I present a new definition of verisimilitude, framed in terms of causes. Roughly speaking, according to it a scientific model is approximately true if it captures accurately the strengths of the causes present in any given situation. Against much of the literature, I argue that any satisfactory account of verisimilitude must inevitably restrict its judgments to context-specific models rather than general theories. We may still endorse—and only need—a relativized notion of scientific progress, understood now not as global advance but rather (...) as the mastering of particular problems. This also sheds new light on longstanding difficulties surrounding language-dependence and models committed to false ontologies. (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)

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)

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)

Do we owe it to future generations, as a requirement of justice, to take action to mitigate anthropogenic climate change? This paper examines the implications of Derek Parfit’s notorious non-identity problem for that question. An argument from Jörg Tremmel that the non-identity effect of climate policy is “insignificant” is examined and found wanting, and a contrastive, difference-making approach for comparing different choices’ non-identity effects is developed. Using the approach, it is argued that the non-identity effect of a given policy response (...) to climate change depends on the contrasting policy. Compared to a baseline scenario without further mitigation, the non-identity effect of choosing to limit climate change to 1.5°C would be highly significant. (shrink)

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.

We propose a novel account of the distinction between innate and acquired biological traits: biological traits are innate to the degree that they are caused by factors intrinsic to the organism at the time of its origin; they are acquired to the degree that they are caused by factors extrinsic to the organism. This account borrows from recent work on causation in order to make rigorous the notion of quantitative contributions to traits by different factors in development. We avoid the (...) pitfalls of previous accounts and argue that the distinction between innate and acquired traits is scientifically useful. We therefore address not only previous accounts of innateness but also skeptics about any account. The two are linked, in that a better account of innateness also enables us better to address the skeptics. (shrink)

We propose a novel account of the distinction between innate and acquired biological traits: biological traits are innate to the degree that they are caused by factors intrinsic to the organism at the time of its origin; they are acquired to the degree that they are caused by factors extrinsic to the organism. This account borrows from recent work on causation in order to make rigorous the notion of quantitative contributions to traits by different factors in development. We avoid the (...) pitfalls of previous accounts and argue that the distinction between innate and acquired traits is scientifically useful. We therefore address not only previous accounts of innateness but also skeptics about any account. The two are linked, in that a better account of innateness also enables us better to address the skeptics. (shrink)

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)