This paper examines the phenomenon of ‘interactive kinds’ first identified by Ian Hacking. An interactive kind is one that is created or significantly modified once a concept of it has been formulated and acted upon in certain ways. Interactive kinds may also ‘loop back’ to influence our concepts and classifications. According to Hacking, interactive kinds are found exclusively in the human domain. After providing a general account of interactive kinds and outlining their philosophical significance, I argue that they are not (...) confined to the human realm, but that they can also occur elsewhere. Hence, I conclude by arguing that interactive kinds pose a challenge to scientific realism about kinds by making it difficult to make a distinction between real and non-real kinds. (shrink)

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)

Woodward's long awaited book is an attempt to construct a comprehensive account of causation explanation that applies to a wide variety of causal and explanatory claims in different areas of science and everyday life. The book engages some of the relevant literature from other disciplines, as Woodward weaves together examples, counterexamples, criticisms, defenses, objections, and replies into a convincing defense of the core of his theory, which is that we can analyze causation by appeal to the notion of manipulation.

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)

This paper defends the notions of an interactive kind and a looping effect as features of social and human scientific classifications and aims to give a realist interpretation of them. I argue that interactive kinds can best be modeled as a special case of changing causal property cluster kinds. In order to do so, I develop a typology of looping effects according to the sort of entities that are affected, the main types of which are individual-looping, category-looping, and kind-looping. Based (...) on this distinction, I identify interactive kinds as those causal property cluster kinds that are subjected to kind-looping. (shrink)

The notion of 'natural kinds' has been central to contemporary discussions of metaphysics and philosophy of science. Although explicitly articulated by nineteenth-century philosophers like Mill, Whewell and Venn, it has a much older history dating back to Plato and Aristotle. In recent years, essentialism has been the dominant account of natural kinds among philosophers, but the essentialist view has encountered resistance, especially among naturalist metaphysicians and philosophers of science. Informed by detailed examination of classification in the natural and social sciences, (...) this book argues against essentialism and for a naturalist account of natural kinds. By looking at case studies drawn from diverse scientific disciplines, from fluid mechanics to virology and polymer science to psychiatry, the author argues that natural kinds are nodes in causal networks. On the basis of this account, he maintains that there can be natural kinds in the social sciences as well as the natural sciences. (shrink)

Between 2001 and 2006 there was an ‘epidemic’ of complete withdrawal from daily life among numerous children in refugee families seeking asylum in Sweden. It became embedded in many distinct controversies, including the politics of immigration, and acrimonious disagreements between pediatricians dealing with individual families, and government-employed sociologists commissioned to report on what was going on. Most of the cases resolved themselves when an amnesty was agreed in 2006, although there remain many doubts about the statistics. After describing this phenomenon, (...) the paper proposes a model called Imitation & Internalisation. Most of the children may have begun by imitating others who had fallen ill, but soon internalized it to the extent that it became an integral part of their psychophysical and social constitution. The model can be applied to phenomena as diverse as hypnotism, the placebo effect, and catching faith by association with believers. (shrink)

In Concepts, Kinds, and Cognitive Development, Frank C. Keil provides a coherent account of how concepts and word meanings develop in children, adding to our understanding of the representational nature of concepts and word meanings at all ages. Keil argues that it is impossible to adequately understand the nature of conceptual representation without also considering the issue of learning. Weaving together issues in cognitive development, philosophy, and cognitive psychology, he reconciles numerous theories, backed by empirical evidence from nominal kinds studies, (...) natural-kinds studies, and studies of fundamental categorical distinctions. He shows that all this evidence, when put together, leads to a better understanding of semantic and conceptual development. The book opens with an analysis of the problems of modeling qualitative changes in conceptual development, investigating how concepts of natural kinds, nominal kinds, and artifacts evolve. The studies on nominal kinds document a powerful and unambiguous developmental pattern indicating a shift from a reliance on global tabulations of characteristic features to what appears to be a small set of defining ones. The studies on natural kinds document an analogous shift toward a core theory instead of simple definition. Both sets of studies are strongly supported by cross cultural data. While these patterns seem to suggest that the young child organizes concepts according to characteristic features, Keil argues that there is a framework of conceptual categories and causal beliefs that enables even very young children to understand kinds at a deeper, theoretically guided, level. This account suggests a new way of understanding qualitative change and carries strong implications for how concepts are represented at any point in development. A Bradford Book. (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)

is a term introduced by Ian Hacking to refer to the kinds of people—child abusers, pregnant teenagers, the unemployed—studied by the human sciences. Hacking argues that classifying and describing human kinds results in feedback, which alters the very kinds under study. This feedback results in human kinds having histories totally unlike those of natural kinds (such as gold, electrons and tigers), leading Hacking to conclude that human kinds are radically unlike natural kinds. Here I argue that Hacking's argument fails and (...) that he has not demonstrated that human kinds cannot be natural kinds. Introduction Natural kinds Hacking's feedback mechanisms 3.1 Cultural feedback 3.2 Conceptual feedback. (shrink)

