It is widely agreed that an artwork having certain non-aesthetic properties explains its having a certain aesthetic property. One interesting feature of such an explanation is its selectivity—it cites only some of the non-aesthetic properties on which the presence of the aesthetic property depends. Hence a question arises as to what distinguishes the selected non-aesthetic properties from the unselected ones. I answer this question by proposing a selection principle modeled on Laura Franklin-Hall’s selection principle for causal explanation, according to which (...) an explanation selects a package of factors that maximizes the ratio of delivery to cost. (shrink)

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)

Though biologists identify individuals as ‘male’ or ‘female’ across a broad range of animal species, the particular traits exhibited by males and females can vary tremendously. This diversity has led some to conclude that cross-animal sexes (males, or females, of whatever animal species) have “little or no explanatory power” (Dupré 1986: 447) and, thus, are not natural kinds in any traditional sense. This essay will explore considerations for and against this conclusion, ultimately arguing that the animal sexes, properly understood, are (...) “historical explanatory kinds”: groupings that can be scientifically significant even while their members differ radically in their current properties and particular histories. Whether this makes them full-fledged natural kinds is a question I take up at the very end. (shrink)

This paper sketches a causal account of scientific explanation designed to sustain the judgment that high-level, detail-sparse explanations—particularly those offered in biology—can be at least as explanatorily valuable as lower-level counterparts. The motivating idea is that complete explanations maximize causal economy: they cite those aspects of an event’s causal run-up that offer the biggest-bang-for-your-buck, by costing less (in virtue of being abstract) and delivering more (in virtue making the event stable or robust).

Our ordinary causal concept seems to fit poorly with how our best physics describes the world. We think of causation as a time-asymmetric dependence relation between relatively local events. Yet fundamental physics describes the world in terms of dynamical laws that are, possible small exceptions aside, time symmetric and that relate global time slices. My goal in this paper is to show why we are successful at using local, time-asymmetric models in causal explanations despite this apparent mismatch with fundamental physics. (...) In particular, I will argue that there is an important connection between time asymmetry and locality, namely: understanding the locality of our causal models is the key to understanding why the physical time asymmetries in our universe give rise to time asymmetry in causal explanation. My theory thus provides a unified account of why causation is local and time asymmetric and thereby enables a reply to Russell’s famous attack on causation. (shrink)

Causal selection has to do with the distinction we make between background conditions and “the” true cause or causes of some outcome of interest. A longstanding consensus in philosophy views causal selection as lacking any objective rationale and as guided, instead, by arbitrary, pragmatic, and non-scientific considerations. I argue against this position in the context of causal selection for disease traits. In this domain, causes are selected on the basis of the type of causal control they exhibit over a disease (...) of interest. My analysis clarifies the principled rationale that guides this selection and how it involves both pragmatic and objective considerations, which have been overlooked in the extant literature. (shrink)

The concept of causal specificity is drawing considerable attention from philosophers of biology. It became the rationale for rejecting (and occasionally, accepting) a thesis of causal parity of developmental factors. This literature assumes that attributing specificity to causal relations is at least in principle a straightforward (if not systematic) task. However, the parity debate in philosophy of biology seems to be stuck at a point where it is not the biological details that will help move forward. In this paper, I (...) take a step back to reexamine the very idea of causal specificity and its intended role in the parity dispute in philosophy of biology. I contend that the idea of causal specificity across variations as currently discussed in the literature is irreducibly twofold in nature: it is about two independent components that are not mutually entailed. I show this to be the source of prior complications with the notion of specificity itself that ultimately affect the purposes for which it is often invoked, notably to settle the parity dispute. (shrink)

The history of developmental biology is interwoven with debates as to whether mechanistic explanations of development are possible or whether alternative explanatory principles or even vital forces need to be assumed. In particular, the demonstrated ability of embryonic cells to tune their developmental fate precisely to their relative position and the overall size of the embryo was once thought to be inexplicable in mechanistic terms. Taking a causal perspective, this Element examines to what extent and how developmental biology, having turned (...) molecular about four decades ago, has been able to meet the vitalist challenge. It focuses not only on the nature of explanations but also on the usefulness of causal knowledge – including the knowledge of classical experimental embryology – for further scientific discovery. It also shows how this causal perspective allows us to understand the nature and significance of some key concepts, including organizer, signal and morphogen. This title is also available as Open Access on Cambridge Core. (shrink)

Hall has recently argued that there are two concepts of causality, picking out two different kinds of causal relation. McGrath, and Hitchcock and Knobe, have recently argued that the facts about causality depend on what counts as a “default” or “normal” state, or even on the moral facts. In the light of these claims you might be tempted to agree with Skyrms that causal relations constitute, metaphysically speaking, an “amiable jumble”, or with Cartwright that ‘causation’, though a single word, encompasses (...) many different kinds of things. This paper argues, drawing on the author’s recent work on explanation, that the evidence adduced in support of causal pluralism can be accommodated easily by a unified theory of causality—a theory according to which all singular causal claims concern the same fundamental causal network. (shrink)

The interventionist account provides us with several notions permitting the qualification of causal relationships. In recent years, there has been a push toward formalizing these notions using information theory. In this paper, I discuss one of them, namely causal specificity. The notion of causal specificity is ambiguous as it can refer to at least two different concepts. After having presented these, I show that current attempts to formalize causal specificity in information theoretic terms have mostly focused on one of these (...) two concepts. I then propose and apply a new information-theoretic measure which captures the other concept. (shrink)

In biology and philosophy of biology, discussing the notion of interaction leads to an examination of interactionism, which is, broadly speaking, the view that rejects gene-centrism and gene determinism and instead emphasizes the fact that traits of organisms are always the result of genes and environments. It has long been asserted that the nature-nurture problem requires an interactionist solution of sorts, the so-called interactionist consensus. This consensus, however, has been deemed insufficient and challenged by several authors triggering an extension of (...) the debate among contestants and defenders. Unfortunately, part of the problem is that the views on causation that would ground claims about interactionism are not always made explicit in this debate, which renders those views somewhat complicated to assess. Moreover, it seems to be assumed that causal complexity excludes the possibility of characterizing, distinguishing, or comparing among causal contributions. By turning to a detailed survey of the origin of the debate and to some developments in the philosophy of causation, we will contend that this view is unwarranted, and that much of the debate around interactionism is based on the drawing of this conclusion. We also examine implications of this analysis for the project to develop a framework based on the notion of inter-identities. (shrink)

I argue that Calcott :481–505, Calcott 2017) mischaracterizes in an important way the notion of causal specificity proposed by Woodward :287–318, Woodward 2010). This leads him to rely too heavily on one single aspect of Woodward’s analysis on causal specificity; propose an information-theoretic measure he calls ‘precision’ which is partly redundant with, but less general than one of the dimensions in Woodward’s analysis of specificity, without acknowledging Woodward’s analysis; and claim that comparing the specificities of two or more causes under (...) what he calls a competitive analysis of causes, does not permit to capture the distinction between permissive and instructive causes. After having restated Woodward’s analysis of causal specificity, I present an information-theoretic measure which, although related to Calcott’s measure, is more general than his and corresponds to the notion of specificity he missed in Woodward's analysis. I then show how this measure can be used, together with mutual causal information, to distinguish permissive from instructive causes in a competitive analysis of causes. (shrink)