This paper argues that emergent conscious properties can't bestow emergent causal powers. It supports this conclusion by way of a dilemma. Necessarily, an emergent conscious property brings about its effects actively or other than actively. If actively, then, the paper argues, the emergent conscious property can't have causal powers at all. And if other than actively, then, the paper argues, the emergentist finds himself committed to incompatible accounts of causation.

Reasoning about causation in fact is an essential element of attributing legal responsibility. Therefore, the automation of the attribution of legal responsibility requires a modelling effort aimed at the following: a thorough understanding of the relation between the legal concepts of responsibility and of causation in fact; a thorough understanding of the relation between causation in fact and the common sense concept of causation; and, finally, the specification of an ontology of the concepts that are minimally required for (automatic) common (...) sense reasoning about causation. This article offers a worked-out example of the indicated analysis. Such example consists of: a definition of the legal concept of responsibility (in terms of liability and accountability); a definition of the legal concept of causation in fact (in terms of the initiation of physical processes by an agent and of the provision of reasons and/or opportunities to other agents); CausatiOnt, an AI-like ontology of the common sense (causal) concepts that are minimally needed for reasoning about the legal concept of causation in fact (in particular, the concepts of category, dimension, object, agent, process, event and act). (shrink)

Situation theory, as developed by Barwise and his collaborators, is used to demonstrate the possibility of defining teleology (and related notions, like that of proper or biological function) in terms of higher order causation, along the lines suggested by Taylor and Wright. This definition avoids the excessive narrowness that results from trying to define teleology in terms of evolutionary history or the effects of natural selection. By legitimating the concept of teleology, this definition also provides promising new avenues for solving (...) long standing problems in the philosophy of mind, such as the problems of intentionality and mental causation. (shrink)

It is often natural to compare two events by describing one as ‘more of a cause’ of some effect than the other. But what do such comparisons amount to, exactly? This paper aims to provide a guided tour of the recent literature on ‘degrees of causation’. Section 2 looks at what I call ‘dependence measures’, which arise from thinking of causes as difference‐makers. Section 3 looks at what I call ‘production measures’, which arise from thinking of causes as jointly sufficient (...) for their effects. Finally, section 4 examines the important question of whether there is any sense in which an agent is more responsible for an outcome in virtue of her action being more of a cause of it. I describe a puzzle that emerges from this question, and explore various strategies for resolving it. (shrink)

Current research in molecular epidemiology uses biomarkers to model the different disease phases from environmental exposure, to early clinical changes, to development of disease. The hope is to get a better understanding of the causal impact of a number of pollutants and chemicals on several diseases, including cancer and allergies. In a recent paper Russo and Williamson address the question of what evidential elements enter the conceptualisation and modelling stages of this type of biomarkers research. Recent research in causality has (...) examined Ned Hall’s distinction between two concepts of causality: production and dependence. In another recent paper, Illari examined the relatively under-explored production approach to causality, arguing that at least one job of an account of causal production is to illuminate our inferential practices concerning causal linking. Illari argued that an informational account solves existing problems with traditional accounts. This paper follows up this previous work by investigating the nature of the causal links established in biomarkers research. We argue that traditional accounts of productive causality are unable to provide a sensible account of the nature of the causal link in biomarkers research, while an informational account is very promising. (shrink)

This paper argues against dismissing the Principle of Alternative Possibilities merely on the ground of so-called Frankfurt-style cases. Its main claims are that the interpretation of such cases depends on which substantive theory of responsibility one endorses and that Frankfurt-style cases all involve some form of causal overdetermination which can be interpreted either as being compatible with the potentially manipulated agent’s ability to act otherwise or as a responsibility undermining constraint. The paper also argues that the possibility of such scenarios (...) can support the truth of classical compatibilism as much as the truth of semicompatibilism. (shrink)

In this paper I analyse who should be able to control the use of human embryonic stem cell lines. I distinguish between different kinds of control and analyse a set of arguments that purport to show that the donors of gametes and embryos should not be able to control the use of stem cell lines derived from their embryos. I show these arguments to be either deficient or of so general a scope that they apply not only to donors but (...) also to those who derived the stem cell lines. Since we normally think that stem cell derivers have the right to control the use of the cell lines they derived, we have no justification for denying donors similar rights of control. In the final section I briefly discuss why informed consent is not an appropriate vehicle for transferring or alienating control rights. (shrink)