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)

Behavioral genetics and cultural evolution have both revolutionized our understanding of human behavior – largely independent of each other. Here, we reconcile these two fields under a dual inheritance framework, offering a more nuanced understanding of the interaction between genes and culture. Going beyond typical analyses of gene–environment interactions, we describe the cultural dynamics that shape these interactions by shaping the environment and population structure. A cultural evolutionary approach can explain, for example, how factors such as rates of innovation and (...) diffusion, density of cultural subgroups, and tolerance for behavioral diversity impact heritability estimates, thus yielding predictions for different social contexts. Moreover, when cumulative culture functionally overlaps with genes, genetic effects become masked, unmasked, or even reversed, and the causal effects of an identified gene become confounded with features of the cultural environment. The manner of confounding is specific to a particular society at a particular time, but a WEIRD (western, educated, industrialized, rich, and democratic) sampling problem obscures this boundedness. Cultural evolutionary dynamics are typically missing from models of gene-to-phenotype causality, hindering generalizability of genetic effects across societies and across time. We lay out a reconciled framework and use it to predict the ways in which heritability should differ between societies, between socioeconomic levels, and other groupings within some societies but not others, and over the life course. An integrated cultural evolutionary behavioral genetic approach cuts through the nature–nurture debate and helps resolve controversies in topics such as IQ. (shrink)

Genome-wide association studies of human complex traits have provided us with new estimates of heritability. These estimates foreground the question of genetic causation. After having presen...

In the last third of the twentieth century, humanists and social scientists argued that attention to genetics would heighten already‐existing genetic determinism, which in turn would intensify negative social outcomes, especially sexism, racism, ableism, and harshness to criminals. They assumed that laypeople are at risk of becoming genetic essentialists. I will call this the “laypeople are genetic essentialists model.” This model has not accurately predicted psychosocial impacts of findings from genetics research. I will be arguing that the failure of the (...) model can be traced to its inability to recognize the complexity of laypeople’s attitudes; its incorrect theory of how beliefs, attitudes, and discourse function; and its blindness to how academics’ own interests can override the available evidence. More specifically, I suggest that the substantial data about laypeople’s deployment of genetics supports what I will call the “laypeople are strategic essentialists model” better than the “laypeople are genetic essentialists model.” The strategic essentialists model holds that people tend to store multiple categories, including multiple causal forces, that they deploy “strategically” to serve context‐dependent goals. It will be difficult for academics to reorient ourselves to model laypeople as sophisticated strategic essentialists rather than as naïve genetic essentialists. Perhaps a little shift, however, will be of value. (shrink)

This paper investigates interactive kinds, a class of kinds suggested by Ian Hacking for which classification generates a feedback loop between the classifiers and what is classified, and argues that human interactive kinds should be distinguished from non-human ones. First, I challenge the claim that there is nothing ontologically special about interactive kinds in virtue of their members being classified as such. To do so, I reject Cooper’s counterexample to Hacking’s thesis that kind descriptions are necessary for intentional action, arguing (...) that classification is required for intentional action. Having considered ways to characterise the metaphysics of interactive kinds and the semantics of kind terms, I argue that the fact that classification facilitates intentional action makes human interactive kinds ontologically distinctive because of the anomalous nature of the change which the kind-classification brings about. I then briefly examine further distinguishing features of human interactive kinds. (shrink)

A high heritability estimate usually corresponds to a situation in which trait variation is largely caused by genetic variation. However, in some cases of gene-environment covariance, causal intuitions about the sources of trait difference can vary, leading experts to disagree as to how the heritability estimate should be interpreted. We argue that the source of contention for these cases is an inconsistency in the interpretation of the concepts ‘genotype’, ‘phenotype’, and ‘environment’. We propose an interpretation of these terms under which (...) trait variance initially caused by genetic variance is subsumed into a heritability for all cases of gene-environment covariance. (shrink)

