In this book, J. L. Mackie makes a careful study of several philosophical issues involved in his account of causation. Mackie follows Hume's distinction between causation as a concept and causation as it is ‘in the objects’ and attempts to provide an account of both aspects. Mackie examines the treatment of causation by philosophers such as Hume, Kant, Mill, Russell, Ducasse, Kneale, Hart and Honore, and von Wright. Mackie's own account involves an analysis of causal statements in terms of counterfactual (...) conditionals though these are judged to be incapable of giving a complete account of causation. Mackie argues that regularity theory too can only offer an incomplete picture of the nature of causation. In the course of his analysis, Mackie critically examines the account of causation offered by Kant, as well as the contemporary Kantian approaches offered by philosophers such as Bennett and Strawson. Also addressed are issues such as the direction of causation, the relation of statistical laws and functional laws, the role of causal statements in legal contexts, and the understanding of causes both as ‘facts’ and ‘events’. Throughout the discussion of these topics, Mackie develops his own complex account of the nature of causation, finally bringing his analysis to bear in regard to the topic of teleology and the question of whether final causes can be justifiably reduced to efficient causes. (shrink)

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. (shrink)

What exactly is a genetic disease? For a phrase one hears on a daily basis, there has been surprisingly little analysis of the underlying concept. Medical doctors seem perfectly willing to admit that the etiology of disease is typically complex, with a great many factors interacting to bring about a given condition. On such a view, descriptions of diseases like cancer as geneticseem at best highly simplistic, and at worst philosophically indefensible. On the other hand, there is clearly some practical (...) value to be had by classifying diseases according to theirpredominant cause when this can be accomplished in a theoretically satisfactory manner. The question therefore becomes exactly how one should go about selecting a single causal factor among many to explain the presence of disease. When an attempt to defend such causal selection is made at all, the standard accounts offered (Koch's postulates, Hill's epidemiological criteria, manipulability) are all clearly inadequate. I propose, however, an epidemiological account of disease causation which walks the fine line between practical applicability and theoretical considerations of causal complexity and attempts to compromise between patient-centered and population-centered concepts of disease. The epidemiological account is the most basic framework consistent with our strongly held intuitions about the causal classification of disease, yet it avoids the difficulties encountered by its competitors. (shrink)

Studies causation both as a concept and as it is 'in the objects.' Offers new accounts of the logic of singular causal statements, the form of causal regularities, the detection of causal relationships, the asymmetry of cause and effect, and necessary connection, and it relates causation to functional and statistical laws and to teleology.

Woodward's long awaited book is an attempt to construct a comprehensive account of causation explanation that applies to a wide variety of causal and explanatory claims in different areas of science and everyday life. The book engages some of the relevant literature from other disciplines, as Woodward weaves together examples, counterexamples, criticisms, defenses, objections, and replies into a convincing defense of the core of his theory, which is that we can analyze causation by appeal to the notion of manipulation.

This paper attempts to elucidate three characteristics of causal relationships that are important in biological contexts. Stability has to do with whether a causal relationship continues to hold under changes in background conditions. Proportionality has to do with whether changes in the state of the cause “line up” in the right way with changes in the state of the effect and with whether the cause and effect are characterized in a way that contains irrelevant detail. Specificity is connected both to (...) David Lewis’ notion of “influence” and also with the extent to which a causal relation approximates to the ideal of one cause–one effect. Interrelations among these notions and their possible biological significance are also discussed. (shrink)