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)

This essay advocates a “functional” approach to causation and causal reasoning: these are to be understood in terms of the goals and purposes of causal thinking. This approach is distinguished from accounts based on metaphysical considerations or on reconstruction of “intuitions.”.

Griffiths et al. (2015) have proposed a quantitative measure of causal specificity and used it to assess various attempts to single out genetic causes as being causally more specific than other cellular mechanisms, for example, alternative splicing. Focusing in particular on developmental processes, they have identified a number of important challenges for this project. In this discussion note, I would like to show how these challenges can be met.

Biologists studying complex causal systems typically identify some factors as causes and treat other factors as background conditions. For example, when geneticists explain biological phenomena, they often foreground genes and relegate the cellular milieu to the background. But factors in the milieu are as causally necessary as genes for the production of phenotypic traits, even traits at the molecular level such as amino acid sequences. Gene-centered biology has been criticized on the grounds that because there is parity among causes, the (...) “privileging” of genes reflects a reductionist bias, not an ontological difference. The idea that there is an ontological parity among causes is related to a philosophical puzzle identified by John Stuart Mill: what, other than our interests or biases, could possibly justify identifying some causes as the actual or operative ones, and other causes as mere background? The aim of this paper is to solve this conceptual puzzle and to explain why there is not an ontological parity among genes and the other factors. It turns out that solving this puzzle helps answer a seemingly unrelated philosophical question: what kind of causal generality matters in biology? (shrink)

Bas C. van Fraassen presents an original exploration of how we represent the world.

(Journal of Philosophy, 1988, 85:303-318).

Causation is widely assumed to be a binary relation: c causes e. I will argue that causation is a quaternary, contrastive relation: c rather than C* causes e rather than E*, where C* and E* are nonempty sets of contrast events. Or at least, I will argue that treating causation as contrastive helps resolve some paradoxes.

Binding specificity is a centrally important concept in molecular biology, yet it has received little philosophical attention. Here I aim to remedy this by analyzing binding specificity as a causal property. I focus on the concept’s role in drug design, where it is highly prized and hence directly studied. From a causal perspective, understanding why binding specificity is a valuable property of drugs contributes to an understanding of causal selection—of how and why scientists distinguish between causes, not just causes from (...) noncauses. In particular, the specificity of drugs is precisely what underwrites their value as experimental interventions on biological processes. (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)

Waters’s (2007) actual difference making and Weber’s (2013, 2017) biological normality approaches to causal selection have received many criticisms, some of which miss their target. Disagreement about whether Waters’s and Weber’s views succeed in providing criteria that uniquely singles out the gene as explanatorily significant in biology has led philosophers to overlook a prior problem. Before one can address whether Waters’s and Weber’s views successfully account for the explanatory significance of genes, one must ask whether either view satisfactorily meets the (...) necessary conditions for causal selection in the first place. An adequate defense of causal selection must meet two desiderata. First, there must be an explanatory property that sets some causes apart from others. Second, the property identified must be one that is recognized by biologists as relevant to their domain(s) of inquiry. I argue that both fall short of meeting the second condition. I demonstrate this by showing how many of the biological technologies crucial to experimentation do not fit either view very well. I offer a more adequate proposal that accommodates non-actual and artificial causal variables. A consequence of my view is the following: When analyzing the causal selection practices of biologists, philosophers should consider the explanatory targets relevant to a research program – including ones whose explanans must appeal to biological technologies. I then explain how this proposal can inform the existing debate between Weber (2017) and Griffiths et al. (2015). (shrink)

Stimulating, thought-provoking text by one of the 20th century’s most creative philosophers clearly and discerningly makes accessible such topics as probability, measurement and quantitative language, structure of space, causality and determinism, theoretical laws and concepts and much more. "...the best book available for the intelligent reader who wants to gain some insight into the nature of contemporary philosophy of science."—Choice.

Reprint of the original, first published in 1869.

Questions about the metaphysics of causation may be usefully divided as follows. First, there are questions about the nature of the causal relata, including (1.1) whether they are in spacetime immanence), (1.2) how fine grained they are individuation), and (1.3) how many there are adicity). Second, there are questions about the metaphysics of the causal relation, including (2.1) what is the difference between causally related and causally unrelated sequences connection), (2.2) what is the difference between sequences related as cause to (...) effect, and those related as effect to cause or as joint effects of a common cause direction), and (2.3) what is the difference between sequences involving the cause, and those involving mere conditions selection). (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)

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)