In cases in which many causes together bring about an effect, it is common to select some as particularly important. Philosophers since Mill have been pessimistic about analyzing this reasoning because of its variability and the multifarious causal and pragmatic details of how it works. I argue Mill was right to think these details matter but wrong that they preclude philosophical analysis of causal selection. I show that analyzing the pragmatic details of scientific debates about the important causes of the (...) Bhopal Gas Tragedy can illuminate causal reasoning about disasters and shed new light on causality and causal selection. (shrink)

In the face of causal complexity, scientists reconstitute phenomena in order to arrive at a more simplified and partial picture that ignores most of the 'bigger picture.' This paper will distinguish between two modes of reconstituting phenomena: one moving down to a level of greater decomposition (toward organizational parts of the original phenomenon), and one moving up to a level of greater abstraction (toward different differences regarding the phenomenon). The first aim of the paper is to illustrate that phenomena are (...) moving targets, i.e., they are not fixed once and for all, but are adapted, if necessary, on the basis of the preferred perspective adopted for pragmatic reasons. The second aim is to analyze in detail the second mode of reconstituting phenomena. This includes an exposition of the kind of pragmatic-pluralistic picture resulting from the fact that phenomena are reconstituted by a move up to a level of greater abstraction. (shrink)

This paper defends a realist account of the composition of Newtonian forces, dubbed ‘residualism’. According to residualism, the resultant force acting on a body is identical to the component forces acting on it that do not prevent each other from bringing about its acceleration. Several reasons to favor residualism over alternative accounts of the composition of forces are advanced. (i) Residualism reconciles realism about component forces with realism about resultant forces while avoiding any threat of causal overdetermination. (ii) Residualism provides (...) a systematic semantics for the term ‘force’ within Newtonian mechanics. (iii) Residualism allows us to precisely apportion the causal responsibility of each component force in the ensuing acceleration. (iv) Residualism handles special cases such as null forces, single forces, and antagonistic forces in a natural way. (v) Residualism provides a neat picture of the causal powers of forces: each force essentially has two causal powers⎯the power to bring about accelerations (sometimes together with other co-directionnal forces) and the power to prevent other forces from doing so⎯exactly one of which is manifested at a time. (vi) Residualism avoids commitment to unobservable effects of forces: forces cause either stresses (tensile or compressive) or accelerations. (shrink)

Human development is a matter of complex interactions between nutritional regimes, genes, educational regimes and other diverse developmental resources. I argue that there is no ethically salient difference between the contributions made to development by genes and the contributions made by these other resources. Since we think nutrition and schooling should be included in the calculus of distributive justice, we should include at least some genes in this calculus too. What is more, under the right circumstances genetic engineering may become (...) a useful tool for the distribution of developmental resources. This said, attention to the parity of genetic and environmental causation can also help to articulate the legitimate suspicions many groups have of genetic engineering. (shrink)

In robustness analysis, hypotheses are supported to the extent that a result proves robust, and a result is robust to the extent that we detect it in diverse ways. But what precise sense of diversity is at work here? In this paper, I show that the formal explications of evidential diversity most often appealed to in work on robustness – which all draw in one way or another on probabilistic independence – fail to shed light on the notion of diversity (...) relevant to robustness analysis. I close by briefly outlining a promising alternative approach inspired by Horwich’s (1982) eliminative account of evidential diversity. (shrink)

