Identifying the necessary and sufficient conditions for individuating and classifying diseases is a matter of great importance in the fields of law, ethics, epidemiology, and of course, medicine. In this paper, I first propose a means of achieving this goal, ensuring that no two distinct disease-types could correctly be ascribed to the same disease-token. I then posit a metaphysical ontology of diseases—that is, I give an account of what a disease is. This is essential to providing the most effective means (...) of interfering with disease processes. Following existing work in the philosophy of medicine and epidemiology (primarily Christopher Boorse; Caroline Whitbeck; Alexander Broadbent), philosophy of biology (Joseph LaPorte; D.L. Hull), conditional analyses of causation (J.L. Mackie; David Lewis), and recent literature on dispositional essentialism (Stephen Mumford and Rani Anjum; Alexander Bird), I endorse a dispositional conception of disease. Following discussion of various conceptions of disease-identity, their relations to the clinical and pathological effects of the diseases in question, and how diseases are treated, I conclude (i) that diseases should be individuated by their causes, and (ii) that diseases are causal processes best seen as simultaneously acting sequences of mutually manifesting dispositions. (shrink)

This paper aims to bridge philosophical and psychological research on causation, counterfactual thought, and the problem of backtracking. Counterfactual approaches to causation such as that by Lewis have ruled out backtracking, while on prominent models of causal inference interventionist counterfactuals do not backtrack. However, on various formal models, certain backtracking counterfactuals end up being true, and psychological evidence shows that people do sometimes backtrack when answering counterfactual questions in causal contexts. On the basis of psychological research, I argue that while (...) ordinarily both kinds of counterfactuals may be employed, non-backtracking counterfactuals are more easily used in causal inference because they are consistent with temporal order information embedded in the mental simulation heuristic, and they match reasoners’ experience of causation. While this approach is incompatible with the ambitions of counterfactual theories that seek to establish the non-backtracking interpretation as the only legitimate one, it can provide support for perspectival views on causation and open further inquiry on the functions of causal and counterfactual thought in the context of causal models. (shrink)

It is natural to think of causes as difference-makers. What exact difference causes make, however, is an open question. In this paper, I argue that the right way of understanding difference-making is in terms of causal processes: causes make a difference to a causal process that leads to the effect. I will show that this way of understanding difference-making nicely captures the distinction between causing an outcome and helping determine how the outcome happens and, thus, explains why causation is not (...) transitive. Moreover, the theory handles tricky cases that are problematic for competing accounts of difference-making. (shrink)

This paper combines the ancient idea that causes necessitate their effects with Angelika Kratzer’s semantics of modality. On the resulting view, causal claims quantify over restricted domains of possible worlds determined by two contextually determined parameters. I argue that this view can explain a number of otherwise puzzling features of the way we use and evaluate causal language, including the difference between causing an effect and being a cause of it, the sensitivity of causal judgements to normative facts, and the (...) semantics of causal disagreements. (shrink)

Knowledge of mechanisms is critical for causal reasoning. We contrasted two possible organizations of causal knowledge—an interconnected causal network, where events are causally connected without any boundaries delineating discrete mechanisms; or a set of disparate mechanisms—causal islands—such that events in different mechanisms are not thought to be related even when they belong to the same causal chain. To distinguish these possibilities, we tested whether people make transitive judgments about causal chains by inferring, given A causes B and B causes C, (...) that A causes C. Specifically, causal chains schematized as one chunk or mechanism in semantic memory led to transitive causal judgments. On the other hand, chains schematized as multiple chunks led to intransitive judgments despite strong intermediate links. Normative accounts of causal intransitivity could not explain these intransitive judgments. (shrink)

This paper examines racial discrimination and algorithmic bias in predictive policing algorithms (PPAs), an emerging technology designed to predict threats and suggest solutions in law enforcement. We first describe what discrimination is in a case study of Chicago’s PPA. We then explain their causes with Broadbent’s contrastive model of causation and causal diagrams. Based on the cognitive science literature, we also explain why fairness is not an objective truth discoverable in laboratories but has context-sensitive social meanings that need to be (...) negotiated through democratic processes. With the above analysis, we next predict why some recommendations given in the bias reduction literature are not as effective as expected. Unlike the cliché highlighting equal participation for all stakeholders in predictive policing, we emphasize power structures to avoid hermeneutical lacunae. Finally, we aim to control PPA discrimination by proposing a governance solution—a framework of a social safety net. (shrink)

What is medicine? One obvious answer in the context of the contemporary clinical tradition is that medicine is the process of curing sick people. However, this “curative thesis” is not satisfactory, even when “cure” is defined generously and even when exceptions such as cosmetic surgery are set aside. Historian of medicine Roy Porter argues that the position of medicine in society has had, and still has, little to do with its ability to make people better. Moreover, the efficacy of medicine (...) for improving population health has been famously doubted by historians and epidemiologists. The curative thesis demands that we have mostly been stupid, duped, or staggeringly hopeful, given that medicine has not until recently offered more than a handful of effective cures. I suggest, in this article, that the core medical competence is neither to cure, nor to prevent, disease, but to understand and to predict it. I argue that this approach does a better job than the curative thesis at explaining why not all medicine is concerned with curative efforts and that it enjoys historical support from the ancient entanglement of prophecy and medicine and from the fact that medicine thrived for centuries with almost no effective cures and continues to thrive today in various forms that are mostly without curative efficacy. I suggest that this approach grounds a fairer approach to alternative, traditional, and other medical practices, as well as some fresh lessons for the development of mainstream medicine. (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)