Cardiff Law School, Museum Avenue, Cardiff CF10 3AX, UK. Tel: +44(0)2920875447, Fax: +44(0)2920874097; Email: Holms{at}cardiff.ac.uk ' + u + '@' + d + ' '//--> Abstract The paper presents a brief overview of current knowledge about (i) the link between parental behaviour and lifestyle and childhood obesity, (ii) the many other factors influencing overweight and obesity rates in children and (iii) the effectiveness of interventions in children who are already overweight and obese. On the basis of this, it is analysed (...) to what extent it is meaningful to attribute causal and moral responsibility to parents in theory and in practice. It is argued that although there is a sense in which many parents are causally and morally responsible for the obesity of their children, most parents are not blameworthy and the attribution of parental responsibility in most cases does not justify intervention in the family context by society on behalf of the children. In the analysis of the possible justification of more general interventions, parallels are drawn to the distinction between hard and soft forms of paternalism. Train up a child in the way he should go; and when he is old, he will not depart from it. (Proverbs 22: 6) For I have told him that I will judge his house for ever for the iniquity which he knoweth; because his sons made themselves vile, and he restrained them not. 1. (Samuel 3: 13) CiteULike Connotea Del.icio.us What's this? (shrink)

This paper develops a general approach to how society should compensate for losses that individuals incur due to public health interventions aimed at controlling the spread of infectious diseases. The paper falls in three parts. The first part provides an initial introduction to the issues and briefly outlines five different kinds of public health interventions that will be used as test cases. They are all directed at individuals and aimed at controlling the spread of infectious diseases (1) isolation, (2) quarantine, (...) (3) recommended voluntary social distancing, (4) changes in health care provision for asymptomatic carriers of multi-resistant microorganisms, and (5) vaccination. The interventions will be briefly described including the various risks, burdens and harms individuals who are subject to these interventions may incur. The second part briefly surveys current compensation mechanisms as far as any exist and argue that even where they exist they are clearly insufficient and do not provide adequate compensation. The third part will then develop a general framework for compensation for losses incurred due to public health interventions in the infectious disease context. This is the major analytical and constructive part of the paper. It first analyses pragmatic and ethical arguments supporting the existence of an obligation on the part of the state to compensate for such losses, and then considers whether this obligation can be defeated by (1) resource considerations, or (2) issues relating to personal responsibility. (shrink)

It is often thought that non-junk or coding DNA is more significant than other cellular elements, including so-called junk DNA. This is for two main reasons: because coding DNA is often targeted by historical or current selection, it is considered functionally special and because its mode of action is uniquely specific amongst the other actual difference makers in the cell, it is considered causally special. Here, we challenge both these presumptions. With respect to function, we argue that there is previously (...) unappreciated reason to think that junk DNA is significant, since it can alter the cellular environment, and those alterations can influence how organism-level selection operates. With respect to causality, we argue that there is again reason to think that junk DNA is significant, since it too is remarkably causally specific. As a result, something is missing from the received view of significance in molecular biology—a view which emphasizes specificity and neglects something we term ‘reach’. With the special case of junk DNA in mind, we explore how to model and understand the causal specificity, reach, and corresponding efficacy of difference makers in biology. The account contains implications for how evolution shapes the genome, as well as advances our understanding of multi-level selection. (shrink)

In the last half century, decision theory has had a deep influence on moral theory. Its impact has largely been beneficial. However, it has also given rise to some problems, two of which are discussed here. First, issues such as risk-taking and risk imposition have been left out of ethics since they are believed to belong to decision theory, and consequently the ethical aspects of these issues have not been treated in either discipline. Secondly, ethics has adopted the decision-theoretical idea (...) that action-guidance has to be based on cause–effect or means–ends relationships between an individual action and its possible outcomes. This is problematic since the morally relevant connections between an action and future events are not fully covered by such relationships. In response to the first problem it is proposed that moral theory should deal directly and extensively with issues such as risk-taking and risk imposition, thereby intruding unabashedly into the traditional territory of decision theory. As a partial response to the second problem it is proposed that moral theorizing should release itself from the decision-theoretical requirement that the moral status of an action has to be derivable from the consequences (or other properties) that are assignable to that action alone. In particular, the effects that an action can have in combination with other actions by the same or other agents are valid arguments in an action-guiding moral discourse, even if its contribution to these combined consequences cannot be isolated and evaluated separately. (shrink)