Embodied cognitive science has argued that cognition is embodied principally in virtue of grossmorphological and sensorimotor features. This thesis argues that cognition is also internally embodied in affective and fine-grained physiological features whose transformative roles remain mostly unnoticed in contemporary cognitive science. I call this ‘proper embodiment’. I approach this larger subject by examining various emotion theories in philosophy and psychology. These tend to emphasise one of the many gross components of emotional processes, such as ‘feeling’ or ‘judgement’ to the (...) detriment of the others, often leading to an artificial emotion-cognition distinction even within emotion science itself. Attempts to reconcile this by putting the gross components back together, such as JessePrinz’s “embodied appraisal theory”, are, I argue, destined to failure because the vernacular concept of emotion which is used as the explanandum is not a natural kind and is not amenable to scientific explication.I examine Antonio Damasio’s proposal that emotion is involved in paradigmatic ‘cognitive’ processing such as rational decision making and argue (1) that the research he discusses does not warrant the particular hypothesis he favours, and (2) that Damasio’s account, though in many ways a step in the right direction, nonetheless continues to endorse a framework which sees affect and cognition as separate (though now highly interacting) faculties. I further argue that the conflation of ‘affect’ and 'emotion' may be the source of some confusion in emotion theory and that affect needs to be properly distinguished from ‘emotion’. I examine some dissociations in the pain literature which give us further empirical evidence that, as with the emotions, affect is a distinct component along with more cognitive elements of pain. I then argue that affect is distinctive in being grounded in homeostatic regulative activity in the body proper. With the distinction between affect, emotion, and cognition in hand, and the associated grounding of affect in bodily activity, I then survey evidence that bodily affect is also involved in perception and in paradigmatic cognitive processes such as attention and executive function. I argue that this relation is not ‘merely’ casual. Instead, affect (grounded in fine-grained details of internal bodily activity) is partially constitutive of cognition, participating in cognitive processing and contributing to perceptual and cognitive phenomenology. Finally I review some work in evolutionary robotics which reaches a similar conclusion, suggesting that the particular fine details of embodiment, such as molecular signalling between both neural and somatic cells matters to cognition. I conclude that cognition is properly embodied’ in that it is partially constituted by the many fine-grained bodily processes involved in affect (as demonstrated in the thesis) and plausibly by a wide variety of other fine-grained bodily processes that likewise tend to escape the net of contemporary cognitive science. (shrink)

A survey of innateness in cognitive science, focusing on (1) what innateness might be, and (2) whether concepts might be innate.

The causal impacts of genes and environment on any one biological trait are inextricably entangled, and consequently it is widely accepted that it makes no sense in singleton cases to privilege either factor for particular credit. On the other hand, at a population level it may well be the case that one of the factors is responsible for more variation than the other. Standard methodological practice in biology uses the statistical technique of analysis of variance to measure this latter kind (...) of causal efficacy. In this paper, I argue that: 1) analysis of variance is in fact badly suited to this role; and. (shrink)

This paper advocates a dispositional account of innate cognitive capacities, which has an illustrious history from Plato to Chomsky. The "triggering model" of innateness, first made explicit by Stich ([1975]), explicates the notion in terms of the relative informational content of the stimulus (input) and the competence (output). The advantage of this model of innateness is that it does not make a problematic reference to normal conditions and avoids relativizing innate traits to specific populations, as biological models of innateness are (...) forced to do. Relativization can be avoided in the case of cognitive capacities precisely because informational content is involved. Even though one cannot measure output relative to input in a precise way, there are indirect and approximate ways of assessing the degree of innateness of a specific cognitive capacity. (shrink)

The notion of credit plays a central role in virtue epistemology and in the literature on moral worth. While virtue epistemologists and ethicists have devoted a significant amount of work to providing an account of creditable success, a unified theory of credit applicable to both epistemology and ethics, as well as a discussion of the general form it should take, are largely missing from the literature. Our goal is to lay out a theory of credit that seems to underlie much (...) of the discussion in virtue epistemology, which we dub the Cake Theory. We argue that given the goals that virtue epistemologists and ethicists who discuss moral worth have, this theory is problematic, for it makes credit depend on the wrong facts. (shrink)

Journal of Philosophy of Education, EarlyView.

This paper examines the complex research landscape of contemporary suicidology from a philosophy of science perspective. I begin by unpacking the methods, concepts, and assumptions of some of the prominent approaches to studying suicide causation, including psychological autopsy studies, epidemiological studies, biological studies, and qualitative studies. I then analyze the different ways these approaches partition the causes of suicide, with particular emphasis on the ways they conceptualize the domain of mental disorder. I argue that these different ways of partitioning the (...) causal space and conceptualizing mental disorder result in incommensurabilities between the approaches. These incommensurabilities restrict the degrees to which the different approaches can be integrated, thus lending support to explanatory pluralism in the study of suicide causation. They also shed light on some of the philosophical underpinnings of the disagreement between mainstream suicidology and the emerging area of critical suicidology. (shrink)

A statement of the form ‘C caused E’ obeys the requirement of proportionality precisely when C says no more than what is necessary to bring about E. The thesis that causal statements must obey this requirement might be given a semantic or a pragmatic justification. We use the idea that causal claims are contrastive to criticize both.

