I use a contrastive theory of causal explanation to analyze the notion of a genetic trait. The resulting definition is relational, an implication of which is that no trait is genetic always and everywhere. Rather, every trait may be either genetic or non-genetic, depending on explanatory context. I also outline some other advantages of connecting the debate to the wider causation literature, including how that yields us an account of the distinction between genetic traits and genetic dispositions.

The statistical technique of analysis of variance is often used by biologists as a measure of causal factors’ relative strength or importance. I argue that it is a tool ill suited to this purpose, on several grounds. I suggest a superior alternative, and outline some implications. I finish with a diagnosis of the source of error – an unwitting inheritance of bad philosophy that now requires the remedy of better philosophy.

Comparing different causes’ importance, and apportioning responsibility between them, requires making good sense of the notion of partial explanation, that is, of degree of explanation. How much is this subjective, how much objective? If the causes in question are probabilistic, how much is the outcome due to them and how much to simple chance? I formulate the notion of degree of causation, or effect size, relating it to influential recent work in the literature on causation. I examine to what extent (...) mainstream social science methods--both quantitative and qualitative--succeed in establishing effect sizes so understood. The answer turns out to be, roughly: only to some extent. Next, the standard understanding of effect size, even though widespread, still has several underappreciated consequences. I detail some of those. Finally, I discuss the separate issue of explanandum-dependence, which is essential to assessing any cause’s explanatory importance and yet which has been comparatively neglected. (shrink)

The concept of innateness is used to make inferences between various better-understood properties, like developmental canalization, evolutionary adaptation, heritability, species-typicality, and so on (‘innateness-related properties’). This article uses a recently-developed account of the representational content carried by inheritance systems like the genome to explain why innateness-related properties cluster together, especially in non-human organisms. Although inferences between innateness-related properties are deductively invalid, and lead to false conclusions in many actual cases, where some aspect of a phenotypic trait develops in reliance on (...) a genetic representation it will tend, better than chance, to have many of the innateness-related properties. The account also shows why inferences between innateness-related properties sometimes fail and argues that such inferences are especially misleading when applied to human psychology and behaviour because human psychological development is especially reliant on non-genetic inherited representations. (shrink)

Denis Walsh has written a striking new defense in this journal of the statisticalist (i.e., noncausalist) position regarding the forces of evolution. I defend the causalist view against his new objections. I argue that the heart of the issue lies in the nature of nonadditive causation. Detailed consideration of that turns out to defuse Walsh’s ‘description‐dependence’ critique of causalism. Nevertheless, the critique does suggest a basis for reconciliation between the two competing views. *Received December 2009; revised December 2009. †To contact (...) the author, please write to: Department of Philosophy, 599 Lucas Hall, One University Boulevard, University of Missouri, St. Louis, MO 63121; e‐mail: [email protected]. (shrink)

, whereby some causes are deemed more important than others, are ubiquitous in historical studies. Drawing from influential recent work on causation, I develop a definition of causal-explanatory strength. This makes clear exactly which aspects of explanatory weighting are subjective and which objective. It also sheds new light on several traditional issues, showing for instance that: underlying causes need not be more important than proximate ones; several different causes can each be responsible for most of an effect; small causes need (...) not be less important than big ones; and non-additive interactive effects between causes present no particular difficulty. Key Words: causation • explanation • history • interaction • proximate • underlying. (shrink)

This volume provides a broad overview of issues in the philosophy of behavioral biology, covering four main themes: genetic, developmental, evolutionary, and neurobiological explanations of behavior. It is both interdisciplinary and empirically informed in its approach, addressing philosophical issues that arise from recent scientific findings in biological research on human and non-human animal behavior. Accordingly, it includes papers by professional philosophers and philosophers of science, as well as practicing scientists. Much of the work in this volume builds on presentations given (...) at the international conference, “Biological Explanations of Behavior: Philosophical Perspectives”, held in 2008 at the Leibniz Universität Hannover in Germany. The volume is intended to be of interest to a broad range of audiences, which includes philosophers (e.g., philosophers of mind, philosophers of biology, and metaethicists), as well as practicing scientists, such as biologists or psychologists whose interests relate to biological explanations of behavior. (shrink)

I argue that causation is a contrastive relation: c-rather-than-C* causes e-rather-than-E*, where C* and E* are contrast classes associated respectively with actual events c and e. I explain why this is an improvement on the traditional binary view, and develop a detailed definition. It turns out that causation is only well defined in ‘uniform’ cases, where either all or none of the members of C* are related appropriately to members of E*.

Heritability is routinely interpreted causally. Yet, what such an interpretation amounts to is often unclear. Here, I provide a causal interpretation of this concept in terms of range of causal influence, one of several causal dimensions proposed within the interventionist account of causation. An information-theoretic measure of range of causal influence has recently been put forward in the literature. Starting from this formalization and relying upon Woodward’s analysis, I show that an important problem associated with interpreting heritability causally, namely the (...) locality problem, amounts, at least partly, to a low invariance and low stability between the genotype/environment and the phenotype of individuals. In light of this, I plead for a causal interpretation of heritability that takes the notions of Woodward’s invariance and stability into consideration. In doing so, I defuse naive causal interpretations of heritability. (shrink)

Partial explanations are everywhere. That is, explanations citing causes that explain some but not all of an effect are ubiquitous across science, and these in turn rely on the notion of degree of explanation. I argue that current accounts are seriously deficient. In particular, they do not incorporate adequately the way in which a cause’s explanatory importance varies with choice of explanandum. Using influential recent contrastive theories, I develop quantitative definitions that remedy this lacuna, and relate it to existing measures (...) of degree of causation. Among other things, this reveals the precise role here of chance, as well as bearing on the relation between causal explanation and causation itself. (shrink)

Lucas Matthews and I substantially revised my SEP entry on Heritability. This version includes discussion of the missing heritability problem and other issues that arise from the use of Genome Wide Association Studies by Behavioral Geneticists.

It is often natural to compare two events by describing one as ‘more of a cause’ of some effect than the other. But what do such comparisons amount to, exactly? This paper aims to provide a guided tour of the recent literature on ‘degrees of causation’. Section 2 looks at what I call ‘dependence measures’, which arise from thinking of causes as difference‐makers. Section 3 looks at what I call ‘production measures’, which arise from thinking of causes as jointly sufficient (...) for their effects. Finally, section 4 examines the important question of whether there is any sense in which an agent is more responsible for an outcome in virtue of her action being more of a cause of it. I describe a puzzle that emerges from this question, and explore various strategies for resolving it. (shrink)