Causal selection is the task of picking out, from a field of known causally relevant factors, some factors as elements of an explanation. The Causal Parity Thesis in the philosophy of biology challenges the usual ways of making such selections among different causes operating in a developing organism. The main target of this thesis is usually gene centrism, the doctrine that genes play some special role in ontogeny, which is often described in terms of information-bearing or programming. This paper is (...) concerned with the attempt of confronting the challenge coming from the Causal Parity Thesis by offering principles of causal selection that are spelled out in terms of an explicit philosophical account of causation, namely an interventionist account. I show that two such accounts that have been developed, although they contain important insights about causation in biology, nonetheless fail to provide an adequate reply to the Causal Parity challenge: Ken Waters's account of actual-difference making and Jim Woodward's account of causal specificity. A combination of the two also doesn't do the trick, nor does Laura Franklin-Hall's account of explanation (in this volume). We need additional conceptual resources. I argue that the resources we need consist in a special class of counterfactual conditionals, namely counterfactuals the antecedents of which describe biologically normal interventions. (shrink)

Much of the philosophical literature on causation has focused on the concept of actual causation, sometimes called token causation. In particular, it is this notion of actual causation that many philosophical theories of causation have attempted to capture.2 In this paper, we address the question: what purpose does this concept serve? As we shall see in the next section, one does not need this concept for purposes of prediction or rational deliberation. What then could the purpose be? We will argue (...) that one can gain an important clue here by looking at the ways in which causal judgments are shaped by people‘s understanding of norms. (shrink)

Several different approaches to the conceptual analysis of causation are guided by the idea that a cause is something that makes a difference to its effects. These approaches seek to elucidate the concept of causation by explicating the concept of a difference-maker in terms of better-understood concepts. There is no better example of such an approach than David Lewis’ analysis of causation, in which he seeks to explain the concept of a difference-maker in counterfactual terms. Lewis introduced his counterfactual theory (...) of causation with these words: 'We think of a cause as something that makes a difference, and the difference it makes must be a difference from what would have happened without it. Had it been absent, its effects—some of them, at least, and usually all—would have been absent as well.' (Lewis 1973b: pp. 160-1) According to Lewis, a cause c makes a difference to an effect e in the sense that if the cause c had not occurred, the effect e would not have occurred either. All we shall see in section 2, Lewis’ theory says there is more to the concept of causation than this counterfactual condition. Lewis is on the right track, I think, in saying that we think of a cause as something that makes a difference and that this thought is best explicated in terms of counterfactual concepts. However, I shall argue that the particular way in which Lewis spells out the concept of a cause as difference-maker is unsatisfactory. For Lewis’ articulation of this concept is distorted by a specific metaphysical assumption: specifically, that causation is an absolute relation, specifiable independently of any contextual factors. The distortion induced by this assumption is reflected in the undiscriminating manner in which his theory generates countless causes for any given effect. However, commonsense judgement is much more discriminating about causes than Lewis’ theory. Accordingly, I claim that Lewis' analysis faces the problem of profligate causes and I outline some specific problem cases in section 3.. (shrink)

In this paper we defend the view that the ordinary notions of cause and effect have a direct and essential connection with our ability to intervene in the world as agents.1 This is a well known but rather unpopular philosophical approach to causation, often called the manipulability theory. In the interests of brevity and accuracy, we prefer to call it the agency theory.2 Thus the central thesis of an agency account of causation is something like this: an event A is (...) a cause of a distinct event B just in case bringing about the occurrence of A would be an effective means by which a free agent could bring about the occurrence of B. In our view the unpopularity of the agency approach to causation may be traced to two factors. The first is a failure to appreciate certain distinctive advantages that this approach has over its various rivals. We have drawn attention to some of these advantages elsewhere, and we summarize below. However, the second and more important factor is the influence of a number of stock objections, objections that seem to have persuaded many philosophers that agency accounts face insuperable obstacles. In this paper we want to show that these objections have been vastly overrated. There are four main objections. (shrink)

According to James Woodward’s influential interventionist account of causation, X is a cause of Y iff, roughly, there is a possible intervention on X that changes Y. Woodward requires that interventions be merely logically possible. I will argue for two claims against this modal character of interventions: First, merely logically possible interventions are dispensable for the semantic project of providing an account of the meaning of causal statements. If interventions are indeed dispensable, the interventionist theory collapses into a counterfactual theory (...) of causation. Thus, the interventionist theory is not tenable as a theory of causation in its own right. Second, if one maintains that merely logically possible interventions are indispensable, then interventions with this modal character lead to the fatal result that interventionist counterfactuals are evaluated inadequately. Consequently, interventionists offer an inadequate theory of causation. I suggest that if we are concerned with explicating causal concepts and stating the truth-conditions of causal claims we best get rid of Woodwardian interventions. (shrink)

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)

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)

Book Information Science, Truth, and Democracy. By Philip Kitcher. Oxford. New York. 2001. Pp. xiii + 219. US$27.50.

An updated and extended second edition supporting the findings of its well-known predecessor which claimed that courts employ common-sense notions of causation in determining legal responsibility.