Gene–environment covariance is the phenomenon whereby genetic differences bias variation in developmental environment, and is particularly problematic for assigning genetic and environmental causation in a heritability analysis. The interpretation of these cases has differed amongst biologists and philosophers, leading some to reject the utility of heritability estimates altogether. This paper examines the factors that influence causal reasoning when G–E covariance is present, leading to interpretive disagreement between scholars. It argues that the causal intuitions elicited are influenced by concepts of agency (...) and blame-worthiness, and are intimately tied with the conceptual understanding of the phenotype under investigation. By considering a phenotype-specific approach, I provide an account as to why causal ascriptions can differ depending on the interpreter. Phenotypes like intelligence, which have been the primary focus of this debate, are more likely to spark disagreement for the interpretation of G–E covariance cases because the concept and ideas about its ‘normal development’ relatively ill-defined and are a subject of debate. I contend that philosophical disagreement about causal attributions in G–E covariance cases are in essence disagreements regarding how a phenotype should be defined and understood. This moves the debate from one of an ontological flavour concerning objective causal claims, to one concerning the conceptual, normative and semantic dependencies. (shrink)

Especially troublesome in this dispute is the status of the natural sciences, and this is where Hacking finds some of his most telling cases, from the conflict ...

The sociogenomics revolution is upon us, we are told. Whether revolutionary or not, sociogenomics is poised to flourish given the ease of incorporating polygenic scores (or PGSs) as “genetic propensities” for complex traits into social science research. Pointing to evidence of ubiquitous heritability and the accessibility of genetic data, scholars have argued that social scientists not only have an opportunity but a duty to add PGSs to social science research. Social science research that ignores genetics is, some proponents argue, at (...) best partial and likely scientifically flawed, misleading, and wasteful. Here, I challenge arguments about the value of genetics for social science and with it the claimed necessity of incorporating PGSs into social science models as measures of genetic influences. In so doing, I discuss the impracticability of distinguishing genetic influences from environmental influences because of non-causal gene–environment correlations, especially population stratification, familial confounding, and downward causation. I explain how environmental effects masquerade as genetic influences in PGSs, which undermines their raison d’être as measures of genetic propensity, especially for complex socially contingent behaviors that are the subject of sociogenomics. Additionally, I draw attention to the partial, unknown biology, while highlighting the persistence of an implicit, unavoidable reductionist genes versus environments approach. Leaving sociopolitical and ethical concerns aside, I argue that the potential scientific rewards of adding PGSs to social science are few and greatly overstated and the scientific costs, which include obscuring structural disadvantages and cultural influences, outweigh these meager benefits for most social science applications. (shrink)

Do newborns think-do they know that 'three' is greater than 'two'? Do they prefer 'right' to 'wrong'? What about emotions--do newborns recognize happiness or anger? If they do, then how are our inborn thoughts and feelings encoded in our bodies? Could they persist after we die? Going all the way back to ancient Greece, human nature and the mind-body link are the topics of age-old scholarly debates. But laypeople also have strong opinions about such matters. Most people believe, for example, (...) that newborn babies don't know the difference between right and wrong-such knowledge, they insist, can only be learned. For emotions, they presume the opposite-that our capacity to feel fear, for example, is both inborn and embodied. These beliefs are stories we tell ourselves about what we know and who we are. They reflect and influence our understanding of ourselves and others and they guide every aspect of our lives. In a twist that could have come out of a Greek tragedy, Berent proposes that our errors are our fate. These mistakes emanate from the very principles that make our minds tick: our blindness to human nature is rooted in human nature itself. An intellectual journey that draws on philosophy, anthropology, linguistics, cognitive science, and Berent's own cutting-edge research, The Blind Storyteller grapples with a host of provocative questions, from why we are so infatuated with our brains to what happens when we die. The end result is a startling new perspective on our humanity. (shrink)

Purpose Genetic research, via the mainstream media, presents the public with novel, profound findings almost on a daily basis. However, it is not clear how much laypeople understand these presentations and how they integrate such new findings into their knowledge base. Genetic knowledge (GK), existing causal beliefs, and genetic essentialist tendencies (GET) have been implicated in such processes; the current study assesses the relationships between these elements and how brief presentations of media releases of scientific findings about genetics are consumed (...) and affect the readers. -/- Methods An Australian national survey of GK, GET, and existing causal beliefs about health phenomena (heart disease and obesity) was conducted. Participants were also exposed to news headlines that offered genetic and non-genetic partial explanations of the same health phenomena and reported their evaluations of these headlines, as well as the effects of the headlines on their personal understanding of the health phenomena. -/- Results GK was negatively-associated with GET. Whereas GK did not directly predict the evaluation and effects of the genetic headlines, GET did. GK predicted the effects of the headlines indirectly via GET and via GET and existing causal beliefs. -/- Conclusion GET seem to predict unwarranted effects of exposure to news headlines about genetic science, whereas GK seems to indirectly mitigate the same unwarranted effects. (shrink)