Alex Broadbent

This chapter explores the idea that causal inference is warranted if and only if the mechanism underlying the inferred causal association is identified. This mechanistic stance is discernible in the epidemiological literature, and in the strategies adopted by epidemiologists seeking to establish causal hypotheses. But the exact opposite methodology is also discernible, the black box stance, which asserts that epidemiologists can and should make causal inferences on the basis of their evidence, without worrying about the mechanisms that might underlie their hypotheses. I argue that the mechanistic stance is indeed a bad methodology for causal inference. However, I detach and defend a mechanistic interpretation of causal generalisations in epidemiology as existence claims about underlying mechanisms.

When is a cause of a cause of an effect also a cause of that effect? The right answer is either Sometimes or Always. In favour of Always, transitivity is considered by some to be necessary for distinguishing causes from redundant non-causal events. Moreover transitivity may be motivated by an interest in an unselective notion of causation, untroubled by principles of invidious discrimination. And causal relations appear to add up like transitive relations, so that the obtaining of the overarching relation is not independent of the obtaining of the intermediaries. On the other hand, in favour of Sometimes, often we seem not to treat events that are very spatiotemporally remote from an effect as its causes, even when connected to the effect in question by a chain of counterfactual or chance-raising dependence. Moreover cases of double prevention provide counterexamples to causal transitivity even over short chains. According to the argument of this paper, causation is non-transitive. Transitizing causation provides no viable account of causal redundancy. An unselective approach to causation may motivate resisting the distance counterexamples to transitivity, but it does not help with double prevention, and even makes it more intractable. The strongest point in favour of transitivity is the adding up of causal relations, and this is the point that extant non-transitizing analyses have not adequately addressed. I propose a necessary condition on causation that explains the adding up phenomenon. In doing so it also provides a unifying explanation of distance and double prevention counterexamples to transitivity.

This paper takes it as a premise that a distinction between matters of fact and of law is important in the causal inquiry. But it argues that separating factual and legal causation as different elements of liability is not the best way to implement the fact/law distinction. What counts as a cause-in-fact is partly a legal question; and certain liability-limiting doctrines under the umbrella of “legal causation” depend on the application of factual-causal concepts. The contrastive account of factual causation proposed in this paper improves matters. This account more clearly distinguishes matters of fact from matters of law within the cause-in-fact inquiry. It also extends the scope of cause-in-fact to answer some questions currently answered by certain doctrines of legal causation—doctrines that, it is argued, are more naturally seen as applications of our ordinary causal concept than as noncausal liability-limiting devices.

We are pleased to once again present to the readers of Theoretical Medicine and Bioethics papers from the Philosophy of Medicine Roundtable. Previous issues have followed the 3rd and 4th Roundtables, and the current issue presents a selection from the more than 20 papers presented at the 5th Philosophy of Medicine Roundtable, which took place in New York, at Columbia University, in November 2013. Like its predecessors, held in Birmingham, AL, Rotterdam, and San Sebastian, this Roundtable attracted speakers from around the world. It also featured keynote presentations from Rita Charon of Columbia University and Ross Upshur of the University of Toronto.It may seem somewhat odd to feature a special issue on philosophy of medicine in a journal that effectively has philosophy of medicine in its title. However, a review of the contents of this journal and similar ones, such as the Journal of Medicine and Philosophy, will quickly reveal such an issue’s purpose. The dominant content of these j ..

If there is any value in the idea that disease is something other than the mere absence of health then that value must lie in the way that diseases are classified. This paper offers further development of a view advanced previously, the 'contrastive model' of disease: it develops the account to handle asymptomatic disease ; and in doing so it relates the model to a broadly biostatistical view of health. The developments are prompted by considering cancers featuring viruses as prominent causes, since these appear to amount to cases where the prescriptions of the contrastive model could be followed, but aren't. The resulting irrelevance objection claims that the contrastive model is irrelevant to medical science and practice. The paper seeks to rebut the irrelevance objection.

The counterfactual analysis of causation has focused on one particular counterfactual conditional, taking as its starting-point the suggestion that C causes E iff (C E). In this paper, some consequences are explored of reversing this counterfactual, and developing an account starting with the idea that C causes E iff (E C). This suggestion is discussed in relation to the problem of pre-emption. It is found that the 'reversed' counterfactual analysis can handle even the most difficult cases of pre-emption with only minimal complications. The paper closes with a discussion of the wider philosophical implications of developing a reversed counterfactual analysis, especially concerning the differentiation of causes from causal conditions, causation by absences, and the extent to which causes suffice for their effects.

Nineteenth-century medical advances were entwined with a conceptual innovation: the idea that many cases of disease which were previously thought to have diverse causes could be explained by the action of a single kind of cause, for example a certain bacterial or parasitic infestation. The focus of modern epidemiology, however, is on chronic non-communicable diseases, which frequently do not seem to be attributable to any single causal factor. This paper is an effort to resolve the resulting tension. The paper criticises the monocausal model of disease, so successful in the nineteenth century. It also argues that a multifactorial model of disease can only be satisfactory if it amounts to more than a mere rejection of the monocausal model. A third alternative, the contrastive model, is proposed and defended on the grounds that it links the notions of disease and of general explanation, while avoiding the philosophical naiveties and practical difficulties of the monocausal model.

In this article I seek to say what it is for something to count as a neglected disease. I argue that neglect should be defined in terms of efforts at prevention, mitigation and cure, and not solely in terms of research dollars per disability-adjusted life-year. I further argue that the trend towards multifactorialism and risk factor thinking in modern epidemiology has lent credibility to the erroneous view that the primary problem with neglected diseases is a lack of research. A more restrictive contrastive model of disease is endorsed as better suited to the definition of neglected disease.