This article illustrates in which sense genetic determinism is still part of the contemporary interactionist consensus in medicine. Three dimensions of this consensus are discussed: kinds of causes, a continuum of traits ranging from monogenetic diseases to car accidents, and different kinds of determination due to different norms of reaction. On this basis, this article explicates in which sense the interactionist consensus presupposes the innate?acquired distinction. After a descriptive Part 1, Part 2 reviews why the innate?acquired distinction is under attack (...) in contemporary philosophy of biology. Three arguments are then presented to provide a limited and pragmatic defense of the distinction: an epistemic, a conceptual, and a historical argument. If interpreted in a certain manner, and if the pragmatic goals of prevention and treatment (ideally specifying what medicine and health care is all about) are taken into account, then the innate?acquired distinction can be a useful epistemic tool. It can help, first, to understand that genetic determination does not mean fatalism, and, second, to maintain a system of checks and balances in the continuing nature?nurture debates. (shrink)

Standard statistical measures of strength of association, although pioneered by Pearson deliberately to be acausal, nowadays are routinely used to measure causal efficacy. But their acausal origins have left them ill suited to this latter purpose. I distinguish between two different conceptions of causal efficacy, and argue that: 1) Both conceptions can be useful 2) The statistical measures only attempt to capture the first of them 3) They are not fully successful even at this 4) An alternative definition more squarely (...) based on causal thinking not only captures the second conception, it can also capture the first one better too. (shrink)

While most researchers who use evolutionary theory to investigatehuman nature especially human sexuality describe themselves as ``interactionists'', there is no clear consensus on the meaning of thisterm in this context. By interactionism most people in the fieldmean something like, both nature and nurture ``count'' in thedevelopment of human psychology and behavior. Nevertheless, themultidisciplinary nature of evolutionary psychology results in a widevariety of interpretations of this general claim. Today, mostdebates within evolutionary psychology about the innateness of agiven behavioral characteristic or over (...) its development turn as muchon which conception of ``innateness'' and ``interactionism'' theresearcher holds as on any empirical data they might derive. (shrink)

Comparisons of rival explanations or theories often involve vague appeals to explanatory power. In this paper, we dissect this metaphor by distinguishing between different dimensions of the goodness of an explanation: non-sensitivity, cognitive salience, precision, factual accuracy and degree of integration. These dimensions are partially independent and often come into conflict. Our main contribution is to go beyond simple stipulation or description by explicating why these factors are taken to be explanatory virtues. We accomplish this by using the contrastive-counterfactual approach (...) to explanation and the view of understanding as an inferential ability. By combining these perspectives, we show how the explanatory power of an explanation in a given dimension can be assessed by showing the range of answers it provides to what-if-things-had-been-different questions and the theoretical and pragmatic importance of these questions. Our account also explains intuitions linking explanation to unification or to exhibition of a mechanism. (shrink)

Is psychopathy born or made? Contemporary psychopathy research shows that there is much wrong with this question. It is increasingly accepted that the development of psychopathy is dependent on multiple causal factors interacting with one another. However, there remains the major theoretical challenge of understanding the relations between these multiple causal factors in the developmental process. In this paper, I argue that the conventional picture of gene-environment interactionism does not offer an adequate account of psychopathy development. Instead, I propose that (...) a theoretical framework from the philosophy of biology, namely developmental systems theory, can facilitate a better understanding of psychopathy development that captures the contingent and dynamic relations between multiple causal factors. Some practical implications of a developmental systems theory approach to psychopathy are also explored. (shrink)

This article illustrates in which sense genetic determinism is still part of the contemporary interactionist consensus in medicine. Three dimensions of this consensus are discussed: kinds of causes, a continuum of traits ranging from monogenetic diseases to car accidents, and different kinds of determination due to different norms of reaction. On this basis, this article explicates in which sense the interactionist consensus presupposes the innate?acquired distinction. After a descriptive Part 1, Part 2 reviews why the innate?acquired distinction is under attack (...) in contemporary philosophy of biology. Three arguments are then presented to provide a limited and pragmatic defense of the distinction: an epistemic, a conceptual, and a historical argument. If interpreted in a certain manner, and if the pragmatic goals of prevention and treatment are taken into account, then the innate?acquired distinction can be a useful epistemic tool. It can help, first, to understand that genetic determination does not mean fatalism, and, second, to maintain a system of checks and balances in the continuing nature?nurture debates. (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)

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)

, 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)