Scientific methods are heuristic in nature. Heuristics are simplifying, incomplete, underdetermined and fallible problem-solving rules that can nevertheless serve certain goals in certain contexts better than truth-preserving algorithms. Because of their goal- and context-dependence, a framework is needed for systematic choosing between them. This is the domain of scientific methodology. Such a methodology, I argue, relies on a form of instrumental rationality. Three challenges to such an instrumentalist account are addressed. First, some authors have argued that the rational choice of (...) at least some methods, namely those supporting belief formation, is not goal-dependent. Second, some authors have observed that some method choices seem intuitively rational, even though relevant goals are lacking. Thirdly, some authors have argued that instrumental rationality itself depends on a goal-independent form of rationality. It is the heuristic nature of scientific methods that affords me the arguments against these challenges. This heuristic-instrumentalist account provides the means-ends analysis needed to evaluate heuristic method choice. The paper thus offers the conceptual basis for a scientific methodology that is both compatible with the heuristic nature of actual scientific practice and also normatively relevant for assessing method choice. (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)

There is a critical inconsistency in the literature on analogical retrieval. On the one hand, a vast set of laboratory studies has found that people often fail to retrieve past experiences that share deep relational commonalities, even when they would be useful for reasoning about a current problem. On the other hand, historical studies and naturalistic research show clear evidence of remindings based on deep relational commonalities. Here, we examine a possible explanation for this inconsistency—namely, that remindings based on relational (...) principles increase as a function of expertise. To test this claim, we devised a simple analogy‐generation task that can be administered across a wide range of expertise. We presented common events as the bases from which to generate analogies. Although the events themselves were unrelated to geoscience, we found that when the event was explainable in terms of a causal principle that is prominent in geoscience, expert geoscientists were likely to spontaneously produce analogies from geoscience that relied on the same principle. Further, for these examples, prompts to produce causal analogies increased their frequency among nonscientists and scientists from another domain, but not among expert geoscientists (whose spontaneous causal retrieval levels were already high). In contrast, when the example was best explained by a principle outside of geoscience, all groups required prompting to produce substantial numbers of analogies based on causal principles. Overall, this pattern suggests that the spontaneous use of causal principles is characteristic of experts. We suggest that expert scientists adopt habitual patterns of encoding according to the key relational principles in their domain, and that this contributes to their propensity to spontaneously retrieve relational matches. We discuss implications for the nature of expertise and for science instruction and assessment. (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)

Philosophical theories of causation are commonly judged by their ability to correctly determine whether there is a causal relation present in intuitively clear example scenarios. If the theories survive this test, they are then used to answer big philosophical questions about causation. This Method of Examples is attractive because it seems to allow us to determine the quality of a theory of causation independently of answering the big philosophical questions; which is good, since it means that we can then non-circularly (...) use the theories judged to be best to answer those questions. However, the current article argues that this virtue of the Method of Examples is an illusion. In particular, I argue that the necessary step of judging whether a proposed analysis of causation is reductive can only be taken after many of the most vexing philosophical questions about causation have already been answered. It is then shown that a rejection of the methodological supremacy of the Method of Examples leads to a more pluralistic method of judging theories of causation, a pluralism that benefits non-standard approaches like interventionism and agency theories. (shrink)

Many methods are used in research on complexity. One of these is qualitative comparative analysis. Although many authors allude to the relationships between complexity and QCA, these links are rarely made explicit. We propose that one way of doing so is by using critical realism as a meta-framework. This article discusses the viability of this approach by examining the extent to which QCA is a complexity-informed method. This question is answered in three steps. First, we discuss the nature of complexity (...) and its epistemological implications. Second, we focus on Bhaskar’s perspective on critical realism and show how it can be used as a framework for understanding social complexity. Third, we examine the ontological and epistemological assumptions underlying QCA and synthesize these with our critical realist approach to complexity. We argue that complex reality is non-decomposable, contingent, non-compressible and time-asymmetric. We conclude that, although QCA is inevitably reductive and partial, its core premises are built upon the notions of contingency and time-asymmetry. Therefore, it is not only a powerful method for doing complexity-informed research, but is also a complexity-informed method by itself. (shrink)

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)

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)