our brains, what causal role is left for our reasons and motives? It would seem that these brain events do all the causal work there is to do, thus robbing the mental of its efficacy altogether or else making it a merely superfluous or redundant causal factor. This essay presents a systematic treatment of this exclusion dilemma from the perspective of a nonreductive physicalist. I argue that both horns of this dilemma can be avoided if we ground mental causation in counterfactual dependence between distinct events and understand the mind-body relation as event realization. Although in the final analysis our actions are overdetermined by their mental and neurophysiological antecedents, this overdetermination is entirely unproblematic. (shrink)

Whether there exist causal relations between guns firing and people dying, between pedals pressed and cars accelerating, or between carbon dioxide emissions and global warming, is typically taken to be a mind-independent, objective, matter of fact. However, recent contributions to the literature on causation, in particular theories of contrastive causation and causal modelling, have undermined this central causal platitude by relativising causal facts to models or to interests. This thesis flies against the prevailing wind by arguing that we must pay (...) greater attention to which elements of our causal talk vary with context and which elements track genuine features of the world around us. I will argue that once these elements are teased apart we will be in a position to better understand some of the most persistent problems in the philosophy of causation: pre-emption cases, absence causation, failures of transitivity and overdetermination. The result is a naturalist account of causation, concordant with the contextual variability we find in our ordinary causal talk, and parsimonious with respect to the theoretical entities posited. (shrink)

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