Can a heritability value tell us something about the weight of genetic versus environmental causes that have acted in the development of a particular individual? Two possible questions arise. Q1: what portion of the phenotype of X is due to its genes and what portion to its environment? Q2: what portion of X’s phenotypic deviation from the mean is a result of its genetic deviation and what portion a result of its environmental deviation? An answer to Q1 provides the full (...) information about X’s development, while an answer to Q2 leaves out a large portion unexplained—that portion which corresponds to the phenotypic mean. Q1 is unanswerable, but I show it is nevertheless legitimate under certain quantitative genetics models. With regard to Q2, opinions in the philosophical and biological literature differ as to its legitimacy. I argue that not only is it legitimate, but in particular, under a few simplifying assumptions, it allows for a quantitative probabilistic answer: for normally distributed quantitative traits with no G-E correlation or statistical G × E interaction, we can assess the probability that X’s genes had a greater effect than its environment on its deviation from the mean population value. This probability is expressed as a function the heritability and the individual’s phenotypic value; we can also provide a quantitative probabilistic answer to Q2 for an arbitrary individual where the probability is a function only of heritability. (shrink)

According to The Bell Curve, Black Americans are genetically inferior to Whites. That's not the only point in Richard Herrnstein and Charles Murray's book. They also argue that there is something called "general intelligence" which is measured by IQ tests, socially important, and 60 percent "heritable" within whites. (I'll explain heritability below.) But the claim about genetic inferiority is my target here. It has been subject to wide-ranging criticism since the book was first published last year. Those criticisms, however, have (...) missed its deepest flaws. Indeed, the Herrnstein/Murray argument depends on conceptual confusions that have been tacitly accepted to some degree by many of the book's sharpest critics. (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.

Comparisons of causal efficacy are ubiquitous in the practice of science and indeed everyday life. I focus on just one aspect of this task – one to my knowledge nowhere yet addressed satisfactorily – namely, comparing the efficacies of two causes that work in apparently incommensurable ways. Contrary to common opinion I argue that, to be comparable, it is neither necessary nor sufficient that two causes also be commensurable.

This edited collection showcases some of the best recent research in the philosophy of science. It comprises of thematically arranged papers presented at the 5th conference of the European Philosophy of Science Association (EPSA15), covering a broad variety of topics within general philosophy of science, and philosophical issues pertaining to specific sciences. The collection will appeal to researchers with an interest in the philosophical underpinnings of their own discipline, and to philosophers who wish to study the latest work on the (...) themes discussed. (shrink)

Okasha claims at the outset of his book "Evolution and the Levels of Selection" (2006) that the Price equation lays bare the fundamentals underlying all selection phenomena. However, the thoroughness of his subsequent analysis of multi-level selection theories leads him to abandon his fundamentalist commitments. At critical points he invokes cost benefit analyses that sometimes favors the Price approach and sometimes the contextual approach, sometimes favors MLS1 and sometimes MLS2. And although he doesn’t acknowledge it, even the Price approach breaks (...) down into a family of alternative equations that parse the causes in different ways, none of which is uniquely correct and none of which achieves the ultimate isolation of effects due to what Okasha believes are the fundamental causes. I argue that his book provides good reason to re-conceive our understanding of evolutionary theorizing in terms of a toolbox view (developed here) and to stop subjecting the analyses of evolutionary concepts to a universalist standard. (shrink)

The idea that some characteristics of an organism are explained by the organism's intrinsic nature, whilst others reflect the influence of the environment is an ancient one. It has even been argued that this distinction is itself part of the evolved psychology of the human species. The distinction played an important role in the history of philosophy as the locus of the dispute between Rationalism and Empiricism discussed in another entry in this encyclopedia. This entry, however, focuses on twentieth-century accounts (...) of the innate/acquired distinction. These accounts have for the most part been inspired by the sciences of mind and behaviour. (shrink)

Biologists and philosophers of science have recently called for an extension of evolutionary theory. This so-called ‘extended evolutionary synthesis’ seeks to integrate developmental processes, extra-genetic forms of inheritance, and niche construction into evolutionary theory in a central way. While there is often agreement in evolutionary biology over the existence of these phenomena, their explanatory relevance is questioned. Advocates of EES posit that their perspective offers better explanations than those provided by ‘standard evolutionary theory’. Still, why this would be the case (...) is unclear. Usually, such claims assume that EES’s superior explanatory status arises from the pluralist structure of EES, its different problem agenda, and a growing body of evidence for the evolutionary relevance of developmental phenomena. However, what is usually neglected in this debate is a discussion of what the explanatory standards of EES actually are, and how they differ from prevailing standards in SET. In other words, what is considered to be a good explanation in EES versus SET? To answer this question, we present a theoretical framework that evaluates the explanatory power of different evolutionary explanations of the same phenomena. This account is able to identify criteria for why and when evolutionary explanations of EES are better than those of SET. Such evaluations will enable evolutionary biology to find potential grounds for theoretical integration. (shrink)

The probability that the fitter of two alleles will increase in frequency in a population goes up as the product of N (the effective population size) and s (the selection coefficient) increases. Discovering the distribution of values for this product across different alleles in different populations is a very important biological task. However, biologists often use the product Ns to define a different concept; they say that drift “dominates” selection or that drift is “stronger than” selection when Ns is much (...) smaller than some threshold quantity (e.g., ½) and that the reverse is true when Ns is much larger than that threshold. We argue that the question of whether drift dominates selection for a single allele in a single population makes no sense. Selection and drift are causes of evolution, but there is no fact of the matter as to which cause is stronger in the evolution of any given allele. (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)

The paper addresses the question of whether heritability can be useful in establishing genetics as an explanation for an individual’s display of some trait or behavior. After reviewing the fundamental philosophical challenge to heritability—that heritability is a population level measure—an argument is presented for rethinking the role heritability occupies in both causal and explanatory claims. It is argued that heritability can be useful for genetically based explanations of individual traits, if the conditions for proper genetic explanation are modestly reconceived, and (...) the measure is seen as an evidential tool which conforms to standard methods for determining causal factors. (shrink)

Selection explanations explain some non-accidental generalizations in virtue of a selection process. Such explanations are not particulaizable - they do not transfer as explanations of the instances of such generalizations. This is unlike many explanations in the physical sciences, where the explanation of the general fact also provides an explanation of its instances (i.e. standard D-N explanations). Are selection explanations (e.g. in biology) therefore a different kind of explanation? I argue that to understand this issue, we need to see that (...) a standard D-N explanation of some non-accidental generalization (al Fs are Gs) may also ipso facto explain its contrapositive (all non-Gs are non-Fs), but the explanation is particularizable with respect to the former but not to the latter. This can be seen by noting that the Raven Paradox counterexample to the H-D model of confirmation also generates a counterexample to the D-N model of explanation (all ravens are black does not explain why the non-black shoe is a non-raven). In such cases it is natural to take the generalization with the positive predicates to have a particularizable explanation. However, this need not be the case, and in selection explanations it is the generalization with the positive predicates whose explanation is no particularizable. Thus there is no need to suppose that selection explanations are fundamentally different. (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.

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)

In reworking a variety of biological concepts, Developmental Systems Theory (DST) has made frequent use of parity of reasoning. We have done this to show, for instance, that factors that have similar sorts of impact on a developing organism tend nevertheless to be invested with quite different causal importance. We have made similar arguments about evolutionary processes. Together, these analyses have allowed DST not only to cut through some age-old muddles about the nature of development, but also to effect a (...) long-delayed reintegration of development into evolutionary theory. Our penchant for causal symmetry, however (or 'causal democracy', as it has recently been termed), has sometimes been misunderstood. This paper shows that causal symmetry is neither a platitude about multiple influences nor a denial of useful distinctions, but a powerful way of exposing hidden assumptions and opening up traditional formulations to fruitful change. (shrink)

How is the human tendency and ability to collaborate acquired and how did it evolve? This paper explores the ontogeny and evolution of human collaboration using a combination of theoretical and empirical resources. We present a game theoretic model of the evolution of learning in the Stag Hunt game, which predicts the evolution of a built-in cooperative bias. We then survey recent empirical results on the ontogeny of collaboration in humans, which suggest the ability to collaborate is developmentally stable across (...) a range of environments. Lastly, we use an account of innateness developed by Ariew (Philos Sci 63:S19–S27, 1996) and Sober (Routledge encyclopedia of philosophy. Routledge, London, pp 794–797, 1998) to assess the extent that (1) the model predicts the fixation of innate collaboration and (2) the empirical studies show a human’s ability to collaborate to be innate. (shrink)